Volume 12, Issue 13

COVID-19
Serum IgM against SARS-CoV-2 correlates with in-hospital mortality in severe/critical patients with COVID-19 in Wuhan, China

Xintian Liu, Xuan Zheng, Bo Liu, Mingxiang Wu, Zhenlu Zhang, Gangcheng Zhang, Xi Su,

https://doi.org/10.18632/aging.103417 pp 12432—12440

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Liu X, Zheng X, Liu B, Wu M, Zhang Z, Zhang G, Su X, . Serum IgM against SARS-CoV-2 correlates with in-hospital mortality in severe/critical patients with COVID-19 in Wuhan, China. . 12:12432-12440. https://doi.org/10.18632/aging.103417

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                TY  - JOUR
                AU  - Liu, Xintian 
                AU  - Zheng, Xuan 
                AU  - Liu, Bo 
                AU  - Wu, Mingxiang 
                AU  - Zhang, Zhenlu 
                AU  - Zhang, Gangcheng 
                AU  - Su, Xi 
                TI  - Serum IgM against SARS-CoV-2 correlates with in-hospital mortality in severe/critical patients with COVID-19 in Wuhan, China
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103417
                DO  - 10.18632/aging.103417
                SP  - 12432
                EP  - 12440
                PY  - 
                AB  - Severe/critical patients with coronavirus disease 2019 (COVID-19) have become the central issue in the current global pandemic due to their high mortality rate. However, the relationship between antibody response and clinical outcomes has not been well described in this group. We conducted a single-center, retrospective, cohort study to investigate the relationship between serum immunoglobulin G (IgG) and IgM and clinical outcomes in severe/critical patients with COVID-19. Seventy-nine severe/critical patients with COVID-19 admitted in Wuhan Asia General Hospital in Wuhan, China during January 22, 2020 to March 6, 2020 were included. Serum antibodies were measured at day 25 (SD, 7) post illness onset. The median IgG titer was 113 (IQR 81-167) AU/ml, and IgM titer was 50 (IQR, 23-105) AU/ml. Patients whose IgM titer &#x2265; 50 AU/ml had higher in-hospital mortality (p=0.026). IgM titer &#x2265; 50 AU/ml was also correlated with higher incidences of Acute Respiratory Distress Syndrome (ARDS) and sepsis shock. Antibody remeasurements were performed in 42 patients, where IgM titer declined significantly in survivors (p=0.031). Serum IgM titer changes according to the COVID-19 progression. The severe/critical patients with COVID-19 have a higher risk of clinical adverse events when IgM titer &#x2265; 50 AU/ml. Further decreasing of IgM could imply a better outcome in severe/critical cases.
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Protein and calorie restriction may improve outcomes in living kidney donors and kidney transplant recipients

Franny Jongbloed, Ron W.F. de Bruin, Harry Van Steeg, Piet Beekhof, Paul Wackers, Dennis A. Hesselink, Jan H.J. Hoeijmakers, Martijn E.T. Dollé, Jan N.M. IJzermans,

https://doi.org/10.18632/aging.103619 pp 12441—12467

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Jongbloed F, de Bruin RW, Steeg HV, Beekhof P, Wackers P, Hesselink DA, Hoeijmakers JH, Dollé ME, IJzermans JN, . Protein and calorie restriction may improve outcomes in living kidney donors and kidney transplant recipients. . 12:12441-12467. https://doi.org/10.18632/aging.103619

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                TY  - JOUR
                AU  - Jongbloed, Franny 
                AU  - de Bruin, Ron W.F. 
                AU  - Steeg, Harry Van 
                AU  - Beekhof, Piet 
                AU  - Wackers, Paul 
                AU  - Hesselink, Dennis A. 
                AU  - Hoeijmakers, Jan H.J. 
                AU  - Dollé, Martijn E.T. 
                AU  - IJzermans, Jan N.M. 
                TI  - Protein and calorie restriction may improve outcomes in living kidney donors and kidney transplant recipients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103619
                DO  - 10.18632/aging.103619
                SP  - 12441
                EP  - 12467
                PY  - 
                AB  - Previously, we and others showed that dietary restriction protects against renal ischemia-reperfusion injury in animals. However, clinical translation of preoperative diets is scarce, and in the setting of kidney transplantation these data are lacking. In this pilot study, we investigated the effects of five days of a preoperative protein and caloric dietary restriction (PCR) diet in living kidney donors on the perioperative effects in donors, recipients and transplanted kidneys. Thirty-five kidney donors were randomized into either the PCR, 30% calorie and 80% protein reduction, or control group without restrictions. Adherence to the diet and kidney function in donors and their kidney recipients were analyzed. Perioperative kidney biopsies were taken in a selected group of transplanted kidneys for gene expression analysis. All donors adhered to the diet. From postoperative day 2 up until month 1, kidney function of donors was significantly better in the PCR-group. PCR-donor kidney recipients showed significantly improved kidney function and lower incidence of slow graft function and acute rejection. PCR inhibited cellular immune response pathways and activated stress-resistance signaling. These observations are the first to show that preoperative dietary restriction induces postoperative recovery benefits in humans and may be beneficial in clinical settings involving ischemia-reperfusion injury.
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COVID-19
Questionnaire assessment helps the self-management of patients with inflammatory bowel disease during the outbreak of Coronavirus Disease 2019

Meiping Yu, Zhenghao Ye, Yu Chen, Tingting Qin, Jiguang Kou, De’an Tian, Fang Xiao,

https://doi.org/10.18632/aging.103525 pp 12468—12478

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Yu M, Ye Z, Chen Y, Qin T, Kou J, Tian D, Xiao F, . Questionnaire assessment helps the self-management of patients with inflammatory bowel disease during the outbreak of Coronavirus Disease 2019. . 12:12468-12478. https://doi.org/10.18632/aging.103525

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                TY  - JOUR
                AU  - Yu, Meiping 
                AU  - Ye, Zhenghao 
                AU  - Chen, Yu 
                AU  - Qin, Tingting 
                AU  - Kou, Jiguang 
                AU  - Tian, De’an 
                AU  - Xiao, Fang 
                TI  - Questionnaire assessment helps the self-management of patients with inflammatory bowel disease during the outbreak of Coronavirus Disease 2019
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103525
                DO  - 10.18632/aging.103525
                SP  - 12468
                EP  - 12478
                PY  - 
                AB  - Objective: This study aimed to assess the disease conditions of patients with inflammatory bowel disease (IBD) in Hubei Province during the outbreak of Coronavirus Disease 2019 (COVID-19) by questionnaire online and guide their self-management during this epidemic.Results: A total of 102 eligible questionnaires were included. No patient we surveyed reported a diagnosis of COVID-19. Our result showed that 67.86% of patients with ulcerative colitis (UC) and 80.43% of patients with Crohn&apos;s disease (CD) were in remission, 85.29%of patients had a good quality of life. Part of the patients (21.57%) reported their disease conditions worsening. The reduction in physical exercise was a risk factor for worsening conditions (OR=17.593, p=0.009). Some patients reported an alteration of medication regimens during the epidemic.Conclusions: The epidemic of COVID-19 might have a certain impact on many aspects of Hubei IBD patients within four weeks after the traffic control. Doctors could utilize the results from our questionnaire to guide IBD patients&#x2019; self-management.Methods: A questionnaire was designed containing the Harvey-Bradshaw Index (HBI), the 6-point Mayo Score, the short inflammatory bowel disease questionnaire (SIBDQ) and distributed to Hubei IBD patients online within four weeks of traffic control after the outbreak, it also included questions about patients&#x2019; self-reported disease conditions and their epidemiological features of COVID-19.
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COVID-19
A qualitative study of the vocational and psychological perceptions and issues of transdisciplinary nurses during the COVID-19 outbreak

Jing Fan, Kaihui Hu, Xueqin Li, Ying Jiang, Xiang Zhou, Xin Gou, Xinyuan Li,

https://doi.org/10.18632/aging.103533 pp 12479—12492

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Fan J, Hu K, Li X, Jiang Y, Zhou X, Gou X, Li X, . A qualitative study of the vocational and psychological perceptions and issues of transdisciplinary nurses during the COVID-19 outbreak. . 12:12479-12492. https://doi.org/10.18632/aging.103533

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                TY  - JOUR
                AU  - Fan, Jing 
                AU  - Hu, Kaihui 
                AU  - Li, Xueqin 
                AU  - Jiang, Ying 
                AU  - Zhou, Xiang 
                AU  - Gou, Xin 
                AU  - Li, Xinyuan 
                TI  - A qualitative study of the vocational and psychological perceptions and issues of transdisciplinary nurses during the COVID-19 outbreak
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103533
                DO  - 10.18632/aging.103533
                SP  - 12479
                EP  - 12492
                PY  - 
                AB  - Background: Due to its high infectivity and concealment, the coronavirus disease 2019 (COVID-19) outbreak that occurred in Wuhan attracted global attention. A special nursing group of transdisciplinary nurses (TNs) who had not worked in respiratory medicine, infection departments, or emergency and intensive medicine but who accounted for a large proportion of all nurses also drew our attention. Few studies have examined this special group of TNs. Therefore, this study collected the experiences and views of TNs at the forefront of the COVID-19 outbreak to investigate their potential problems.Results: Twenty-five TNs and 19 nurses with experience in infectious diseases (non-TNs) were enrolled in the study. Compared with non-TNs, TNs showed higher levels of perceived stress and relatively less perceived social support. For TNs, the ambiguous roles, transition of operating mode, unfamiliar work content, and reversal of their daily schedule were the most common vocational problems. Additionally, most TNs had psychological problems such as anxiety, pain and insomnia. The incomprehension of parents, concern for family members and long-term isolation were the most common causes of psychological stress.Conclusion: This survey is the first to focus on the group of TNs at the forefront of the COVID-19 outbreak and to investigate their experiences, vocational issues and psychological stresses qualitatively and quantificationally. We found that TNs had more perceived stress and less perceived social support than non-TNs. The vocational and psychological issues of TNs should be highlighted. These findings identify important issues and offer insights into the underlying issues to help TNs ultimately win the battle against novel coronavirus epidemics.Methods: Semi-structured and face-to-face individual interviews and quantitative assessments were conducted. The Braun Clarke Thematic Analysis method and the strategy outlined by Miles and Huberman were used in the data analysis process of the qualitative study. The perceived stress scale and perceived social support scale were utilized to quantificationally evaluate the perceived stress level and the amount of perceived social support. Both qualitative and quantitative methods were adopted to assess the vocational and psychological perceptions and issues.
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COVID-19
Epidemiological, comorbidity factors with severity and prognosis of COVID-19: a systematic review and meta-analysis

Xiaoyu Fang, Shen Li, Hao Yu, Penghao Wang, Yao Zhang, Zheng Chen, Yang Li, Liqing Cheng, Wenbin Li, Hong Jia, Xiangyu Ma,

https://doi.org/10.18632/aging.103579 pp 12493—12503

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Fang X, Li S, Yu H, Wang P, Zhang Y, Chen Z, Li Y, Cheng L, Li W, Jia H, Ma X, . Epidemiological, comorbidity factors with severity and prognosis of COVID-19: a systematic review and meta-analysis. . 12:12493-12503. https://doi.org/10.18632/aging.103579

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                TY  - JOUR
                AU  - Fang, Xiaoyu 
                AU  - Li, Shen 
                AU  - Yu, Hao 
                AU  - Wang, Penghao 
                AU  - Zhang, Yao 
                AU  - Chen, Zheng 
                AU  - Li, Yang 
                AU  - Cheng, Liqing 
                AU  - Li, Wenbin 
                AU  - Jia, Hong 
                AU  - Ma, Xiangyu 
                TI  - Epidemiological, comorbidity factors with severity and prognosis of COVID-19: a systematic review and meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103579
                DO  - 10.18632/aging.103579
                SP  - 12493
                EP  - 12503
                PY  - 
                AB  - A systematic review and meta-analysis was conducted in an attempt to systematically collect and evaluate the associations of epidemiological, comorbidity factors with the severity and prognosis of coronavirus disease 2019 (COVID-19). The systematic review and meta-analysis was conducted according to the guidelines proposed by the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Sixty nine publications met our study criteria, and 61 studies with more than 10,000 COVID-19 cases were eligible for the quantitative synthesis. We found that the males had significantly higher disease severity (RR: 1.20, 95% CI: 1.13-1.27, P &lt;0.001) and more prognostic endpoints. Older age was found to be significantly associated with the disease severity and six prognostic endpoints. Chronic kidney disease contributed mostly for death (RR: 7.10, 95% CI: 3.14-16.02), chronic obstructive pulmonary disease (COPD) for disease severity (RR: 4.20, 95% CI: 2.82-6.25), admission to intensive care unit (ICU) (RR: 5.61, 95% CI: 2.68-11.76), the composite endpoint (RR: 8.52, 95% CI: 4.36-16.65,), invasive ventilation (RR: 6.53, 95% CI: 2.70-15.84), and disease progression (RR: 7.48, 95% CI: 1.60-35.05), cerebrovascular disease for acute respiratory distress syndrome (ARDS) (RR: 3.15, 95% CI: 1.23-8.04), coronary heart disease for cardiac abnormality (RR: 5.37, 95% CI: 1.74-16.54). Our study highlighted that the male gender, older age and comorbidities owned strong epidemiological evidence of associations with the severity and prognosis of COVID-19.
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COVID-19
Risk factors influencing the prognosis of elderly patients infected with COVID-19: a clinical retrospective study in Wuhan, China

Shan Gao, Fang Jiang, Wei Jin, Yuan Shi, Leilei Yang, Yanqiong Xia, Linyan Jia, Bo Wang, Han Lin, Yin Cai, Zhengyuan Xia, Jian Peng,

https://doi.org/10.18632/aging.103631 pp 12504—12516

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Gao S, Jiang F, Jin W, Shi Y, Yang L, Xia Y, Jia L, Wang B, Lin H, Cai Y, Xia Z, Peng J, . Risk factors influencing the prognosis of elderly patients infected with COVID-19: a clinical retrospective study in Wuhan, China. . 12:12504-12516. https://doi.org/10.18632/aging.103631

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                TY  - JOUR
                AU  - Gao, Shan 
                AU  - Jiang, Fang 
                AU  - Jin, Wei 
                AU  - Shi, Yuan 
                AU  - Yang, Leilei 
                AU  - Xia, Yanqiong 
                AU  - Jia, Linyan 
                AU  - Wang, Bo 
                AU  - Lin, Han 
                AU  - Cai, Yin 
                AU  - Xia, Zhengyuan 
                AU  - Peng, Jian 
                TI  - Risk factors influencing the prognosis of elderly patients infected with COVID-19: a clinical retrospective study in Wuhan, China
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103631
                DO  - 10.18632/aging.103631
                SP  - 12504
                EP  - 12516
                PY  - 
                AB  - The mortality rate of elderly patients with Coronavirus Disease 2019 (COVID-19) was significantly higher than the overall mortality rate. However, besides age, leading death risk factors for the high mortality in elderly patients remain unidentified. This retrospective study included 210 elderly COVID-19 patients (aged &#x2265; 65 years), of whom 175 patients were discharged and 35 died. All deceased patients had at least one comorbidity. A significantly higher proportion of patients in the deceased group had cardiovascular diseases (49% vs. 20%), respiratory diseases (51% vs. 11%), chronic kidney disease (29% vs. 5%) and cerebrovascular disease (20% vs. 3%) than that in the discharged group. The median levels of C-reactive protein (125.8mg/L vs. 9.3mg/L) and blood urea nitrogen (7.2mmol/L vs. 4.4mmol/L) were significantly higher and median lymphocyte counts (0.7&#xD7;109/L vs. 1.1&#xD7;109/L) significantly lower in the deceased group than those in the discharged group. The survival curve analysis showed that higher C-reactive protein (&#x2265;5mg/L) plus any other abnormalities of lymphocyte, blood urea nitrogen or lactate dehydrogenase significantly predicted poor prognosis of COVID-19 infected elderly patients. This study revealed that the risk factors for the death in these elderly patients included comorbidities, increased levels of C-reactive protein and blood urea nitrogen, and lymphopenia during hospitalization.
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Untargeted metabolomics for uncovering biological markers of human skeletal muscle ageing

Daniel J. Wilkinson, Giovanny Rodriguez-Blanco, Warwick B. Dunn, Bethan E. Phillips, John P. Williams, Paul L. Greenhaff, Kenneth Smith, Iain J. Gallagher, Philip J. Atherton,

https://doi.org/10.18632/aging.103513 pp 12517—12533

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Wilkinson DJ, Rodriguez-Blanco G, Dunn WB, Phillips BE, Williams JP, Greenhaff PL, Smith K, Gallagher IJ, Atherton PJ, . Untargeted metabolomics for uncovering biological markers of human skeletal muscle ageing. . 12:12517-12533. https://doi.org/10.18632/aging.103513

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                TY  - JOUR
                AU  - Wilkinson, Daniel J. 
                AU  - Rodriguez-Blanco, Giovanny 
                AU  - Dunn, Warwick B. 
                AU  - Phillips, Bethan E. 
                AU  - Williams, John P. 
                AU  - Greenhaff, Paul L. 
                AU  - Smith, Kenneth 
                AU  - Gallagher, Iain J. 
                AU  - Atherton, Philip J. 
                TI  - Untargeted metabolomics for uncovering biological markers of human skeletal muscle ageing
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103513
                DO  - 10.18632/aging.103513
                SP  - 12517
                EP  - 12533
                PY  - 
                AB  - Ageing compromises skeletal muscle mass and function through poorly defined molecular aetiology. Here we have used untargeted metabolomics using UHPLC-MS to profile muscle tissue from young (n=10, 25&#xB1;4y), middle aged (n=18, 50&#xB1;4y) and older (n=18, 70&#xB1;3y) men and women (50:50). Random Forest was used to prioritise metabolite features most informative in stratifying older age, with potential biological context examined using the prize-collecting Steiner forest algorithm embedded in the PIUMet software, to identify metabolic pathways likely perturbed in ageing. This approach was able to filter a large dataset of several thousand metabolites down to subnetworks of age important metabolites. Identified networks included the common age-associated metabolites such as androgens, (poly)amines/amino acids and lipid metabolites, in addition to some potentially novel ageing related markers such as dihydrothymine and imidazolone-5-proprionic acid. The present study reveals that this approach is a potentially useful tool to identify processes underlying human tissue ageing, and could therefore be utilised in future studies to investigate the links between age predictive metabolites and common biomarkers linked to health and disease across age.
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Healthspan pathway maps in C. elegans and humans highlight transcription, proliferation/biosynthesis and lipids

Steffen Möller, Nadine Saul, Alan A. Cohen, Rüdiger Köhling, Sina Sender, Hugo Murua Escobar, Christian Junghanss, Francesca Cirulli, Alessandra Berry, Peter Antal, Priit Adler, Jaak Vilo, Michele Boiani, Ludger Jansen, Dirk Repsilber, Hans Jörgen Grabe, Stephan Struckmann, Israel Barrantes, Mohamed Hamed, Brecht Wouters, Liliane Schoofs, Walter Luyten, Georg Fuellen,

https://doi.org/10.18632/aging.103514 pp 12534—12581

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Möller S, Saul N, Cohen AA, Köhling R, Sender S, Murua Escobar H, Junghanss C, Cirulli F, Berry A, Antal P, Adler P, Vilo J, Boiani M, et al, . Healthspan pathway maps in C. elegans and humans highlight transcription, proliferation/biosynthesis and lipids. . 12:12534-12581. https://doi.org/10.18632/aging.103514

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 TY - JOUR
 AU - Möller, Steffen 
 AU - Saul, Nadine 
 AU - Cohen, Alan A. 
 AU - Köhling, Rüdiger 
 AU - Sender, Sina 
 AU - Murua Escobar, Hugo 
 AU - Junghanss, Christian 
 AU - Cirulli, Francesca 
 AU - Berry, Alessandra 
 AU - Antal, Peter 
 AU - Adler, Priit 
 AU - Vilo, Jaak 
 AU - Boiani, Michele 
 AU - Jansen, Ludger 
 AU - Repsilber, Dirk 
 AU - Grabe, Hans Jörgen 
 AU - Struckmann, Stephan 
 AU - Barrantes, Israel 
 AU - Hamed, Mohamed 
 AU - Wouters, Brecht 
 AU - Schoofs, Liliane 
 AU - Luyten, Walter 
 AU - Fuellen, Georg 
 TI - Healthspan pathway maps in C. elegans and humans highlight transcription, proliferation/biosynthesis and lipids
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103514
 DO - 10.18632/aging.103514
 SP - 12534
 EP - 12581
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Möller, Steffen 
 AU - Saul, Nadine 
 AU - Cohen, Alan A. 
 AU - Köhling, Rüdiger 
 AU - Sender, Sina 
 AU - Murua Escobar, Hugo 
 AU - Junghanss, Christian 
 AU - Cirulli, Francesca 
 AU - Berry, Alessandra 
 AU - Antal, Peter 
 AU - Adler, Priit 
 AU - Vilo, Jaak 
 AU - Boiani, Michele 
 AU - Jansen, Ludger 
 AU - Repsilber, Dirk 
 AU - Grabe, Hans Jörgen 
 AU - Struckmann, Stephan 
 AU - Barrantes, Israel 
 AU - Hamed, Mohamed 
 AU - Wouters, Brecht 
 AU - Schoofs, Liliane 
 AU - Luyten, Walter 
 AU - Fuellen, Georg 
 TI - Healthspan pathway maps in C. elegans and humans highlight transcription, proliferation/biosynthesis and lipids
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103514
 DO - 10.18632/aging.103514
 SP - 12534
 EP - 12581
 PY - 
 AB - The molecular basis of aging and of aging-associated diseases is being unraveled at an increasing pace. An extended healthspan, and not merely an extension of lifespan, has become the aim of medical practice. Here, we define health based on the absence of diseases and dysfunctions. Based on an extensive review of the literature, in particular for humans and C. elegans, we compile a list of features of health and of the genes associated with them. These genes may or may not be associated with survival/lifespan. In turn, survival/lifespan genes that are not known to be directly associated with health are not considered. Clusters of these genes based on molecular interaction data give rise to maps of healthspan pathways for humans and for C. elegans. Overlaying healthspan-related gene expression data onto the healthspan pathway maps, we observe the downregulation of (pro-inflammatory) Notch signaling in humans and of proliferation in C. elegans. We identify transcription, proliferation/biosynthesis and lipids as a common theme on the annotation level, and proliferation-related kinases on the gene/protein level. Our literature-based data corpus, including visualization, should be seen as a pilot investigation of the molecular underpinnings of health in two different species. Web address: http://pathways.h2020awe.eu.
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Modulation of attention networks serving reorientation in healthy aging

Yasra Arif, Rachel K. Spooner, Alex I. Wiesman, Christine M. Embury, Amy L. Proskovec, Tony W. Wilson,

https://doi.org/10.18632/aging.103515 pp 12582—12597

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Arif Y, Spooner RK, Wiesman AI, Embury CM, Proskovec AL, Wilson TW, . Modulation of attention networks serving reorientation in healthy aging. . 12:12582-12597. https://doi.org/10.18632/aging.103515

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                TY  - JOUR
                AU  - Arif, Yasra 
                AU  - Spooner, Rachel K. 
                AU  - Wiesman, Alex I. 
                AU  - Embury, Christine M. 
                AU  - Proskovec, Amy L. 
                AU  - Wilson, Tony W. 
                TI  - Modulation of attention networks serving reorientation in healthy aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103515
                DO  - 10.18632/aging.103515
                SP  - 12582
                EP  - 12597
                PY  - 
                AB  - Orienting attention to behaviorally relevant stimuli is essential for everyday functioning and mainly involves activity in the dorsal and ventral frontoparietal networks. Many studies have shown declines in the speed and accuracy of attentional reallocation with advancing age, but the underlying neural dynamics remain less understood. We investigated this age-related decline using magnetoencephalography (MEG) and a Posner task in 94 healthy adults (22-72 years old). MEG data were examined in the time-frequency domain, and significant oscillatory responses were imaged using a beamformer. We found that participants responded slower when attention reallocation was needed (i.e., the validity effect) and that this effect was positively correlated with age. We also found age-related validity effects on alpha activity in the left parietal and beta in the left frontal-eye fields from 350-950 ms. Overall, stronger alpha and beta responses were observed in younger participants during attention reallocation trials, but this pattern was reversed in the older participants. Interestingly, this alpha validity effect fully mediated the relationship between age and behavioral performance. In conclusion, older adults were slower in reorienting attention and exhibited age-related alterations in alpha and beta responses within parietal and frontal regions, which may reflect increased task demands depleting their compensatory resources.
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Increased expression of connexin 43 in a mouse model of spinal motoneuronal loss

Federica Maria Spitale, Nunzio Vicario, Michelino Di Rosa, Daniele Tibullo, Michele Vecchio, Rosario Gulino, Rosalba Parenti,

https://doi.org/10.18632/aging.103561 pp 12598—12608

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Spitale FM, Vicario N, Rosa MD, Tibullo D, Vecchio M, Gulino R, Parenti R, . Increased expression of connexin 43 in a mouse model of spinal motoneuronal loss. . 12:12598-12608. https://doi.org/10.18632/aging.103561

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                TY  - JOUR
                AU  - Spitale, Federica Maria 
                AU  - Vicario, Nunzio 
                AU  - Rosa, Michelino Di 
                AU  - Tibullo, Daniele 
                AU  - Vecchio, Michele 
                AU  - Gulino, Rosario 
                AU  - Parenti, Rosalba 
                TI  - Increased expression of connexin 43 in a mouse model of spinal motoneuronal loss
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103561
                DO  - 10.18632/aging.103561
                SP  - 12598
                EP  - 12608
                PY  - 
                AB  - Amyotrophic lateral sclerosis (ALS) is one of the most common motoneuronal disease, characterized by motoneuronal loss and progressive paralysis. Despite research efforts, ALS remains a fatal disease, with a survival of 2-5 years after disease onset. Numerous gene mutations have been correlated with both sporadic (sALS) and familiar forms of the disease, but the pathophysiological mechanisms of ALS onset and progression are still largely uncertain. However, a common profile is emerging in ALS pathological features, including misfolded protein accumulation and a cross-talk between neuroinflammatory and degenerative processes. In particular, astrocytes and microglial cells have been proposed as detrimental influencers of perineuronal microenvironment, and this role may be exerted via gap junctions (GJs)- and hemichannels (HCs)-mediated communications. Herein we investigated the role of the main astroglial GJs-forming connexin, Cx43, in human ALS and the effects of focal spinal cord motoneuronal depletion onto the resident glial cells and Cx43 levels. Our data support the hypothesis that motoneuronal depletion may affect glial activity, which in turn results in reactive Cx43 expression, further promoting neuronal suffering and degeneration.
                ER  -

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Obesity is associated with senescence of mesenchymal stromal cells derived from bone marrow, subcutaneous and visceral fat of young mice

Nicola Alessio, Mustafa B. Acar, Ibrahim H. Demirsoy, Tiziana Squillaro, Dario Siniscalco, Giovanni Di Bernardo, Gianfranco Peluso, Servet Özcan, Umberto Galderisi,

https://doi.org/10.18632/aging.103606 pp 12609—12621

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Alessio N, Acar MB, Demirsoy IH, Squillaro T, Siniscalco D, Bernardo GD, Peluso G, Özcan S, Galderisi U, . Obesity is associated with senescence of mesenchymal stromal cells derived from bone marrow, subcutaneous and visceral fat of young mice. . 12:12609-12621. https://doi.org/10.18632/aging.103606

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                TY  - JOUR
                AU  - Alessio, Nicola 
                AU  - Acar, Mustafa B. 
                AU  - Demirsoy, Ibrahim H. 
                AU  - Squillaro, Tiziana 
                AU  - Siniscalco, Dario 
                AU  - Bernardo, Giovanni Di 
                AU  - Peluso, Gianfranco 
                AU  - Özcan, Servet 
                AU  - Galderisi, Umberto 
                TI  - Obesity is associated with senescence of mesenchymal stromal cells derived from bone marrow, subcutaneous and visceral fat of young mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103606
                DO  - 10.18632/aging.103606
                SP  - 12609
                EP  - 12621
                PY  - 
                AB  - White adipose tissue (WAT) is distributed in several depots with distinct metabolic and inflammatory functions. In our body there are subcutaneous (sWAT), visceral (vWAT) and bone marrow (bWAT) fat depots. Obesity affects the size, function and inflammatory state of WATs. In particular, obesity may affect the activity of mesenchymal stromal cells (MSCs) present in WAT. MSCs are a heterogeneous population containing stromal cells, progenitor cells, fibroblasts and stem cells that are able to differentiate among adipocytes, chondrocytes, osteocytes and other mesodermal derivatives.
                In the first study of this kind, we performed a comparison of the effects of obesity on MSCs obtained from sWAT, vWAT and bWAT. Our study showed that obesity affects mainly the biological functions of MSCs obtained from bone marrow and vWAT by decreasing the proliferation rate, reducing the percentage of cells in S phase and triggering senescence. The onset of senescence was confirmed by expression of genes belonging to RB and P53 pathways.
                Our study revealed that the negative consequences of obesity on body physiology may also be related to impairment in the functions of the stromal compartment present in the several adipose tissues. This finding provides new insights as to the targets that should be considered for an effective treatment of obesity-related diseases.
                ER  -

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Fully bayesian longitudinal unsupervised learning for the assessment and visualization of AD heterogeneity and progression

Konstantinos Poulakis, Daniel Ferreira, Joana B. Pereira, Örjan Smedby, Prashanthi Vemuri, Eric Westman,

https://doi.org/10.18632/aging.103623 pp 12622—12647

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Poulakis K, Ferreira D, Pereira JB, Smedby Ö, Vemuri P, Westman E, . Fully bayesian longitudinal unsupervised learning for the assessment and visualization of AD heterogeneity and progression. . 12:12622-12647. https://doi.org/10.18632/aging.103623

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                TY  - JOUR
                AU  - Poulakis, Konstantinos 
                AU  - Ferreira, Daniel 
                AU  - Pereira, Joana B. 
                AU  - Smedby, Örjan 
                AU  - Vemuri, Prashanthi 
                AU  - Westman, Eric 
                TI  - Fully bayesian longitudinal unsupervised learning for the assessment and visualization of AD heterogeneity and progression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103623
                DO  - 10.18632/aging.103623
                SP  - 12622
                EP  - 12647
                PY  - 
                AB  - Tau pathology and brain atrophy are the closest correlate of cognitive decline in Alzheimer&#x2019;s disease (AD). Understanding heterogeneity and longitudinal progression of atrophy during the disease course will play a key role in understanding AD pathogenesis. We propose a framework for longitudinal clustering that simultaneously: 1) incorporates whole brain data, 2) leverages unequal visits per individual, 3) compares clusters with a control group, 4) allows for study confounding effects, 5) provides cluster visualization, 6) measures clustering uncertainty. We used amyloid-&#x3B2; positive AD and negative healthy subjects, three longitudinal structural magnetic resonance imaging scans (cortical thickness and subcortical volume) over two years. We found three distinct longitudinal AD brain atrophy patterns: one typical diffuse pattern (n=34, 47.2%), and two atypical patterns: minimal atrophy (n=23 31.9%) and hippocampal sparing (n=9, 12.5%). We also identified outliers (n=3, 4.2%) and observations with uncertain classification (n=3, 4.2%). The clusters differed not only in regional distributions of atrophy at baseline, but also longitudinal atrophy progression, age at AD onset, and cognitive decline. A framework for the longitudinal assessment of variability in cohorts with several neuroimaging measures was successfully developed. We believe this framework may aid in disentangling distinct subtypes of AD from disease staging.
                ER  -

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Lack of retinoid acid receptor-related orphan receptor alpha accelerates and melatonin supplementation prevents testicular aging

Ramy K. A. Sayed, Doaa M. Mokhtar, Marisol Fernández-Ortiz, José Fernández-Martínez, Paula Aranda-Martínez, Germaine Escames, Darío Acuña-Castroviejo,

https://doi.org/10.18632/aging.103654 pp 12648—12668

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Sayed RKA, Mokhtar DM, Fernández-Ortiz M, Fernández-Martínez J, Aranda-Martínez P, Escames G, Acuña-Castroviejo D, . Lack of retinoid acid receptor-related orphan receptor alpha accelerates and melatonin supplementation prevents testicular aging. . 12:12648-12668. https://doi.org/10.18632/aging.103654

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                TY  - JOUR
                AU  - Sayed, Ramy K. A. 
                AU  - Mokhtar, Doaa M. 
                AU  - Fernández-Ortiz, Marisol 
                AU  - Fernández-Martínez, José 
                AU  - Aranda-Martínez, Paula 
                AU  - Escames, Germaine 
                AU  - Acuña-Castroviejo, Darío 
                TI  - Lack of retinoid acid receptor-related orphan receptor alpha accelerates and melatonin supplementation prevents testicular aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103654
                DO  - 10.18632/aging.103654
                SP  - 12648
                EP  - 12668
                PY  - 
                AB  - The role of retinoid acid receptor-related orphan receptor alpha (ROR&#x3B1;) on male reproductive functions during aging is unclear. Here, we analyze the morphological changes in the testis of both young and aged ROR&#x3B1;-deficient mice, with and without melatonin supplementation. Young mutants showed vacuolation, degeneration and pyknosis of spermatogenic epithelium and Sertoli cells. Aged mutants showed atrophy of the seminiferous tubules and absence of mitotic spermatogenic cells. Absence of sperms in many tubules, loss of acrosomal cap, vacuolation and hypertrophy of Sertoli cells were detected in aged mice, with a significant reduction in the number of seminiferous tubules and a significant increase in the number of Leydig cells and telocytes. Repair in seminiferous tubules and interstitial tissues with enhancement of spermatogenesis was observed in melatonin-treated aged mice. Young mutants overexpressed VEGF that was weaker in aged animals and observed only in the spermatocytes, while melatonin increased VEGF expression in spermatocytes and spermatids. Caspase 3 increased in both young and aged mutant mice in all seminiferous tubules and interstitium; caspase 3 immunostaining in seminiferous tubules, however, showed a normal pattern of apoptosis with melatonin supplementation. The present study reports that age-dependent testicular changes in ROR&#x3B1; mutant mice were recovered by melatonin treatment.
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Extracellular vesicles derived from microRNA-150-5p-overexpressing mesenchymal stem cells protect rat hearts against ischemia/reperfusion

Hesheng Ou, Hongli Teng, Yuwang Qin, Xuelan Luo, Peng Yang, Wenyu Zhang, Wei Chen, Dongning Lv, Huamin Tang,

https://doi.org/10.18632/aging.102792 pp 12669—12683

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Ou H, Teng H, Qin Y, Luo X, Yang P, Zhang W, Chen W, Lv D, Tang H, . Extracellular vesicles derived from microRNA-150-5p-overexpressing mesenchymal stem cells protect rat hearts against ischemia/reperfusion. . 12:12669-12683. https://doi.org/10.18632/aging.102792

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                TY  - JOUR
                AU  - Ou, Hesheng 
                AU  - Teng, Hongli 
                AU  - Qin, Yuwang 
                AU  - Luo, Xuelan 
                AU  - Yang, Peng 
                AU  - Zhang, Wenyu 
                AU  - Chen, Wei 
                AU  - Lv, Dongning 
                AU  - Tang, Huamin 
                TI  - Extracellular vesicles derived from microRNA-150-5p-overexpressing mesenchymal stem cells protect rat hearts against ischemia/reperfusion
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102792
                DO  - 10.18632/aging.102792
                SP  - 12669
                EP  - 12683
                PY  - 
                AB  - An intriguing area of research has demonstrated the ability of extracellular vesicles (EVs) as biological vehicles for microRNAs (miRNAs) transfer. Mesenchymal stem cells (MSCs) produce large amounts of EVs. Rat models of ischemia/reperfusion (I/R) were established to explore the expression profile of thioredoxin-interacting protein (TXNIP), which was then knocked-down to investigate its effects on myocardial remodeling, followed by detection on myocardial infarction size (MIS), myocardial collagen volume fraction (CVF) and cardiomyocyte apoptosis. MSCs-derived EVs carrying miR-150-5p were cultured with neonatal cardiomyocytes under hypoxia/hypoglycemia condition for in vitro exploration and intramyocardially injected into I/R rats for in vivo exploration. I/R-induced rats presented higher TXNIP levels and lower miR-150-5p levels, along with increased cardiomyocyte apoptosis. miR-150-5p in MSCs was transferred through EVs to cardiomyocytes, leading to suppressed myocardial remodeling, as reflected by smaller MIS and CVF and suppressed cardiomyocyte apoptosis. I/R-treated rats injected with MSCs-derived EVs containing miR-150-5p showed a reduction in myocardial remodeling associated with the downregulation of TXNIP, which may be clinically applicable for treatment of I/R.
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Silencing of long non-coding RNA Sox2ot inhibits oxidative stress and inflammation of vascular smooth muscle cells in abdominal aortic aneurysm via microRNA-145-mediated Egr1 inhibition

Huyu Lin, Bin You, Xiandong Lin, Xiaohu Wang, Dongsheng Zhou, Zhiqun Chen, Yuanxiang Chen, Ren Wang,

https://doi.org/10.18632/aging.103077 pp 12684—12702

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Lin H, You B, Lin X, Wang X, Zhou D, Chen Z, Chen Y, Wang R, . Silencing of long non-coding RNA Sox2ot inhibits oxidative stress and inflammation of vascular smooth muscle cells in abdominal aortic aneurysm via microRNA-145-mediated Egr1 inhibition. . 12:12684-12702. https://doi.org/10.18632/aging.103077

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                TY  - JOUR
                AU  - Lin, Huyu 
                AU  - You, Bin 
                AU  - Lin, Xiandong 
                AU  - Wang, Xiaohu 
                AU  - Zhou, Dongsheng 
                AU  - Chen, Zhiqun 
                AU  - Chen, Yuanxiang 
                AU  - Wang, Ren 
                TI  - Silencing of long non-coding RNA Sox2ot inhibits oxidative stress and inflammation of vascular smooth muscle cells in abdominal aortic aneurysm via microRNA-145-mediated Egr1 inhibition
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103077
                DO  - 10.18632/aging.103077
                SP  - 12684
                EP  - 12702
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) have been largely reported to contribute to the development and progression of abdominal aortic aneurysm (AAA), a common vascular degenerative disease. The present study was set out with the aim to investigate the possible role of lncRNA Sox2ot in the development of AAA. In this study, we found that lncRNA Sox2ot and early growth response factor-1 (Egr1) were highly expressed, while microRNA (miR)-145 was poorly expressed in Ang II-induced AAA mice and oxidative stress-provoked vascular smooth muscle cell (VSMC) model. Egr1 was a potential target gene of miR-145, and lncRNA Sox2ot could competitively bind to miR-145 to upregulate Egr1 expression. Overexpression of miR-145-5p was found to attenuate oxidative stress and inflammation by inhibiting Egr1 both in vivo and in vitro, which was counteracted by lncRNA Sox2ot. Taken together, the present study provides evidence that downregulation of lncRNA Sox2ot suppressed the expression of Egr1 through regulating miR-145, thus inhibiting the development of AAA, highlighting a theoretical basis for AAA treatment.
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Epigenomic and genomic analysis of transcriptome modulation in skin cutaneous melanoma

Wuzhen Chen, Pu Cheng, Jingxin Jiang, Yunqing Ren, Dang Wu, Dan Xue,

https://doi.org/10.18632/aging.103115 pp 12703—12725

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Chen W, Cheng P, Jiang J, Ren Y, Wu D, Xue D, . Epigenomic and genomic analysis of transcriptome modulation in skin cutaneous melanoma. . 12:12703-12725. https://doi.org/10.18632/aging.103115

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                TY  - JOUR
                AU  - Chen, Wuzhen 
                AU  - Cheng, Pu 
                AU  - Jiang, Jingxin 
                AU  - Ren, Yunqing 
                AU  - Wu, Dang 
                AU  - Xue, Dan 
                TI  - Epigenomic and genomic analysis of transcriptome modulation in skin cutaneous melanoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103115
                DO  - 10.18632/aging.103115
                SP  - 12703
                EP  - 12725
                PY  - 
                AB  - Skin cutaneous melanoma (SKCM) is characterized by both epigenetic DNA methylation (MET) abnormalities and genomic copy number variations (CNVs). The resulting transcriptome dysregulation promotes progression of many cancers. In this study, DNA copy numbers and MET, as well as mRNA expression, were examined in 466 SKCM samples from The Cancer Genome Atlas. Our results indicate that CNVs-correlated (CNVcor) genes and MET-correlated (METcor) genes are coregulated to a remarkable degree. In addition, integrative multi-omics analysis of both METcor and CNVcor genes revealed four SKCM subtypes with differing prognoses; these subtypes were validated with independent data. Immune cell scores were markedly elevated in the iC1 subtype, which had the best prognosis. Immune cell infiltration correlated with DNA MET or CNV level in SKCM. In the iC3 subtype, which was associated with the most aggressive SKCM cases, FAM135B gene mutation frequencies were increased, while CD8A, GBP5, KIAA0040, and SAMHD1 expression were downregulated, suggesting that these genes play important roles in cancer development and immune responses. Taken together, the results of our epigenetic and genomic transcriptome modulation analysis improve our understanding of SKCM pathobiology and may aid in the development of more effective therapies.
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EZH2-mediated inhibition of microRNA-22 promotes differentiation of hair follicle stem cells by elevating STK40 expression

Bingjie Cai, Min Li, Yunpeng Zheng, Yakun Yin, Fangcao Jin, Xuyang Li, Juan Dong, Xiaoyan Jiao, Xiaojun Liu, Kun Zhang, Dongqin Li, Junmin Wang, Guangwen Yin,

https://doi.org/10.18632/aging.103165 pp 12726—12739

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Cai B, Li M, Zheng Y, Yin Y, Jin F, Li X, Dong J, Jiao X, Liu X, Zhang K, Li D, Wang J, Yin G, . EZH2-mediated inhibition of microRNA-22 promotes differentiation of hair follicle stem cells by elevating STK40 expression. . 12:12726-12739. https://doi.org/10.18632/aging.103165

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                TY  - JOUR
                AU  - Cai, Bingjie 
                AU  - Li, Min 
                AU  - Zheng, Yunpeng 
                AU  - Yin, Yakun 
                AU  - Jin, Fangcao 
                AU  - Li, Xuyang 
                AU  - Dong, Juan 
                AU  - Jiao, Xiaoyan 
                AU  - Liu, Xiaojun 
                AU  - Zhang, Kun 
                AU  - Li, Dongqin 
                AU  - Wang, Junmin 
                AU  - Yin, Guangwen 
                TI  - EZH2-mediated inhibition of microRNA-22 promotes differentiation of hair follicle stem cells by elevating STK40 expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103165
                DO  - 10.18632/aging.103165
                SP  - 12726
                EP  - 12739
                PY  - 
                AB  - Hair follicle stem cells (HFSCs) contribute to the regeneration of hair follicles (HFs), thus accelerating hair growth. microRNAs (miRs) are potential regulators in various cellular processes, including HFSC proliferation and differentiation. This study proposed a potential target, enhancer of zeste homolog 2 (EZH2) for facilitating hair growth, due to its function over HFSC activities by mediating the miR-22/serine/threonine kinase 40 (STK40)/myocyte enhancer factor 2 (MEF2)/alkaline phosphatase (ALP) axis. Gain- and loss-of-function approaches were adopted to explore the roles of EZH2, miR-22, and STK40 in the proliferation and apoptosis of HFSCs, along with the functional relevance of MEF2-ALP activity. STK40 was elevated during HFSC differentiation, which was found to facilitate HFSC proliferation, but impede their apoptosis by activating MEF2-ALP. Mechanically, miR-22 targeted and inversely regulated STK40, which inhibited MEF2-ALP activity to impede HFSC proliferation and differentiation. Moreover, EZH2 elevated the STK40 expression by repressing miR-22 to promote the proliferation and differentiation of HFSCs. Furthermore, in vivo experiments further validated the roles of EZH2 and STK40 on hair follicle neogenesis and hair growth. Collectively, EZH2 elevated the STK40 expression by downregulating miR-22, consequently accelerating differentiation of HFSCs and hair growth, which sheds light on the underlying molecular mechanism responsible for hair growth.
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PAK4 suppresses TNF-induced release of endothelial microparticles in HUVECs cells

Shouqin Zhang, Yingjie Yin, Congye Li, Yi Zhao, Qixing Wang, Xiangyu Zhang,

https://doi.org/10.18632/aging.103173 pp 12740—12749

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Zhang S, Yin Y, Li C, Zhao Y, Wang Q, Zhang X, . PAK4 suppresses TNF-induced release of endothelial microparticles in HUVECs cells. . 12:12740-12749. https://doi.org/10.18632/aging.103173

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                TY  - JOUR
                AU  - Zhang, Shouqin 
                AU  - Yin, Yingjie 
                AU  - Li, Congye 
                AU  - Zhao, Yi 
                AU  - Wang, Qixing 
                AU  - Zhang, Xiangyu 
                TI  - PAK4 suppresses TNF-induced release of endothelial microparticles in HUVECs cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103173
                DO  - 10.18632/aging.103173
                SP  - 12740
                EP  - 12749
                PY  - 
                AB  - Tumor necrosis factor-&#x3B1; (TNF) is a pro-inflammatory cytokine upregulated in many inflammatory diseases, and a potent inducer of endothelial cell-derived microparticle (EMP) formation. In this study, we identified the protein kinase PAK4 as a key regulator of the TNF-induced EMP release from human umbilical vein endothelial cells (HUVECs). TNF induces dose- and time-dependent EMP release and downregulation of PAK4 and upstream cdc42 in HUVECs. PAK4 suppression or inhibition of its kinase activity increases TNF-induced EMP release and apoptosis in HUVECs, while PAK4 overexpression reduces EMP release and apoptosis in TNF-stimulated cells. Collectively, these data indicate that PAK4 suppresses TNF-induced EMP generation occurring during apoptosis, and suggest that modulation of PAK4 activity may represent a novel approach to suppress the TNF-induced EMP levels in pro-inflammatory disorders and other pathological conditions.
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Navitoclax (ABT263) reduces inflammation and promotes chondrogenic phenotype by clearing senescent osteoarthritic chondrocytes in osteoarthritis

Hao Yang, Cheng Chen, Hao Chen, Xiaojun Duan, Juan Li, Yi Zhou, Weinan Zeng, Liu Yang,

https://doi.org/10.18632/aging.103177 pp 12750—12770

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Yang H, Chen C, Chen H, Duan X, Li J, Zhou Y, Zeng W, Yang L, . Navitoclax (ABT263) reduces inflammation and promotes chondrogenic phenotype by clearing senescent osteoarthritic chondrocytes in osteoarthritis. . 12:12750-12770. https://doi.org/10.18632/aging.103177

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                TY  - JOUR
                AU  - Yang, Hao 
                AU  - Chen, Cheng 
                AU  - Chen, Hao 
                AU  - Duan, Xiaojun 
                AU  - Li, Juan 
                AU  - Zhou, Yi 
                AU  - Zeng, Weinan 
                AU  - Yang, Liu 
                TI  - Navitoclax (ABT263) reduces inflammation and promotes chondrogenic phenotype by clearing senescent osteoarthritic chondrocytes in osteoarthritis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103177
                DO  - 10.18632/aging.103177
                SP  - 12750
                EP  - 12770
                PY  - 
                AB  - Cell senescence is a chronic process associated with age-related degenerative diseases such as osteoarthritis (OA). Senescent cells (SnCs) accumulate in the articular cartilage and synovium, leading to OA pathologies. The accumulation of SnCs in the cartilage results in a senescence-associated secretory phenotype (SASP) and age-related inflammation and dysfunction. Selective removal of SnCs by senolytic agent as a therapeutic strategy has been developed recently. In this study, we examined the ability of the senolytic drug ABT263 (navitoclax) to clear SnCs and further evaluated the therapeutic effect of ABT263 on post-traumatic OA. Monolayer and 3D pellet cultured osteoarthritic chondrocytes were used to evaluate the effect of ABT263 in vitro and a DMM rat model was established for in vivo experiments. We found that ABT263 reduced the expression of inflammatory cytokines and promoted cartilage matrix aggregation in OA chondrocyte pellet culture by inducing SnC apoptosis. Moreover, OA pathological changes in the cartilage and subchondral bone in post-traumatic OA rat were alleviated by ABT263 intra-articular injection. These results demonstrated that ABT263 not only improves inflammatory microenvironment but also promotes cartilage phenotype maintenance in vitro. Furthermore, ABT263 might play a protective role against post-traumatic OA development. Therefore, strategies targeting SnC elimination might be promising for the clinical therapy of OA.
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HOTAIR expands the population of prostatic cancer stem-like cells and causes Docetaxel resistance via activating STAT3 signaling

Ning Wang, Yaodong Jiang, Shidong Lv, Haoran Wen, Dehua Wu, Qiang Wei, Qiang Dang,

https://doi.org/10.18632/aging.103188 pp 12771—12782

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Wang N, Jiang Y, Lv S, Wen H, Wu D, Wei Q, Dang Q, . HOTAIR expands the population of prostatic cancer stem-like cells and causes Docetaxel resistance via activating STAT3 signaling. . 12:12771-12782. https://doi.org/10.18632/aging.103188

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                TY  - JOUR
                AU  - Wang, Ning 
                AU  - Jiang, Yaodong 
                AU  - Lv, Shidong 
                AU  - Wen, Haoran 
                AU  - Wu, Dehua 
                AU  - Wei, Qiang 
                AU  - Dang, Qiang 
                TI  - HOTAIR expands the population of prostatic cancer stem-like cells and causes Docetaxel resistance via activating STAT3 signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103188
                DO  - 10.18632/aging.103188
                SP  - 12771
                EP  - 12782
                PY  - 
                AB  - Prostatic cancer stem-like cells (PCSLCs) play an essential role in PCa development. Accumulating evidence suggests that androgen deprivation therapy (ADT) or chemotherapy using docetaxel could expand the population of PCSLCs. Therefore, understanding the underlying mechanisms responsible for PCSLCs expansion has broadly scientific interest. Here, our results revealed that lncRNA HOTAIR could increase PCSLCs population via activating STAT3 signaling. Mechanistically, HOTAIR functioned as miR-590-5p sponge and prevented it from targeting the 3&#x2019;UTR of IL-10, one upstream molecule of STAT3 signaling, leading to IL-10 upregulation and STAT3 activation. We also found that HOTAIR was required and sufficient to cause Docetaxel resistance (DocR) in C4-2 PCa cells. Moreover, our in vivo animal study also confirmed that Du145-HOTAIR mice had a faster tumor growth rate and a poorer survival rate compared to control cohorts. Our data build compelling rationale to target HOTAIR for the depletion of PCSLCs and alleviation of Docetaxel resistance.
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Genetic association of hypoxia inducible factor 1-alpha (HIF1A) Pro582Ser polymorphism with risk of diabetes and diabetic complications

Huan Ren, Jian-Quan Luo, Yong-Chao Gao, Man-Yun Chen, Xiao-Ping Chen, Hong-Hao Zhou, Ying Jiang, Wei Zhang,

https://doi.org/10.18632/aging.103213 pp 12783—12798

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Ren H, Luo J, Gao Y, Chen M, Chen X, Zhou H, Jiang Y, Zhang W, . Genetic association of hypoxia inducible factor 1-alpha (HIF1A) Pro582Ser polymorphism with risk of diabetes and diabetic complications. . 12:12783-12798. https://doi.org/10.18632/aging.103213

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Provider: 
 TY - JOUR
 AU - Ren, Huan 
 AU - Luo, Jian-Quan 
 AU - Gao, Yong-Chao 
 AU - Chen, Man-Yun 
 AU - Chen, Xiao-Ping 
 AU - Zhou, Hong-Hao 
 AU - Jiang, Ying 
 AU - Zhang, Wei 
 TI - Genetic association of hypoxia inducible factor 1-alpha (HIF1A) Pro582Ser polymorphism with risk of diabetes and diabetic complications
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103213
 DO - 10.18632/aging.103213
 SP - 12783
 EP - 12798
 PY - 
 AB - Diabetes is an age-related chronic disease associated with a number of complications, emerging as one of the major causes of morbidity and mortality worldwide. Several studies indicated that hypoxia-inducible factor 1-alpha (HIF1A) genetic polymorphisms may be associated with diabetes and diabetic complications. However, this association remains ambiguous. Thus, we performed a meta-analysis to provide more precise conclusion on this issue. Odds ratios (OR) with corresponding 95% confidence intervals (CI) were applied to assess the strength of the relationships. There was a protective association between HIF1A Pro582Ser polymorphism and diabetes under the heterozygous genetic model (OR = 0.70, 95% CI = 0.55-0.91; P = 0.007). Similar associations were observed in diabetic complications risk under the allelic (OR = 0.69, 95% CI = 0.57-0.83; P &lt; 0.001), homozygous (OR = 0.51, 95% CI = 0.30-0.87; P = 0.014), recessive (OR = 0.73, 95% CI = 0.59-0.90; P = 0.004) and dominant (OR = 0.40, 95% CI = 0.25-0.65; P &lt; 0.001) genetic models. No effects of the HIF1A Ala588Thr polymorphism were found in risk of diabetes and diabetic complications. Taken together, these findings revealed the protective effect of HIF1A Pro582Ser polymorphism against diabetes and diabetic complications.
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Tomatidine suppresses inflammation in primary articular chondrocytes and attenuates cartilage degradation in osteoarthritic rats

Xiangyu Chu, Tao Yu, Xiaojian Huang, Yang Xi, Bowei Ni, Rui Zhang, Hongbo You,

https://doi.org/10.18632/aging.103222 pp 12799—12811

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Chu X, Yu T, Huang X, Xi Y, Ni B, Zhang R, You H, . Tomatidine suppresses inflammation in primary articular chondrocytes and attenuates cartilage degradation in osteoarthritic rats. . 12:12799-12811. https://doi.org/10.18632/aging.103222

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Provider: 
                TY  - JOUR
                AU  - Chu, Xiangyu 
                AU  - Yu, Tao 
                AU  - Huang, Xiaojian 
                AU  - Xi, Yang 
                AU  - Ni, Bowei 
                AU  - Zhang, Rui 
                AU  - You, Hongbo 
                TI  - Tomatidine suppresses inflammation in primary articular chondrocytes and attenuates cartilage degradation in osteoarthritic rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103222
                DO  - 10.18632/aging.103222
                SP  - 12799
                EP  - 12811
                PY  - 
                AB  - In this study, we investigated whether the anti-inflammatory effects of tomatidine alleviate osteoarthritis (OA)-related pathology in primary articular chondrocytes and a rat OA model. STITCH database analysis identified 22 tomatidine-target genes that were enriched in 78 Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Moreover,39 of the 105 OA-related KEGG pathways were related to tomatidine-target genes. The top two OA-related KEGG pathways with tomatidine-target genes were the MAPK and neutrophin signaling pathways. Pretreating primary chondrocytes with tomatidine suppressed interleukin-1&#x3B2; (IL-1&#x3B2;)-induced expression of iNOS, COX-2, MMP1, MMP3, MMP13, and ADAMTS-5. Tomatidine also suppressed IL-1&#x3B2;-induced degradation of collagen-II and aggrecan proteins by inhibiting NF-&#x3BA;B and MAPK signaling. In a rat OA model, histological and immunohistochemical analyses showed significantly less cartilage degeneration in thetibiofemoral joints of rats treated for 12 weeks with tomatidine after OA induction (experimental group) than in untreated OA group rats. However, micro-computed tomography (&#x3BC;-CT) showed that tomatidine did not affect remodeling of the subchondral bone at the tibial plateau. These data shows that tomatidine suppresses IL-1&#x3B2;-induced inflammation in primary chondrocytes by inhibiting the NF-&#x3BA;B and MAPK signaling pathways, and protects against cartilage destruction in a rat OA model.
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PHLPP2 is regulated by competing endogenous RNA network in pathogenesis of colon cancer

Hong-Kun Wu, Chang Liu, Xin-Xing Li, Wei Ji, Chen-De Xin, Zhi-Qian Hu, Lin Zhou,

https://doi.org/10.18632/aging.103246 pp 12812—12840

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Wu H, Liu C, Li X, Ji W, Xin C, Hu Z, Zhou L, . PHLPP2 is regulated by competing endogenous RNA network in pathogenesis of colon cancer. . 12:12812-12840. https://doi.org/10.18632/aging.103246

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                TY  - JOUR
                AU  - Wu, Hong-Kun 
                AU  - Liu, Chang 
                AU  - Li, Xin-Xing 
                AU  - Ji, Wei 
                AU  - Xin, Chen-De 
                AU  - Hu, Zhi-Qian 
                AU  - Zhou, Lin 
                TI  - PHLPP2 is regulated by competing endogenous RNA network in pathogenesis of colon cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103246
                DO  - 10.18632/aging.103246
                SP  - 12812
                EP  - 12840
                PY  - 
                AB  - Recently, homologous pleckstrin-homology (PH)-domain leucine-rich-repeat protein phosphatases (PHLPP2) has been reported as a tumor suppressor in colon cancer. This study aimed to unravel the possible involvement of long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) regulating PHLPP2 in colon cancer. Expressions of candidate lncRNAs and miRNAs were verified by the RT-qPCR and Western blot analyses in colon cancer. The roles of candidate genes in colon cancer were investigated in HT-29 cells in vitro and in mouse tumor xenograft model in vivo. PHLPP2, a target of miR-141 and miR-424, was downregulated in colon cancer. PHLPP2 upregulation and miR-141 and miR-424 downregulation suppressed the colon cancer cell proliferation, migration, invasion, and epithelial-mesenchymal transition, and promote cell apoptosis, which also resulted in suppression of tumor metastasis and formation. Furthermore, LINC00402, LINC00461, and SFTA1P were identified as the targets of miR-141 and miR-424 and acted as competitive endogenous RNAs (ceRNAs) of PHLPP2. The upregulation of LINC00402, LINC00461, and SFTA1P was verified to enhance the suppressive effects of PHLPP2 in the pathogenesis of colon cancer. Conjointly, our results demonstrated the suppressive effects of PHLPP2 in colon cancer and proved that LINC00402, LINC00461, and SFTA1P acted as ceRNAs of PHLPP2 by competitive binding to miR-141 and miR-424.
                ER  -

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miR-27-3p inhibition restore fibroblasts viability in diabetic wound by targeting NOVA1

Peng Zhang, Xiaomei Song, Qirong Dong, Long Zhou, Lei Wang,

https://doi.org/10.18632/aging.103266 pp 12841—12849

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Zhang P, Song X, Dong Q, Zhou L, Wang L, . miR-27-3p inhibition restore fibroblasts viability in diabetic wound by targeting NOVA1. . 12:12841-12849. https://doi.org/10.18632/aging.103266

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                TY  - JOUR
                AU  - Zhang, Peng 
                AU  - Song, Xiaomei 
                AU  - Dong, Qirong 
                AU  - Zhou, Long 
                AU  - Wang, Lei 
                TI  - miR-27-3p inhibition restore fibroblasts viability in diabetic wound by targeting NOVA1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103266
                DO  - 10.18632/aging.103266
                SP  - 12841
                EP  - 12849
                PY  - 
                AB  - Diabetic wounds increase morbidity and decrease quality of life in patients with type 2 diabetes. Serum miR-27-3p levels are reportedly elevated in type 2 diabetic patients. In the present study, we explored the role of miR-27-3p during wound healing. We found that miR-27-3p is overexpressed in cutaneous fibroblasts of diabetic patients and mice. miR-27-3p knockdown enhanced the proliferation and migration of fibroblasts, while suppressing the incidence of fibroblast apoptosis. Overexpressing miR-27-3p in fibroblasts had the opposite effects. We also identified neuro-oncological ventral antigen 1 (NOVA1) as a target of miR-27-3p in fibroblasts. Knocking down NOVA1 using targeted siRNA mimicked the effects of miR-27-3p overexpression in fibroblasts. Administration of miR-27-3p to the area around wounds inflicted in mice delayed healing of those wounds. This suggests that miR-27-3p suppresses fibroblast function by targeting NOVA1, which results in the slowing of wound healing. These findings may offer a new approach to the treatment of diabetic wound healing.
                ER  -

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Glycosylation end products mediate damage and apoptosis of periodontal ligament stem cells induced by the JNK-mitochondrial pathway

Hui Fang, Kun Yang, Ping Tang, Na Zhao, Rui Ma, Xin Luo, Qi Liu,

https://doi.org/10.18632/aging.103304 pp 12850—12868

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Fang H, Yang K, Tang P, Zhao N, Ma R, Luo X, Liu Q, . Glycosylation end products mediate damage and apoptosis of periodontal ligament stem cells induced by the JNK-mitochondrial pathway. . 12:12850-12868. https://doi.org/10.18632/aging.103304

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Provider: 
                TY  - JOUR
                AU  - Fang, Hui 
                AU  - Yang, Kun 
                AU  - Tang, Ping 
                AU  - Zhao, Na 
                AU  - Ma, Rui 
                AU  - Luo, Xin 
                AU  - Liu, Qi 
                TI  - Glycosylation end products mediate damage and apoptosis of periodontal ligament stem cells induced by the JNK-mitochondrial pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103304
                DO  - 10.18632/aging.103304
                SP  - 12850
                EP  - 12868
                PY  - 
                AB  - Background: Recent studies have confirmed the bidirectional relationship between the two and the exacerbation of periodontitis by type II diabetes mellitus (T2DM), the pathogenic mechanism has not yet been clarified, AGEs has been linked to the pathogenesis of both periodontitis and T2DM, JNK signaling pathway might play a important role to explain the inner mechanism.Objectives: To study advanced glycation end products (AGEs) activate the innate immune system of the host by activating oxidative stress and affecting cellular signal transduction in periodontal ligament stem cells (PDLSCs);Results: TNF-&#x3B1; and/or AGEs can induce the formation of endogenous ROS in PDLSCs, thereby activating the downstream JNK signalling pathway, leading to the initiation of the mitochondria-mediated apoptotic pathway and the induction of PDLSC apoptosis.Conclusion: we hypothesized that the JNK pathway is a key link in the apoptosis of PDLSCs mediated by TNF-&#x3B1; and/or AGEs.Materials and Methods: PDLSCs from healthy volunteers were extracted, cultured and stimulated with TNF-a and/or AGEs, Flow cytometry, CCK-8, multidifferential assay, RT-PCR, apoptosis assay, Transmission electron microscopy and Western blotting were recruit to detect the internal relations between AGEs and PDLSCs.
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miR-183-5p alleviates early injury after intracerebral hemorrhage by inhibiting heme oxygenase-1 expression

Yu Wang, Yuejia Song, Yuxin Pang, Zihan Yu, Wei Hua, Yunhe Gu, Jiping Qi, He Wu,

https://doi.org/10.18632/aging.103343 pp 12869—12895

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Wang Y, Song Y, Pang Y, Yu Z, Hua W, Gu Y, Qi J, Wu H, . miR-183-5p alleviates early injury after intracerebral hemorrhage by inhibiting heme oxygenase-1 expression. . 12:12869-12895. https://doi.org/10.18632/aging.103343

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                TY  - JOUR
                AU  - Wang, Yu 
                AU  - Song, Yuejia 
                AU  - Pang, Yuxin 
                AU  - Yu, Zihan 
                AU  - Hua, Wei 
                AU  - Gu, Yunhe 
                AU  - Qi, Jiping 
                AU  - Wu, He 
                TI  - miR-183-5p alleviates early injury after intracerebral hemorrhage by inhibiting heme oxygenase-1 expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103343
                DO  - 10.18632/aging.103343
                SP  - 12869
                EP  - 12895
                PY  - 
                AB  - Differences in microRNA (miRNA) expression after intracerebral hemorrhage (ICH) have been reported in human and animal models, and miRNAs are being investigated as a new treatment for inflammation and oxidative stress after ICH. In this study, we found that microRNA-183-5p expression was decreased in the mouse brain after ICH. To investigate the effect of miRNA-183-5p on injury and repair of brain tissue after ICH, saline, miRNA-183-5p agomir, or miRNA-183-5p antagomir were injected into the lateral ventricles of 8-week-old mice with collagenase-induced ICH. Three days after ICH, mice treated with exogenous miRNA-183-5p showed less brain edema, neurobehavioral defects, inflammation, oxidative stress, and ferrous deposition than control mice. In addition, by alternately treating mice with a heme oxygenase-1 (HO-1) inducer, a HO-1 inhibitor, a nuclear factor erythroid 2-related factor (Nrf2) activator, and Nrf2 knockout, we demonstrated an indirect, HO-1-dependent regulatory relationship between miRNA-183-5p and Nrf2. Our results indicate that miRNA-183-5p and HO-1 are promising therapeutic targets for controlling inflammation and oxidative damage after hemorrhagic stroke.
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A novel molecular-clinicopathologic nomogram to improve prognosis prediction of hepatocellular carcinoma

Zhongjing Zhang, Wanqing Weng, Weiguo Huang, Boda Wu, Yi Zhou, Jie Zhang, Tuo Deng, Wen Ye, Jiecheng Zhang, Jianyang Ao, Qiyu Zhang, Keqing Shi,

https://doi.org/10.18632/aging.103350 pp 12896—12920

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Zhang Z, Weng W, Huang W, Wu B, Zhou Y, Zhang J, Deng T, Ye W, Zhang J, Ao J, Zhang Q, Shi K, . A novel molecular-clinicopathologic nomogram to improve prognosis prediction of hepatocellular carcinoma. . 12:12896-12920. https://doi.org/10.18632/aging.103350

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                TY  - JOUR
                AU  - Zhang, Zhongjing 
                AU  - Weng, Wanqing 
                AU  - Huang, Weiguo 
                AU  - Wu, Boda 
                AU  - Zhou, Yi 
                AU  - Zhang, Jie 
                AU  - Deng, Tuo 
                AU  - Ye, Wen 
                AU  - Zhang, Jiecheng 
                AU  - Ao, Jianyang 
                AU  - Zhang, Qiyu 
                AU  - Shi, Keqing 
                TI  - A novel molecular-clinicopathologic nomogram to improve prognosis prediction of hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103350
                DO  - 10.18632/aging.103350
                SP  - 12896
                EP  - 12920
                PY  - 
                AB  - Background: Emerging evidence suggests that long non-coding RNA (lncRNA) plays a crucial part in the development and progress of hepatocellular carcinoma (HCC). The objective was to develop novel molecular-clinicopathological prediction methods for overall survival (OS) and recurrence of HCC.Results: An 8-lncRNA-based classifier for OS and a 14-lncRNA-based classifier for recurrence were developed by LASSO COX regression analysis, both of which had high accuracy. The tdROC of OS-nomogram and recurrence-nomogram indicates the satisfactory accuracy and predictive power. The classifiers and nomograms for predicting OS and recurrence of HCC were validated in the Test and GEO cohorts.Conclusions: These two lncRNA-based classifiers could be independent prognostic factors for OS and recurrence. The molecule-clinicopathological nomograms based on the classifiers could increase the prognostic value.Methods: HCC lncRNA expression profiles from the cancer genome atlas (TCGA) were randomly divided into 1:1 training and test cohorts. Based on least absolute shrinkage and selection operator method (LASSO) COX regression model, lncRNA-based classifiers were established to predict OS and recurrence, respectively. OS-nomogram and recurrence-nomogram were developed by combining lncRNA-based classifiers and clinicopathological characterization to predict OS and recurrence, respectively. The prognostic value was accessed by the time-dependent receiver operating characteristic (tdROC) and the concordance index (C-index).
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Relationship between the expression of oestrogen receptor and progesterone receptor and ¹⁸F-FDG uptake in endometrial cancer

Chunhua Wu, Ruohua Chen, Lian Xu, Yumei Chen, Yining Wang, Gan Huang, Jianjun Liu,

https://doi.org/10.18632/aging.103352 pp 12921—12929

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Wu C, Chen R, Xu L, Chen Y, Wang Y, Huang G, Liu J, . Relationship between the expression of oestrogen receptor and progesterone receptor and ¹⁸F-FDG uptake in endometrial cancer. . 12:12921-12929. https://doi.org/10.18632/aging.103352

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Provider: 
 TY - JOUR
 AU - Wu, Chunhua 
 AU - Chen, Ruohua 
 AU - Xu, Lian 
 AU - Chen, Yumei 
 AU - Wang, Yining 
 AU - Huang, Gan 
 AU - Liu, Jianjun 
 TI - Relationship between the expression of oestrogen receptor and progesterone receptor and 18F-FDG uptake in endometrial cancer
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103352
 DO - 10.18632/aging.103352
 SP - 12921
 EP - 12929
 PY - 
 AB - Background: Progestogens have been widely used for the treatment of inoperable endometrial cancer or younger patients with endometrial cancer. Identifying markers that are predictive of a response to progestogens is critical for successful therapy. Molecular imaging with 18F-fluorodeoxyglucose positron emission tomography (18F-FDG PET) can provide metabolic phenotypic information of many malignancies. We investigated whether estrogen receptor (ER)/progestogen receptor (PR) status is correlated with 18F-FDG uptake, and whether 18F-FDG PET/CT could be useful for predicting ER/PR status in endometrial cancer.Results: Endometrial cancers in the ER-positive group had lower SUVmax than those in the ER-negative group (12.3 &#xB1; 6.2 vs. 19.9 &#xB1; 6.6, respectively; P = 0.003). Endometrial cancers in the PR-positive group also had lower SUVmax than those in the PR-negative group (12.4 &#xB1; 6.2 vs. 20.0 &#xB1; 6.9, respectively; P = 0.005). Multivariate analysis indicated that SUVmax and tumour differentiation grade were significantly associated with both ER and PR status (P = 0.027 and P = 0.044, respectively). ER expression was predicted with an accuracy of 74.2% when a SUVmax value of 15.3 was used as a cutoff point for analysis. Similarly, PR expression was predicted with an accuracy of 74.2%, when a SUVmax value of 15.95 was used as the threshold for analysis.Conclusion: Higher 18F-FDG accumulation in endometrial cancers is correlated with negative ER/PR expression. 18F-FDG PET/CT may be used to predict the status of ER/PR and thus aid in optimal treatment decision in endometrial cancers.Methods: We carried out a retrospective analysis on 62 endometrial cancer patients who underwent 18F-FDG PET/CT before radical treatment. The maximum of standardized uptake value (SUVmax) was calculated from the 18F-FDG accumulation of the primary tumor. The relationship between SUVmax and ER/PR status was analyzed.
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Efficacy and safety of an antithrombotic regimen for atrial fibrillation patients with acute coronary syndrome or those undergoing percutaneous coronary intervention: a meta-analysis

Wenqin Guo, Xiehui Chen, Yunling Hao, Qiang Liu, Changnong Peng, Lingyue Zhao, Zongming Feng, Xiaoqing Wang, Huanjun Ruan, Lang Li,

https://doi.org/10.18632/aging.103359 pp 12930—12942

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Guo W, Chen X, Hao Y, Liu Q, Peng C, Zhao L, Feng Z, Wang X, Ruan H, Li L, . Efficacy and safety of an antithrombotic regimen for atrial fibrillation patients with acute coronary syndrome or those undergoing percutaneous coronary intervention: a meta-analysis. . 12:12930-12942. https://doi.org/10.18632/aging.103359

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                TY  - JOUR
                AU  - Guo, Wenqin 
                AU  - Chen, Xiehui 
                AU  - Hao, Yunling 
                AU  - Liu, Qiang 
                AU  - Peng, Changnong 
                AU  - Zhao, Lingyue 
                AU  - Feng, Zongming 
                AU  - Wang, Xiaoqing 
                AU  - Ruan, Huanjun 
                AU  - Li, Lang 
                TI  - Efficacy and safety of an antithrombotic regimen for atrial fibrillation patients with acute coronary syndrome or those undergoing percutaneous coronary intervention: a meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103359
                DO  - 10.18632/aging.103359
                SP  - 12930
                EP  - 12942
                PY  - 
                AB  - This study evaluated the benefit of dual therapy in reducing ischemic events in atrial fibrillation (AF) patients presenting with acute coronary syndrome (ACS) or undergoing percutaneous coronary intervention (PCI). We searched PubMed, Cochrane Library, and ClinicalTrials.gov for randomized controlled trials (RCTs) comparing dual and triple therapies (oral anticoagulation plus aspirin and P2Y12 inhibitor) for AF patients with ACS or those undergoing PCI. The composite primary outcome included all-cause death, myocardial infarction (MI), stent thrombosis (ST), or stroke. Relative risk (RR) and the corresponding 95% confidence interval (CI) was used as the measure of effect size. Four RCTs with 10,969 patients were included. Dual therapy had a higher event rate of primary outcome than triple therapy (RR, 1.15; 95%CI, 1.03&#x2013;1.28; P&lt;0.0001). Dual therapy was associated with significantly higher MI risk, insignificantly higher ST risk, and significantly lower major bleeding risk than triple therapy (RR1.23, 95%CI 1.01&#x2013;1.49, P = 0.036; RR 1.43, 95 %CI 0.98&#x2013;2.09, P = 0.064; and RR0.58, 95%CI 0.45&#x2013;0.76, P&lt;0.0001, respectively). Dual antithrombotic therapy was associated with higher ischemic risk but lower major bleeding risk than triple therapy. The data suggest that antithrombotic regimens should be based on tradeoffs between ischemia and bleeding risk.
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Nrf2 inhibits ferroptosis and protects against acute lung injury due to intestinal ischemia reperfusion via regulating SLC7A11 and HO-1

Hui Dong, Zhuanzhuan Qiang, Dongdong Chai, Jiali Peng, Yangyang Xia, Rong Hu, Hong Jiang,

https://doi.org/10.18632/aging.103378 pp 12943—12959

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Dong H, Qiang Z, Chai D, Peng J, Xia Y, Hu R, Jiang H, . Nrf2 inhibits ferroptosis and protects against acute lung injury due to intestinal ischemia reperfusion via regulating SLC7A11 and HO-1. . 12:12943-12959. https://doi.org/10.18632/aging.103378

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                TY  - JOUR
                AU  - Dong, Hui 
                AU  - Qiang, Zhuanzhuan 
                AU  - Chai, Dongdong 
                AU  - Peng, Jiali 
                AU  - Xia, Yangyang 
                AU  - Hu, Rong 
                AU  - Jiang, Hong 
                TI  - Nrf2 inhibits ferroptosis and protects against acute lung injury due to intestinal ischemia reperfusion via regulating SLC7A11 and HO-1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103378
                DO  - 10.18632/aging.103378
                SP  - 12943
                EP  - 12959
                PY  - 
                AB  - Acute lung injury (ALI) is a syndrome associated with a high mortality rate. Nrf2 is a key regulator of intracellular oxidation homeostasis that plays a pivotal role in controlling lipid peroxidation, which is closely related to the process of ferroptosis. However, the intrinsic effect of Nrf2 on ferroptosis remains to be investigated in ALI. We found that MDA expression increased while GSH and GPX4 decreased in ALI models. Furthermore, the characteristic mitochondrial morphological changes of ferroptosis appear in type II alveolar epithelial cells in IIR models. Additional pre-treatment of Fe and Ferrostatin-1 in ALI significantly aggravated or ameliorated the pathological injuries of lung tissue, pulmonary edema, lipid peroxidation, as well as promoted or prevented cell death, respectively. Knocking down Nrf2 notably decreased the expression of SLC7A11 and HO-1. Interference with SLC7A11 markedly increased Nrf2-HO-1 and dramatically attenuated cell death in OGD/R models. These findings indicate that ferroptosis can be inhibited by Nrf2 through regulating SLC7A11 and HO-1, which may provide a potential therapeutic strategy for IIR-ALI.
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LOXL2 from human amniotic mesenchymal stem cells accelerates wound epithelialization by promoting differentiation and migration of keratinocytes

Dan He, Feng Zhao, Han Jiang, Yue Kang, Yang Song, Xuewen Lin, Ping Shi, Tao Zhang, Xining Pang,

https://doi.org/10.18632/aging.103384 pp 12960—12986

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He D, Zhao F, Jiang H, Kang Y, Song Y, Lin X, Shi P, Zhang T, Pang X, . LOXL2 from human amniotic mesenchymal stem cells accelerates wound epithelialization by promoting differentiation and migration of keratinocytes. . 12:12960-12986. https://doi.org/10.18632/aging.103384

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                TY  - JOUR
                AU  - He, Dan 
                AU  - Zhao, Feng 
                AU  - Jiang, Han 
                AU  - Kang, Yue 
                AU  - Song, Yang 
                AU  - Lin, Xuewen 
                AU  - Shi, Ping 
                AU  - Zhang, Tao 
                AU  - Pang, Xining 
                TI  - LOXL2 from human amniotic mesenchymal stem cells accelerates wound epithelialization by promoting differentiation and migration of keratinocytes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103384
                DO  - 10.18632/aging.103384
                SP  - 12960
                EP  - 12986
                PY  - 
                AB  - In this study, we identified wound healing-related proteins secreted by human amniotic epithelial cells (hAECs) and human amniotic mesenchymal stem cells (hAMSCs). We observed increased migration and reduced proliferation and differentiation when keratinocytes were co-cultured in media conditioned by hAECs (hAECs-CM) and hAMSCs (hAMSCs-CM). Label-free mass spectrometry and bioinformatic analyses of the hAECs-CM and hAMSCs-CM proteome revealed several proteins associated with wound healing, angiogenesis, cellular differentiation, immune response and cell motility. The levels of the proteins related to wound healing, including CTHRC1, LOXL2 and LGALS1, were significantly higher in hAMSCs-CM than hAECs-CM. LOXL2 significantly enhanced in vitro keratinocyte migration and differentiation compared to CTHRC1 and LGALS1. Moreover, LOXL2 enhanced keratinocyte migration and differentiation by activating the JNK signaling pathway. We observed significant reduction in the in vitro migration and differentiation of keratinocytes when co-cultured with medium conditioned by LOXL2-silenced hAMSCs and when treated with 10 &#x3BC;M SP600125, a specific JNK inhibitor. Treatment with hAMSCs-CM and LOXL2 significantly accelerated wound healing in the murine skin wound model. These findings show that LOXL2 promotes wound healing by inducing keratinocyte migration and differentiation via a JNK signaling pathway.
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Transcriptome analysis of common and diverged circulating miRNAs between arterial and venous during aging

Hao Wang, Yuan Zhou, Zhongnan Yin, Li Chen, Ling Jin, Qinghua Cui, Lixiang Xue,

https://doi.org/10.18632/aging.103385 pp 12987—13004

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Wang H, Zhou Y, Yin Z, Chen L, Jin L, Cui Q, Xue L, . Transcriptome analysis of common and diverged circulating miRNAs between arterial and venous during aging. . 12:12987-13004. https://doi.org/10.18632/aging.103385

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                TY  - JOUR
                AU  - Wang, Hao 
                AU  - Zhou, Yuan 
                AU  - Yin, Zhongnan 
                AU  - Chen, Li 
                AU  - Jin, Ling 
                AU  - Cui, Qinghua 
                AU  - Xue, Lixiang 
                TI  - Transcriptome analysis of common and diverged circulating miRNAs between arterial and venous during aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103385
                DO  - 10.18632/aging.103385
                SP  - 12987
                EP  - 13004
                PY  - 
                AB  - Circulating miRNAs have received extensive attention as non-invasive biomarkers for prediction and diagnosis of disease. However, most samples have been obtained from peripheral venous blood. To evaluate whether peripheral venous miRNAs represent circulating miRNAs from all blood vessels under a given condition, such as aging, we compared the miRNA profiles of venous and arterial plasma between young and aged rats by Illumina next-generation sequencing. The DEseq2 tool was used to obtain differentially-expressed miRNAs. We observed 105 aging-related deregulated miRNAs in vein and 62 in artery, which were highly associated with cell survival and inflammation, respectively. On the other hand, the young and aged groups exhibited a unique arterial-venous bias. There were 54 differentially-expressed miRNAs in the young group and 42 in the aged group; only 8 miRNAs were shared. Further transcriptional factors enrichment analysis found that the shared miRNAs could be partially upregulated by NF-&#x3BA;B and SIRT1. These transcriptional factors could be organ-specific and/or regulated in physiological and aging states as possible causal factors. This study suggested the potential application of circulating miRNAs, which reflect the systematic response to certain conditions, such as aging, and the importance of origin selection for candidate circulating miRNAs.
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MicroRNA-124 inhibits macrophage cell apoptosis via targeting p38/MAPK signaling pathway in atherosclerosis development

Xue Liang, Lijun Wang, Manman Wang, Zhaohong Liu, Xing Liu, Baoshuai Zhang, Enzhao Liu, Guangping Li,

https://doi.org/10.18632/aging.103387 pp 13005—13022

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Liang X, Wang L, Wang M, Liu Z, Liu X, Zhang B, Liu E, Li G, . MicroRNA-124 inhibits macrophage cell apoptosis via targeting p38/MAPK signaling pathway in atherosclerosis development. . 12:13005-13022. https://doi.org/10.18632/aging.103387

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                TY  - JOUR
                AU  - Liang, Xue 
                AU  - Wang, Lijun 
                AU  - Wang, Manman 
                AU  - Liu, Zhaohong 
                AU  - Liu, Xing 
                AU  - Zhang, Baoshuai 
                AU  - Liu, Enzhao 
                AU  - Li, Guangping 
                TI  - MicroRNA-124 inhibits macrophage cell apoptosis via targeting p38/MAPK signaling pathway in atherosclerosis development
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103387
                DO  - 10.18632/aging.103387
                SP  - 13005
                EP  - 13022
                PY  - 
                AB  - The objective of this study is to characterize the function of microRNA (miR)-124 in the process of coronary artery disease (CAD). Eighty patients, including 40 CAD patients and 40 non-CAD control patients were enrolled in this study. Atherosclerosis model was established in vivo in ApoE-/- mice and in vitro in RAW264.7 cells. Expression of miR-124 and p38 in patients, animal models and cell models were measured by qRT-PCR, western blot and immunohistochemistry assay. Overexpression or suppression of miR-124 was introduced in vitro and in vivo and the expression levels of p38, miR-124, pro- and anti-inflammatory cytokines, and pro- and anti-apoptotic factors were examined. Results showed that miR-124 was decreased, while p38 was increased in CAD patients and atherosclerosis models compared with control group. MiR-124 could target p38 by binding its 3&#x2019; untranslated region and negatively regulated the protein expression of p38. Overexpression of miR-124 increased the expression of anti-inflammatory cytokines, reduced the expression of pro- inflammatory cytokines, and inhibited macrophage apoptosis. MiR-124 overexpression may be a promising treatment for atherosclerosis and CAD via inhibiting p38.
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The Gαh/phospholipase C-δ1 interaction promotes autophagosome degradation by activating the Akt/mTORC1 pathway in metastatic triple-negative breast cancer

Hui-Yu Lin, Chia-Hao Kuei, Hsun-Hua Lee, Che-Hsuan Lin, Jing-Quan Zheng, Hui-Wen Chiu, Chi-Long Chen, Yuan-Feng Lin,

https://doi.org/10.18632/aging.103390 pp 13023—13037

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Lin H, Kuei C, Lee H, Lin C, Zheng J, Chiu H, Chen C, Lin Y, . The Gαh/phospholipase C-δ1 interaction promotes autophagosome degradation by activating the Akt/mTORC1 pathway in metastatic triple-negative breast cancer. . 12:13023-13037. https://doi.org/10.18632/aging.103390

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                TY  - JOUR
                AU  - Lin, Hui-Yu 
                AU  - Kuei, Chia-Hao 
                AU  - Lee, Hsun-Hua 
                AU  - Lin, Che-Hsuan 
                AU  - Zheng, Jing-Quan 
                AU  - Chiu, Hui-Wen 
                AU  - Chen, Chi-Long 
                AU  - Lin, Yuan-Feng 
                TI  - The Gαh/phospholipase C-δ1 interaction promotes autophagosome degradation by activating the Akt/mTORC1 pathway in metastatic triple-negative breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103390
                DO  - 10.18632/aging.103390
                SP  - 13023
                EP  - 13037
                PY  - 
                AB  - Lung metastasis (LM) is commonly found in triple-negative breast cancer (TNBC); however, the molecular mechanism underlying TNBC metastasis to lungs remains largely unknown. We thus aimed to uncover a possible mechanism for the LM of TNBC. Here we show that the phosphorylation of Akt and mTORC1 was positively but the autophagy activity was negatively correlated with endogenous G&#x3B1;h levels and cell invasion ability in TNBC cell lines. Whereas the knockdown of G&#x3B1;h, as well as blocking its binding with PLC-&#x3B4;1 by a synthetic peptide inhibitor, in the highly invasive MDA-MB231 cells dramatically suppressed Akt/mTORC1 phosphorylation and blocked autophagosome degradation, the overexpression of G&#x3B1;h in the poorly invasive HCC1806 cells enhanced Akt/mTORC1 phosphorylation but promoted autophagosome degradation. The pharmaceutical inhibition of autophagy initiation by 3-methyladenine was found to rescue the cell invasion ability and LM potential of G&#x3B1;h-silenced MDA-MB231 cells. In contrast, the inhibition of mTORC1 activity by rapamycin suppressed autophagosome degradation but mitigated the cell invasion ability and LM potential of G&#x3B1;h-overexpressing HCC1806 cells. These findings demonstrate that the induction of autophagy activity or the inhibition of Akt-mTORC1 axis provides a useful strategy to combat the G&#x3B1;h/PLC-&#x3B4;1-driven LM of TNBC.
                ER  -

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circMET promotes NSCLC cell proliferation, metastasis, and immune evasion by regulating the miR-145-5p/CXCL3 axis

Xu Pei, Shi-Wei Chen, Xiang Long, Shu-Qiang Zhu, Bai-Quan Qiu, Kun Lin, Feng Lu, Jian-Jun Xu, Peng-Fei Zhang, Yong-Bing Wu,

https://doi.org/10.18632/aging.103392 pp 13038—13058

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Pei X, Chen S, Long X, Zhu S, Qiu B, Lin K, Lu F, Xu J, Zhang P, Wu Y, . circMET promotes NSCLC cell proliferation, metastasis, and immune evasion by regulating the miR-145-5p/CXCL3 axis. . 12:13038-13058. https://doi.org/10.18632/aging.103392

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                TY  - JOUR
                AU  - Pei, Xu 
                AU  - Chen, Shi-Wei 
                AU  - Long, Xiang 
                AU  - Zhu, Shu-Qiang 
                AU  - Qiu, Bai-Quan 
                AU  - Lin, Kun 
                AU  - Lu, Feng 
                AU  - Xu, Jian-Jun 
                AU  - Zhang, Peng-Fei 
                AU  - Wu, Yong-Bing 
                TI  - circMET promotes NSCLC cell proliferation, metastasis, and immune evasion by regulating the miR-145-5p/CXCL3 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103392
                DO  - 10.18632/aging.103392
                SP  - 13038
                EP  - 13058
                PY  - 
                AB  - In recent years, circular RNAs (circRNAs) have been increasingly reported to play a crucial role in the proliferation, migration, and invasion of non-small-cell lung cancer (NSCLC) cells. However, the circRNA MET (circMET) oncogenic mechanism that drives NSCLC development and progression remains largely unknown. In this study, the present results demonstrated that circMET expression was significantly higher in NSCLC tissues than in peritumoral tissues using quantitative real-time polymerase chain reaction. Notably, NSCLC patients with a large tumor diameter, poor differentiation and lymphatic metastasis had high RNA levels of circMET. Moreover, high circMET expression served as an independent risk factor for short overall survival (OS) and progression-free survival (PFS) in NSCLC patients. Next, we validated that circMET overexpression can enhance NSCLC cell proliferation, metastasis, and immune evasion in vitro. Mechanistically, our study uncovers that circMET acts as a miR-145-5p sponge to upregulate CXCL3 expression. Collectively, circMET regulates the miR-145-5p/CXCL3 axis and serves as a novel, promising diagnostic and prognostic biomarker in patients with NSCLC.
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Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway

Yizhou Yao, Xuchao Wang, Diyuan Zhou, Hao Li, Huan Qian, Jiawen Zhang, Linhua Jiang, Bin Wang, Qi Lin, Xinguo Zhu,

https://doi.org/10.18632/aging.103393 pp 13059—13075

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Yao Y, Wang X, Zhou D, Li H, Qian H, Zhang J, Jiang L, Wang B, Lin Q, Zhu X, . Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway. . 12:13059-13075. https://doi.org/10.18632/aging.103393

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                TY  - JOUR
                AU  - Yao, Yizhou 
                AU  - Wang, Xuchao 
                AU  - Zhou, Diyuan 
                AU  - Li, Hao 
                AU  - Qian, Huan 
                AU  - Zhang, Jiawen 
                AU  - Jiang, Linhua 
                AU  - Wang, Bin 
                AU  - Lin, Qi 
                AU  - Zhu, Xinguo 
                TI  - Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103393
                DO  - 10.18632/aging.103393
                SP  - 13059
                EP  - 13075
                PY  - 
                AB  - Colorectal cancer (CRC) is a common malignancy worldwide with poor prognosis and survival rates. The aldo-keto reductase family 1 member B10 (AKR1B10) plays an important role in metabolism, cell proliferation and mobility, and is downregulated in CRC. We hypothesized that AKR1B10 would promote CRC genesis via a noncanonical oncogenic pathway and is a novel therapeutic target. In this study, AKR1B10 expression levels in 135 pairs of CRC and para-tumor tissues were examined, and its oncogenic role was determined using in vitro and in vivo functional assays following genetic manipulation of CRC cells. AKR1B10 was downregulated in CRC tissues compared to the adjacent normal colorectal tissues, and associated with the clinicopathological status of the patients. AKR1B10 depletion promoted the proliferation and migration of CRC cells in vitro, while its ectopic expression had the opposite effect. AKR1B10 was also significantly correlated with FGF1 gene and protein levels. Knockdown of AKR1B10 promoted tumor growth in vivo, and increased the expression of FGF1. Finally, AKR1B10 inhibited FGF1, and suppressed the proliferation and migration ability of CRC cells in an FGF1-dependent manner. In conclusion, AKR1B10 acts as a tumor suppressor in CRC by inactivating FGF1, and is a novel target for combination therapy of CRC.
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CircFOXO3 rs12196996, a polymorphism at the gene flanking intron, is associated with circFOXO3 levels and the risk of coronary artery disease

Yu-Lan Zhou, Wei-Peng Wu, Jie Cheng, Li-Li Liang, Jin-Ming Cen, Can Chen, Xinguang Liu, Xing-Dong Xiong,

https://doi.org/10.18632/aging.103398 pp 13076—13089

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Zhou Y, Wu W, Cheng J, Liang L, Cen J, Chen C, Liu X, Xiong X, . CircFOXO3 rs12196996, a polymorphism at the gene flanking intron, is associated with circFOXO3 levels and the risk of coronary artery disease. . 12:13076-13089. https://doi.org/10.18632/aging.103398

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Provider: 
 TY - JOUR
 AU - Zhou, Yu-Lan 
 AU - Wu, Wei-Peng 
 AU - Cheng, Jie 
 AU - Liang, Li-Li 
 AU - Cen, Jin-Ming 
 AU - Chen, Can 
 AU - Liu, Xinguang 
 AU - Xiong, Xing-Dong 
 TI - CircFOXO3 rs12196996, a polymorphism at the gene flanking intron, is associated with circFOXO3 levels and the risk of coronary artery disease
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103398
 DO - 10.18632/aging.103398
 SP - 13076
 EP - 13089
 PY - 
 AB - CircFOXO3 plays an important role in the pathogenesis of coronary artery disease (CAD). Single nucleotide polymorphisms (SNPs) at circRNA flanking introns may change its back-splicing and influence circRNA formation. Here, we aimed to investigate the influence of the polymorphisms at the circFOXO3 flanking introns on individual susceptibility to CAD. A total of 1185 individuals were included in the case-control study. In a multivariate logistic regression analysis, we determined that the rs12196996 G variant was significantly associated with increased CAD risk (OR = 1.36, P = 0.014). A similar trend of the association was observed in the recessive model (OR = 2.57, P = 0.003). Stratified analysis revealed a more significant association with CAD risk among younger subjects and non-smokers. Consistent with these results, the haplotype rs12196996G-rs9398171C containing rs12196996G allele was also associated with increased CAD risk (OR = 1.31, P = 0.013). Further investigation revealed that the rs12196996 GG genotype was associated with decreased circFOXO3 expression, but not linear FOXO3 levels. Taken together, our data provide the first evidence that the rs12196996 polymorphism at the circFOXO3 gene flanking intron is associated with CAD risk in the Chinese Han population, which is probably due to influence circFOXO3 levels.
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Changes of saliva microbiota in the onset and after the treatment of diabetes in patients with periodontitis

Ying Yang, Shili Liu, Yihua Wang, Zhibin Wang, Wenyu Ding, Xiaoyuan Sun, Kunlun He, Qiang Feng, Xiandang Zhang,

https://doi.org/10.18632/aging.103399 pp 13090—13114

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Yang Y, Liu S, Wang Y, Wang Z, Ding W, Sun X, He K, Feng Q, Zhang X, . Changes of saliva microbiota in the onset and after the treatment of diabetes in patients with periodontitis. . 12:13090-13114. https://doi.org/10.18632/aging.103399

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                TY  - JOUR
                AU  - Yang, Ying 
                AU  - Liu, Shili 
                AU  - Wang, Yihua 
                AU  - Wang, Zhibin 
                AU  - Ding, Wenyu 
                AU  - Sun, Xiaoyuan 
                AU  - He, Kunlun 
                AU  - Feng, Qiang 
                AU  - Zhang, Xiandang 
                TI  - Changes of saliva microbiota in the onset and after the treatment of diabetes in patients with periodontitis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103399
                DO  - 10.18632/aging.103399
                SP  - 13090
                EP  - 13114
                PY  - 
                AB  - The relationship between type 2 diabetes mellitus (T2DM) and oral microbiota is still insufficiently recognized. In the present study, we compared the salivary microbiome of nondiabetic individuals, treatment-na&#xEF;ve diabetic patients, and diabetic patients treated with metformin or a combination of insulin and other drugs. The &#x3B1;- and &#x3B2;-diversity demonstrated significant differences in the salivary microbiome between the nondiabetic people and patients with a history of diabetes, while little divergence was found among individuals with a history of diabetes. After characterizing the effects of periodontitis on the microbial composition of each group, the salivary microbiome of the treatment-na&#xEF;ve diabetic patient group was compared with that of nondiabetic people and the metformin/combined treatment groups. The results revealed changes in the contents of certain bacteria after both the onset and the treatment of diabetes; among these differential bacteria, Blautia_wexlerae, Lactobacillus_fermentum, Nocardia_coeliaca and Selenomonas_artemidis varied in all processes. A subsequent correlational analysis of the differential bacteria and clinical characteristics demonstrated that salivary microbes were related to drug treatment and certain pathological changes. Finally, the four common differential bacteria were employed for distinguishing the treatment-na&#xEF;ve diabetic patients from the nondiabetic people and the treated patients, with prediction accuracies of 83.3%, 75% and 75%, respectively.
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ROR2 knockdown suppresses breast cancer growth through PI3K/ATK signaling

Muhong Guo, Ge Ma, Xiaolan Zhang, Weiwei Tang, Junfeng Shi, Qian Wang, Ye Cheng, Bin Zhang, Jin Xu,

https://doi.org/10.18632/aging.103400 pp 13115—13127

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Guo M, Ma G, Zhang X, Tang W, Shi J, Wang Q, Cheng Y, Zhang B, Xu J, . ROR2 knockdown suppresses breast cancer growth through PI3K/ATK signaling. . 12:13115-13127. https://doi.org/10.18632/aging.103400

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                TY  - JOUR
                AU  - Guo, Muhong 
                AU  - Ma, Ge 
                AU  - Zhang, Xiaolan 
                AU  - Tang, Weiwei 
                AU  - Shi, Junfeng 
                AU  - Wang, Qian 
                AU  - Cheng, Ye 
                AU  - Zhang, Bin 
                AU  - Xu, Jin 
                TI  - ROR2 knockdown suppresses breast cancer growth through PI3K/ATK signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103400
                DO  - 10.18632/aging.103400
                SP  - 13115
                EP  - 13127
                PY  - 
                AB  - The receptor tyrosine kinase like orphan receptor 2 (ROR2) has been implicated in the pathogenesis of a variety of human cancers, including breast cancer. Here, we analyzed the clinical significance of ROR2 in breast cancer (BC) progression, and its function in the regulation of BC cell proliferation and growth. Analysis of ROR2 mRNA levels in 45 BC tissues and adjacent non-tumor tissues revealed that ROR2 expression was significantly increased in BC tissues, and that it correlated with tumor diameter. Kaplan-Meier disease-free survival (DFS) analysis demonstrated that BC patients with higher ROR2 expression had lower DFS. Knockdown of ROR2 suppressed in vitro proliferation of BC cells and promoted apoptosis, while ROR2 overexpression induced BC cell proliferation and suppressed apoptosis. Importantly, ROR2 suppression also reduced the tumor growth in mouse BC xenografts, indicating that ROR2 promotes BC tumorigenesis in vivo. In addition, our data revealed that ROR2 promotes proliferation of BC cells by activating the PI3K/AKT signaling pathway. Together, our results indicate that ROR2 acts as an oncogenic gene in breast cancer, and suggest that the ROR2/PI3K/AKT regulatory network contributes to breast cancer progression.
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Long-term low-dose ethanol intake improves healthspan and resists high-fat diet-induced obesity in mice

Yan Diao, Junhui Nie, Peizhu Tan, Yuchen Zhao, Tingting Zhao, Jiajie Tu, Heng Ji, Yuwei Cao, Zhaojing Wu, Huan Liang, Hui Huang, Yanze Li, Xu Gao, Lingyun Zhou,

https://doi.org/10.18632/aging.103401 pp 13128—13146

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Diao Y, Nie J, Tan P, Zhao Y, Zhao T, Tu J, Ji H, Cao Y, Wu Z, Liang H, Huang H, Li Y, Gao X, et al, . Long-term low-dose ethanol intake improves healthspan and resists high-fat diet-induced obesity in mice. . 12:13128-13146. https://doi.org/10.18632/aging.103401

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                TY  - JOUR
                AU  - Diao, Yan 
                AU  - Nie, Junhui 
                AU  - Tan, Peizhu 
                AU  - Zhao, Yuchen 
                AU  - Zhao, Tingting 
                AU  - Tu, Jiajie 
                AU  - Ji, Heng 
                AU  - Cao, Yuwei 
                AU  - Wu, Zhaojing 
                AU  - Liang, Huan 
                AU  - Huang, Hui 
                AU  - Li, Yanze 
                AU  - Gao, Xu 
                AU  - Zhou, Lingyun 
                TI  - Long-term low-dose ethanol intake improves healthspan and resists high-fat diet-induced obesity in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103401
                DO  - 10.18632/aging.103401
                SP  - 13128
                EP  - 13146
                PY  - 
                AB  - Numerous epidemiological studies have reported that moderate alcohol drinking has beneficial effects. However, few studies have focused on the beneficial effects of ethanol, the common component in alcoholic beverages. Here we fed the C57BL/6 mice with 3.5% v/v ethanol as drinking water substitute to investigate the effects of long-term low-dose ethanol intake in vivo. We evaluated the metabolic rate and mitochondrial function of the long-term low-dose ethanol-intake (LLE) mice, assessed the exercise ability of LLE mice, and fed the LLE mice with a high-fat diet to investigate the potential impact of ethanol on it. The LLE mice showed improved thermogenic activity, physical performance, and mitochondrial function, as well as resistance against the high-fat diet-induced obesity with elevated insulin sensitivity and subdued inflammation. Our results suggest that long-term low-dose ethanol intake can improve healthspan and resist high-fat diet-induced obesity in mice. It may provide new insight into understanding the protective effects of moderate alcohol drinking.
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Articulation rehabilitation induces cortical plasticity in adults with non-syndromic cleft lip and palate

Zhen Li, Wenjing Zhang, Chunlin Li, Mengyue Wang, Songjian Wang, Renji Chen, Xu Zhang,

https://doi.org/10.18632/aging.103402 pp 13147—13159

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Li Z, Zhang W, Li C, Wang M, Wang S, Chen R, Zhang X, . Articulation rehabilitation induces cortical plasticity in adults with non-syndromic cleft lip and palate. . 12:13147-13159. https://doi.org/10.18632/aging.103402

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                TY  - JOUR
                AU  - Li, Zhen 
                AU  - Zhang, Wenjing 
                AU  - Li, Chunlin 
                AU  - Wang, Mengyue 
                AU  - Wang, Songjian 
                AU  - Chen, Renji 
                AU  - Zhang, Xu 
                TI  - Articulation rehabilitation induces cortical plasticity in adults with non-syndromic cleft lip and palate
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103402
                DO  - 10.18632/aging.103402
                SP  - 13147
                EP  - 13159
                PY  - 
                AB  - In this study, we investigated brain morphological changes in adults with non-syndromic cleft lip and palate (NSCLP) after articulation rehabilitation (AR). High-resolution T1 weighted brain magnetic resonance imaging data were analyzed from 45 adults with NSCLP after palatoplasty: 24 subjects were assessed before AR (bNSCLP) and 21 subjects were assessed after AR (aNSCLP). In addition, there were 24 age and sex matched controls. Intergroup differences of grey matter volume were evaluated as a comprehensive measure of the cortex; cortical thickness and cortical complexity (gyrification and fractal dimensions) were also analyzed. As compared to controls, the bNSCLP subjects exhibited altered indexes in frontal, temporal, and parietal lobes; these morphological changes are characteristic for adults with NSCLP. Importantly, as compared to the bNSCLP and control subjects, the aNSCLP subjects exhibited cortical plasticity in the regions involved in language, auditory, pronunciation planning, and execution functions. The AR-mediated cortical plasticity in aNSCLP subjects may be caused by AR-induced cortical neurogenesis, which might reflect the underlying neural mechanism during AR.
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A validated survival nomogram for early-onset diffuse gastric cancer

Fei Liao, Xufeng Guo, Xiaohong Lu, Weiguo Dong,

https://doi.org/10.18632/aging.103406 pp 13160—13171

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Liao F, Guo X, Lu X, Dong W, . A validated survival nomogram for early-onset diffuse gastric cancer. . 12:13160-13171. https://doi.org/10.18632/aging.103406

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                TY  - JOUR
                AU  - Liao, Fei 
                AU  - Guo, Xufeng 
                AU  - Lu, Xiaohong 
                AU  - Dong, Weiguo 
                TI  - A validated survival nomogram for early-onset diffuse gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103406
                DO  - 10.18632/aging.103406
                SP  - 13160
                EP  - 13171
                PY  - 
                AB  - This study aimed to establish and independently validate a prognostic nomogram for individual risk prediction in patients with early-onset diffuse gastric cancer (EODGC). Data for 794 patients with EODGC from the SEER database were randomly assigned to training (N=558) and internal validation (N=236) sets, and data for 82 patients from the Renmin Hospital of Wuhan University (RMHWHU) were used as an independent validation cohort. Our LASSO regression analyses of the training set yielded five clinicopathological features (race, AJCC stage, surgery for primary site, chemotherapy and tumor size), which were used to create a survival nomogram. Our survival nomogram achieved better predictive performance than the AJCC staging system, the current standard. Additionally, the calibration curves of the prognostic nomogram revealed good agreement between the predicted survival probabilities and the ground truth values. Indeed, our nomogram, which estimates individualized survival probabilities for patients with EODGC, shows good predictive accuracy and calibration ability for both the SEER and RMHWHU cohorts. These results suggest that a survival nomogram may be better at predicting OS for EODGC patients than the AJCC staging system.
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An individualized transcriptional signature to predict the epithelial-mesenchymal transition based on relative expression ordering

Tingting Chen, Zhangxiang Zhao, Bo Chen, Yuquan Wang, Fan Yang, Chengyu Wang, Qi Dong, Yaoyao Liu, Haihai Liang, Wenyuan Zhao, Lishuang Qi, Yan Xu, Yunyan Gu,

https://doi.org/10.18632/aging.103407 pp 13172—13186

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Chen T, Zhao Z, Chen B, Wang Y, Yang F, Wang C, Dong Q, Liu Y, Liang H, Zhao W, Qi L, Xu Y, Gu Y, . An individualized transcriptional signature to predict the epithelial-mesenchymal transition based on relative expression ordering. . 12:13172-13186. https://doi.org/10.18632/aging.103407

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                TY  - JOUR
                AU  - Chen, Tingting 
                AU  - Zhao, Zhangxiang 
                AU  - Chen, Bo 
                AU  - Wang, Yuquan 
                AU  - Yang, Fan 
                AU  - Wang, Chengyu 
                AU  - Dong, Qi 
                AU  - Liu, Yaoyao 
                AU  - Liang, Haihai 
                AU  - Zhao, Wenyuan 
                AU  - Qi, Lishuang 
                AU  - Xu, Yan 
                AU  - Gu, Yunyan 
                TI  - An individualized transcriptional signature to predict the epithelial-mesenchymal transition based on relative expression ordering
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103407
                DO  - 10.18632/aging.103407
                SP  - 13172
                EP  - 13186
                PY  - 
                AB  - The epithelial-mesenchymal transition (EMT) process is involved in cancer cell metastasis and immune system activation. Hence, identification of gene expression signatures capable of predicting the EMT status of cancer cells is essential for development of therapeutic strategies. However, quantitative identification of EMT markers is limited by batch effects, the platform used, or normalization methods. We hypothesized that a set of EMT-related relative expression orderings are highly stable in epithelial samples yet are reversed in mesenchymal samples. To test this hypothesis, we analyzed transcriptome data for ovarian cancer cohorts from publicly available databases, to develop a qualitative 16-gene pair signature (16-GPS) that effectively distinguishes the mesenchymal from epithelial phenotype. Our method was superior to previous quantitative methods in terms of classification accuracy and applicability to individualized patients without requiring data normalization. Patients with mesenchymal-like ovarian cancer showed poorer overall survival compared to patients with epithelial-like ovarian cancer. Additionally, EMT score was positively correlated with expression of immune checkpoint genes and metastasis. We, therefore, established a robust EMT 16-GPS that is independent of detection platform, batch effects and individual variations, and which represents a qualitative signature for investigating the EMT and providing insights into immunotherapy for ovarian cancer patients.
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Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway

Zhi-Gang Mei, Ya-Guang Huang, Zhi-Tao Feng, Ya-Nan Luo, Song-Bai Yang, Li-Peng Du, Kang Jiang, Xiao-Lu Liu, Xian-Yun Fu, Yi-Hui Deng, Hua-Jun Zhou,

https://doi.org/10.18632/aging.103420 pp 13187—13205

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Mei Z, Huang Y, Feng Z, Luo Y, Yang S, Du L, Jiang K, Liu X, Fu X, Deng Y, Zhou H, . Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway. . 12:13187-13205. https://doi.org/10.18632/aging.103420

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Provider: 
 TY - JOUR
 AU - Mei, Zhi-Gang 
 AU - Huang, Ya-Guang 
 AU - Feng, Zhi-Tao 
 AU - Luo, Ya-Nan 
 AU - Yang, Song-Bai 
 AU - Du, Li-Peng 
 AU - Jiang, Kang 
 AU - Liu, Xiao-Lu 
 AU - Fu, Xian-Yun 
 AU - Deng, Yi-Hui 
 AU - Zhou, Hua-Jun 
 TI - Electroacupuncture ameliorates cerebral ischemia/reperfusion injury by suppressing autophagy via the SIRT1-FOXO1 signaling pathway
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103420
 DO - 10.18632/aging.103420
 SP - 13187
 EP - 13205
 PY - 
 AB - Cerebral ischemia/reperfusion (CIR) injury occurs when blood flow is restored in the brain, causing secondary damage to the ischemic tissues. Previous studies have shown that electroacupuncture (EA) treatment contributes to brain protection against CIR injury through modulating autophagy. Studies indicated that SIRT1-FOXO1 plays a crucial role in regulating autophagy. Here we investigated the mechanisms underlying the neuroprotective effect of EA and its role in modulating autophagy via the SIRT1-FOXO1 signaling pathway in rats with CIR injury. EA pretreatment at &#x201C;Baihui&#x201D;, &#x201C;Quchi&#x201D; and &#x201C;Zusanli&#x201D; acupoints (2/15Hz, 1mA, 30 min/day) was performed for 5 days before the rats were subjected to middle cerebral artery occlusion, and the results indicated that EA pretreatment substantially reduced the Longa score and infarct volume, increased the dendritic spine density and lessened autophagosomes in the peri-ischemic cortex of rats. Additionally, EA pretreatment also reduced the ratio of LC3-II/LC3-I, the levels of Ac-FOXO1 and Atg7, and the interaction of Ac-FOXO1 and Atg7, but increased the levels of p62, SIRT1, and FOXO1. The above effects were abrogated by the SIRT1 inhibitor EX527. Thus, we presume that EA pretreatment elicits a neuroprotective effect against CIR injury, potentially by suppressing autophagy via activating the SIRT1-FOXO1 signaling pathway.
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Altered circular RNA expression profiles in the non-ischemic thalamus in focal cortical infarction mice

Fangming Li, Chuqiao Li, Xiaoqiang Li, Yudi Li, Yulan Zhong, Li Ling,

https://doi.org/10.18632/aging.103424 pp 13206—13219

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Li F, Li C, Li X, Li Y, Zhong Y, Ling L, . Altered circular RNA expression profiles in the non-ischemic thalamus in focal cortical infarction mice. . 12:13206-13219. https://doi.org/10.18632/aging.103424

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                TY  - JOUR
                AU  - Li, Fangming 
                AU  - Li, Chuqiao 
                AU  - Li, Xiaoqiang 
                AU  - Li, Yudi 
                AU  - Zhong, Yulan 
                AU  - Ling, Li 
                TI  - Altered circular RNA expression profiles in the non-ischemic thalamus in focal cortical infarction mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103424
                DO  - 10.18632/aging.103424
                SP  - 13206
                EP  - 13219
                PY  - 
                AB  - Focal cerebral infarction leads to secondary changes in non-ischemic areas remote from but connected to the infarct site. Circular RNAs (circRNAs) are involved in the pathophysiological processes of many diseases. However, the expression and roles of circRNAs in non-ischemic remote regions after ischemic stroke remain unknown. In this study, adult male C57BL/6J mice were subjected to permanent distal middle cerebral artery occlusion (MCAO) to establish focal cortical infarction. High-throughput sequencing was used to profile the circRNA expression in the mouse ipsilateral thalamus at 7 and 14 d after MCAO. Bioinformatics analyses were conducted to predict the function of the differential expressed circRNAs&#x2019; host and target genes. Compared with sham group, a total of 2659 circRNAs were significantly altered in the ipsilateral thalamus at 7 or 14 d after MCAO in mice. Among them, 73 circRNAs were significantly altered at both two time points after stroke. GO and KEGG analyses indicated that circRNAs plays important roles in secondary thalamic neurodegeneration and remodeling after focal cortical infarction. This is the first study to profile the circRNA expression in non-ischemic region of ischemic stroke, suggesting that circRNAs may be therapeutic targets for reducing post-stroke secondary remote neurodegeneration.
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Cancer-associated fibroblasts-derived gamma-glutamyltransferase 5 promotes tumor growth and drug resistance in lung adenocarcinoma

Jia-Ru Wei, Jun Dong, Lei Li,

https://doi.org/10.18632/aging.103429 pp 13220—13233

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Wei J, Dong J, Li L, . Cancer-associated fibroblasts-derived gamma-glutamyltransferase 5 promotes tumor growth and drug resistance in lung adenocarcinoma. . 12:13220-13233. https://doi.org/10.18632/aging.103429

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                TY  - JOUR
                AU  - Wei, Jia-Ru 
                AU  - Dong, Jun 
                AU  - Li, Lei 
                TI  - Cancer-associated fibroblasts-derived gamma-glutamyltransferase 5 promotes tumor growth and drug resistance in lung adenocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103429
                DO  - 10.18632/aging.103429
                SP  - 13220
                EP  - 13233
                PY  - 
                AB  - Gamma-glutamyltransferase 5 (GGT5) is a member of the gamma-glutamyl transpeptidase gene family with the capacity of cleaving the gamma-glutamyl moiety of glutathione, but its role in cancer progression has never been revealed. In this study, we found that gene GGT5 was highly expressed in cancer-associated fibroblasts (CAFs) in lung adenocarcinoma, predicting the unfavorable survival of patients with lung adenocarcinoma. Cell growth, foci formation and spheres formation analyses showed that cancer cell proliferation was attenuated under treatment with the conditioned media from GGT5-silenced CAFs. Moreover, high expression of GGT5 in CAFs enhanced the drug resistance of cancer cells by increasing intracellular glutathione and reducing the intracellular reactive oxygen species in cancer cells. In mouse xenograft model, we proved that targeting GGT5 with a small-molecule inhibitor GGsTop could inhibit tumor growth and increase the chemosensitivity of cancer cells. Taken together, our study illuminates that high level of GGT5 in CAFs contributes to cancer cell survival and drug resistance, indicating that GGT5 may be a promising therapeutic target in lung adenocarcinoma.
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Increasing the expression of microRNA-126-5p in the temporal muscle can promote angiogenesis in the chronically ischemic brains of rats subjected to two-vessel occlusion plus encephalo-myo-synangiosis

Chuan Chen, Cong Ling, Jin Gong, Chao Li, Liying Zhang, Shuangqi Gao, Zhangyu Li, Tengchao Huang, Hui Wang, Ying Guo,

https://doi.org/10.18632/aging.103431 pp 13234—13254

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Chen C, Ling C, Gong J, Li C, Zhang L, Gao S, Li Z, Huang T, Wang H, Guo Y, . Increasing the expression of microRNA-126-5p in the temporal muscle can promote angiogenesis in the chronically ischemic brains of rats subjected to two-vessel occlusion plus encephalo-myo-synangiosis. . 12:13234-13254. https://doi.org/10.18632/aging.103431

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                TY  - JOUR
                AU  - Chen, Chuan 
                AU  - Ling, Cong 
                AU  - Gong, Jin 
                AU  - Li, Chao 
                AU  - Zhang, Liying 
                AU  - Gao, Shuangqi 
                AU  - Li, Zhangyu 
                AU  - Huang, Tengchao 
                AU  - Wang, Hui 
                AU  - Guo, Ying 
                TI  - Increasing the expression of microRNA-126-5p in the temporal muscle can promote angiogenesis in the chronically ischemic brains of rats subjected to two-vessel occlusion plus encephalo-myo-synangiosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103431
                DO  - 10.18632/aging.103431
                SP  - 13234
                EP  - 13254
                PY  - 
                AB  - Background: miR-126-5p plays an important role in promoting endothelial cell (EC) proliferation. We thus explored whether miR-126-5p can promote EC proliferation and angiogenesis in chronically ischemic brains (CIBs).Results: Improved revascularization in moyamoya patients was correlated with upregulated miR-126-5p expression in the TM and DM. In vitro experiments showed that miR-126-5p promoted EC proliferation through the PI3K/Akt pathway. CIBs from the agomir group exhibited significantly higher p-Akt, VEGF, CD31 and eNOS expression compared with the control CIBs. The ICBP and the RCF were significantly better in the agomir compared with the control group.Conclusion: Increasing miR-126-5p expression in the TM can promote EC proliferation and angiogenesis in CIBs of 2VO+EMS rats through the PI3K/Akt pathway.Methods: We assessed the correlation between revascularization and miR-126-5p expression in the temporal muscle (TM) and dura mater (DM) of moyamoya patients. The effect of miR-126-5p on EC proliferation and downstream signaling pathways was explored in vitro. We established an animal model of two-vessel occlusion plus encephalo-myo-synangiosis (2VO+EMS), transfected the TM with miR-126-5p agomir/antagomir, compared the expression of miR-126-5p and relevant downstream cytokines in brain tissue among different groups, and investigated the improvement in cerebral blood perfusion (ICBP) and the recovery of cognitive function (RCF).
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Circular RNA circMBOAT2 promotes prostate cancer progression via a miR-1271-5p/mTOR axis

Juanyi Shi, Cheng Liu, Changhao Chen, Kaixuan Guo, Zhuang Tang, Yuming Luo, Luping Chen, Yinjie Su, Kewei Xu,

https://doi.org/10.18632/aging.103432 pp 13255—13280

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Shi J, Liu C, Chen C, Guo K, Tang Z, Luo Y, Chen L, Su Y, Xu K, . Circular RNA circMBOAT2 promotes prostate cancer progression via a miR-1271-5p/mTOR axis. . 12:13255-13280. https://doi.org/10.18632/aging.103432

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                TY  - JOUR
                AU  - Shi, Juanyi 
                AU  - Liu, Cheng 
                AU  - Chen, Changhao 
                AU  - Guo, Kaixuan 
                AU  - Tang, Zhuang 
                AU  - Luo, Yuming 
                AU  - Chen, Luping 
                AU  - Su, Yinjie 
                AU  - Xu, Kewei 
                TI  - Circular RNA circMBOAT2 promotes prostate cancer progression via a miR-1271-5p/mTOR axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103432
                DO  - 10.18632/aging.103432
                SP  - 13255
                EP  - 13280
                PY  - 
                AB  - Patients with advanced prostate cancer (PCa) have poor prognosis. Circular RNAs (circRNAs) regulate biological processes in a variety of cancers, but the precise roles of circRNAs in PCa are poorly understood. Herein, we identified a novel circRNA, termed circMBOAT2 (has_circ_0007334), which was significantly overexpressed in PCa tissues and cell lines. Overexpression of circMBOAT2 was associated with high Gleason score, advanced pathological T stage, and poor prognosis. Overexpression of circMBOAT2 promoted proliferation, migration, and invasion of PCa cells in vitro, and enhanced tumorigenesis and metastasis in vivo. Mechanistically, circMBOAT2 overexpression upregulated the expression of mTOR by acting as a decoy for miR-1271-5p, resulting in the activation of the PI3K/Akt pathway, ultimately promoting the progression of PCa. Importantly, application of an inhibitor of mTOR significantly antagonized circMBOAT2-mediated PCa tumorigenesis in vivo. circMBOAT2 promotes proliferation and metastasis of PCa through miR-1271-5p/mTOR axis-mediated activation of the PI3K/Akt pathway. In summary, our findings uncover a molecular mechanism in the progression of PCa and indicate that circMBOAT2 may be a useful prognostic biomarker and therapeutic target in PCa.
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SLC7A2 serves as a potential biomarker and therapeutic target for ovarian cancer

Tianshui Sun, Fangfang Bi, Zhuonan Liu, Qing Yang,

https://doi.org/10.18632/aging.103433 pp 13281—13296

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Sun T, Bi F, Liu Z, Yang Q, . SLC7A2 serves as a potential biomarker and therapeutic target for ovarian cancer. . 12:13281-13296. https://doi.org/10.18632/aging.103433

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                TY  - JOUR
                AU  - Sun, Tianshui 
                AU  - Bi, Fangfang 
                AU  - Liu, Zhuonan 
                AU  - Yang, Qing 
                TI  - SLC7A2 serves as a potential biomarker and therapeutic target for ovarian cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103433
                DO  - 10.18632/aging.103433
                SP  - 13281
                EP  - 13296
                PY  - 
                AB  - The solute carrier (SLC) family is the largest group of membrane transporters, but their functions in ovarian cancer (OV) remain unclear. We analyzed SLC family members with amino acids-transporting functions in OV. The mRNA expression levels and prognostic values of SLCs in OV were analyzed in the Gene Expression Profiling Interactive Analysis and Kaplan&#x2013;Meier Plotter database. Solute carrier family 7 member 2 (SLC7A2), which showed differential expression and the most significant prognostic value, was selected for further analyses. The cBioPortal database, Gene Set Enrichment Analysis and Weighted Correlation Network Analysis were used to explore the potential functions and molecular mechanisms of SLC7A2 in OV. Validations in our own samples and in Gene Expression Omnibus datasets were conducted. Functional validation in OV cell lines was carried out. In total, 73 SLC family members were analyzed. Seven members were upregulated while 11 members were downregulated in OV and 15 members were protective factors for prognosis while 12 members were risk factors. SLC7A2 was downregulated in OV, and it was positively associated with prognosis. Knockdown of SLC7A2 promoted viability, invasion and migration of OV cells. These SLC family members and in particular SLC7A2 represented novel biomarkers for diagnosis and treatment for OV.
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Cytoplasmic PCNA is located in the actin belt and involved in osteoclast differentiation

Donge Tang, Xiaohui Liu, Kezhi Chen, Zhipeng Li, Yong Dai, Jiake Xu, Huan-Tian Zhang, Xuejuan Gao, Langxia Liu,

https://doi.org/10.18632/aging.103434 pp 13297—13317

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Tang D, Liu X, Chen K, Li Z, Dai Y, Xu J, Zhang H, Gao X, Liu L, . Cytoplasmic PCNA is located in the actin belt and involved in osteoclast differentiation. . 12:13297-13317. https://doi.org/10.18632/aging.103434

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                TY  - JOUR
                AU  - Tang, Donge 
                AU  - Liu, Xiaohui 
                AU  - Chen, Kezhi 
                AU  - Li, Zhipeng 
                AU  - Dai, Yong 
                AU  - Xu, Jiake 
                AU  - Zhang, Huan-Tian 
                AU  - Gao, Xuejuan 
                AU  - Liu, Langxia 
                TI  - Cytoplasmic PCNA is located in the actin belt and involved in osteoclast differentiation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103434
                DO  - 10.18632/aging.103434
                SP  - 13297
                EP  - 13317
                PY  - 
                AB  - Osteoporosis (OP) is an age-related osteolytic disease and characterized by low bone mass and more prone to fracture due to active osteoclasts. Proliferating cell nuclear antigen (PCNA) has been long identified as a nuclear protein playing critical roles in the regulation of DNA replication and repair. Recently, a few studies have demonstrated the cytoplasmic localization of PCNA and its function associated with apoptosis in neutrophil and neuroblastoma cells. However, the involvement of PCNA, including the cytoplasmic PCNA, in the osteoclast differentiation remains unclear. In the present study, we show that PCNA is translocated from nucleus to cytoplasm during the RANKL-induced osteoclast differentiation, and localized in the actin belt of mature osteoclast. Knockdown of PCNA significantly affected the integrity of actin belt, the formation of multinucleated osteoclasts, the expression of osteoclast-specific genes, and the in vitro bone resorption. Interactomic study has revealed &#x3B2;-actin as the major interacting partner of the cytoplasmic PCNA, suggesting that cytoplasmic PCNA might play a critical role in the differentiation of osteoclast through regulation of actin-cytoskeleton remodeling. Taken together, our results demonstrate the critical role of cytoplasmic PCNA during the process of osteoclast differentiation, and provided a potential therapeutic target for treatment of osteoclast-related bone diseases.
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Subtype-specific risk models for accurately predicting the prognosis of breast cancer using differentially expressed autophagy-related genes

Baoai Han, He Zhang, Yuying Zhu, Xingxing Han, Zhiyong Wang, Zicong Gao, Yue Yuan, Ruinan Tian, Fei Zhang, Ruifang Niu,

https://doi.org/10.18632/aging.103437 pp 13318—13337

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Han B, Zhang H, Zhu Y, Han X, Wang Z, Gao Z, Yuan Y, Tian R, Zhang F, Niu R, . Subtype-specific risk models for accurately predicting the prognosis of breast cancer using differentially expressed autophagy-related genes. . 12:13318-13337. https://doi.org/10.18632/aging.103437

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                TY  - JOUR
                AU  - Han, Baoai 
                AU  - Zhang, He 
                AU  - Zhu, Yuying 
                AU  - Han, Xingxing 
                AU  - Wang, Zhiyong 
                AU  - Gao, Zicong 
                AU  - Yuan, Yue 
                AU  - Tian, Ruinan 
                AU  - Zhang, Fei 
                AU  - Niu, Ruifang 
                TI  - Subtype-specific risk models for accurately predicting the prognosis of breast cancer using differentially expressed autophagy-related genes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103437
                DO  - 10.18632/aging.103437
                SP  - 13318
                EP  - 13337
                PY  - 
                AB  - Emerging evidence suggests that the dysregulation of autophagy-related genes (ARGs) is coupled with the carcinogenesis and progression of breast cancer (BRCA). We constructed three subtype-specific risk models using differentially expressed ARGs. In Luminal, Her-2, and Basal-like BRCA, four- (BIRC5, PARP1, ATG9B, and TP63), three- (ITPR1, CCL2, and GAPDH), and five-gene (PRKN, FOS, BAX, IFNG, and EIF4EBP1) risk models were identified, which all have a receiver operating characteristic &gt; 0.65 in the training and testing dataset. Multivariable Cox analysis showed that those risk models can accurately and independently predict the overall survival of BRCA patients. Comprehensive analysis showed that the 12 identified ARGs were correlated with the overall survival of BRCA patients; six of the ARGs (PARP1, TP63, CCL2, GAPDH, FOS, and EIF4EBP1) were differentially expressed between BRCA and normal breast tissue at the protein level. In addition, the 12 identified ARGs were highly interconnected and displayed high frequency of copy number variation in BRCA samples. Gene set enrichment analysis suggested that the deactivation of the immune system was the important driving force for the progression of Basal-like BRCA. This study demonstrated that the 12 ARG signatures were potential multi-dimensional biomarkers for the diagnosis, prognosis, and treatment of BRCA.
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circRNA_100859 functions as an oncogene in colon cancer by sponging the miR-217-HIF-1α pathway

Peng Zhou, Wei Xie, Hua-Lin Huang, Rong-Qi Huang, Chao Tian, Hong-Bo Zhu, Ying-Huan Dai, Zhi-Yuan Li,

https://doi.org/10.18632/aging.103438 pp 13338—13353

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Zhou P, Xie W, Huang H, Huang R, Tian C, Zhu H, Dai Y, Li Z, . circRNA_100859 functions as an oncogene in colon cancer by sponging the miR-217-HIF-1α pathway. . 12:13338-13353. https://doi.org/10.18632/aging.103438

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                TY  - JOUR
                AU  - Zhou, Peng 
                AU  - Xie, Wei 
                AU  - Huang, Hua-Lin 
                AU  - Huang, Rong-Qi 
                AU  - Tian, Chao 
                AU  - Zhu, Hong-Bo 
                AU  - Dai, Ying-Huan 
                AU  - Li, Zhi-Yuan 
                TI  - circRNA_100859 functions as an oncogene in colon cancer by sponging the miR-217-HIF-1α pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103438
                DO  - 10.18632/aging.103438
                SP  - 13338
                EP  - 13353
                PY  - 
                AB  - Circular RNAs (circRNAs) play an important role in cancer development and progression by regulating gene expression. The present study aimed to investigate the function of circRNA_100859 in colon cancer. circRNA expression profiles from a human circRNAs chip were analyzed. The effects of circRNA_100859 on cell proliferation and apoptosis were assessed in vitro and interactions between circRNA_100859 and its micro (mi)RNA and target genes were analyzed. The diagnostic and prognostic significance of circRNA_100859 was also investigated. It was identified that circRNA_100859 was overexpressed in colon cancer tissues and promoted cell proliferation and inhibited cell apoptosis. Additionally, bioinformatics and a dual-luciferase reporter assay confirmed that circRNA_100859 acted as a miR-217 sponge, and miR-217 directly targeted hypoxia-inducible factor (HIF)-1&#x3B1;. Rescue assays demonstrated that HIF-1&#x3B1; protein and mRNA expression levels and cell proliferation were regulated by the circRNA_100859/miR-217 axis (P&lt;0.05). Furthermore, statistical analysis showed that the circRNA_100859-miR-217-HIF-1&#x3B1; axis was associated with Tumor-Node-Metastasis (TNM) stage, histological grade, and KRAS mutations, and also showed high diagnostic and prognostic value for patients with colon cancer (P&lt;0.05). Therefore, it was concluded that circRNA_100859 functions as an oncogene in colon cancer by sponging the miR-217-HIF-1&#x3B1; pathway. In addition, the circRNA_100859-miR-217-HIF-1&#x3B1; axis may serve as a novel diagnostic and prognostic biomarker for patients with colon cancer.
                ER  -

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IL-22 promotes tumor growth of breast cancer cells in mice

Ying Zhang, Cong Liu, Jun Gao, Siqi Shao, Yingying Cui, Songlou Yin, Bin Pan,

https://doi.org/10.18632/aging.103439 pp 13354—13364

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Zhang Y, Liu C, Gao J, Shao S, Cui Y, Yin S, Pan B, . IL-22 promotes tumor growth of breast cancer cells in mice. . 12:13354-13364. https://doi.org/10.18632/aging.103439

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                TY  - JOUR
                AU  - Zhang, Ying 
                AU  - Liu, Cong 
                AU  - Gao, Jun 
                AU  - Shao, Siqi 
                AU  - Cui, Yingying 
                AU  - Yin, Songlou 
                AU  - Pan, Bin 
                TI  - IL-22 promotes tumor growth of breast cancer cells in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103439
                DO  - 10.18632/aging.103439
                SP  - 13354
                EP  - 13364
                PY  - 
                AB  - Increased interleukin-22 (IL-22) level was reported to associate with progression of breast cancer. Regulation of IL-22 in breast cancer still needs to be elucidated. We assessed the effect of giving IL-22 in tumor growth of mice inoculated with 4T1, MCF7 and MDA-MB-231 breast cancer cells. IL-22-producing cells were analyzed in tumor tissues. We also analyzed the impact of giving IL-1&#x3B2; and IL-23 on IL-22 levels in tumor tissues. Giving exogenous IL-22 increased tumor size and intra-tumor Ki-67-positive cells in vivo. IL-22 increased phosphorylated STAT3 level and proliferation of breast cancer cells in vitro, an effect blocked by a STAT3-inhibitor stattic. Endogenous IL-22 mRNA level was up-regulated in tumor tissue, compared with normal mammary tissue. Innate lymphoid cell group 3 (ILC3) is a major producer of IL-22 in 4T1 tumor. Giving IL-1&#x3B2; and/or IL-23 increased cell proliferation in 4T1 tumor, which was reversed by concurrent use of an IL-22 neutralization antibody. IL-1&#x3B2; and IL-23 increased levels of IL-22 mRNA and IL-22-producing ILC3 in 4T1 tumor. Our findings suggest a mechanism for how IL-22 regulates tumor growth in breast cancer, and indicate blocking IL-22 function might reduce IL-1&#x3B2;- and IL-23-induced tumor progression of breast cancer.
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TCF7L2 rs290487 C allele aberrantly enhances hepatic gluconeogenesis through allele-specific changes in transcription and chromatin binding

Xueyou Zhang, Panpan Ye, Haitao Huang, Baohong Wang, Fengqin Dong, Qi Ling,

https://doi.org/10.18632/aging.103442 pp 13365—13387

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Zhang X, Ye P, Huang H, Wang B, Dong F, Ling Q, . TCF7L2 rs290487 C allele aberrantly enhances hepatic gluconeogenesis through allele-specific changes in transcription and chromatin binding. . 12:13365-13387. https://doi.org/10.18632/aging.103442

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Provider: 
 TY - JOUR
 AU - Zhang, Xueyou 
 AU - Ye, Panpan 
 AU - Huang, Haitao 
 AU - Wang, Baohong 
 AU - Dong, Fengqin 
 AU - Ling, Qi 
 TI - TCF7L2 rs290487 C allele aberrantly enhances hepatic gluconeogenesis through allele-specific changes in transcription and chromatin binding
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103442
 DO - 10.18632/aging.103442
 SP - 13365
 EP - 13387
 PY - 
 AB - In this study, we investigated the mechanisms underlying the altered hepatic glucose metabolism and enhanced diabetes risk in individuals with the TCF7L2 rs290487 C allele. Analysis of 195 cirrhotic patients revealed a higher insulin resistance index and incidence of hepatogenous diabetes in patients with the rs290487 C/C genotype compared to those with the C/T or T/T genotype. The in vitro experiments using targeted mutant PLC-PRF-5 cell line showed that cells with the rs290487 C/C genotype (C/C cells) had higher glucose production, lower glucose uptake, and lower TCF7L2 mRNA and protein levels than those with the C/T genotype (C/T cells). Integrated multi-omics analysis of ChIP-seq, ATAC-seq, RNA-seq, and metabolomics data showed genome-wide alterations in the DNA binding affinity of TCF7L2 in the C/C cells, including gain (e.g., PFKP and PPARGC1A) and loss (e.g., PGK1 and PGM1) of binding sites in several glucose metabolism-related genes. These allele-specific changes in transcriptional regulation lead to increased expression of gluconeogenesis-related genes (PCK1, G6PC and PPARGC1A) and their downstream metabolites (oxaloacetate and &#x3B2;-D-fructose 2,6-bisphosphate). These findings demonstrate that the TCF7L2 rs290487 C allele enhances gluconeogenesis through allele-specific changes in transcription and chromatin binding.
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PGK1 inhibitor CBR-470-1 protects neuronal cells from MPP⁺

Jinyu Zheng, Jian-liang Zhu, Yufeng Zhang, Hao Zhang, Yu Yang, De-Rong Tang, Jian Sun,

https://doi.org/10.18632/aging.103443 pp 13388—13399

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Zheng J, Zhu J, Zhang Y, Zhang H, Yang Y, Tang D, Sun J, . PGK1 inhibitor CBR-470-1 protects neuronal cells from MPP⁺. . 12:13388-13399. https://doi.org/10.18632/aging.103443

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Provider: 
 TY - JOUR
 AU - Zheng, Jinyu 
 AU - Zhu, Jian-liang 
 AU - Zhang, Yufeng 
 AU - Zhang, Hao 
 AU - Yang, Yu 
 AU - Tang, De-Rong 
 AU - Sun, Jian 
 TI - PGK1 inhibitor CBR-470-1 protects neuronal cells from MPP+
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103443
 DO - 10.18632/aging.103443
 SP - 13388
 EP - 13399
 PY - 
 AB - The neurotoxin MPP+ (1-methyl-4-phenylpyridinium ion) disrupts mitochondrial function leading to oxidative stress and neuronal death. Here we examine whether activation of the Keap1-Nrf2 cascade can protect SH-SY5Y neuroblastoma cells from MPP+-induced cytotoxicity. Treatment of SH-SY5Y cells with CBR-470-1, an inhibitor of the glycolytic enzyme phosphoglycerate kinase 1 (PGK1), leads to methylglyoxal modification of Keap1, Keap1-Nrf2 disassociation, and increased expression of Nrf2 responsive genes. Pretreatment with CBR-470-1 potently attenuated MPP+-induced oxidative injury and SH-SY5Y cell apoptosis. CBR-470-1 neuroprotection is dependent upon Nrf2, as Nrf2 shRNA or CRISPR/Cas9-mediated Nrf2 knockout, abolished CBR-470-1-induced SH-SY5Y cytoprotection against MPP+. Consistent with these findings, PGK1 depletion or knockout mimicked CBR-470-1-induced actions and rendered SH-SY5Y cells resistant to MPP+-induced cytotoxicity. Furthermore, activation of the Nrf2 cascade by CRISPR/Cas9-induced Keap1 knockout protected SH-SY5Y cells from MPP+. In Keap1 or PGK1 knockout SH-SY5Y cells,CBR-470-1 failed to offer further cytoprotection against MPP+. Collectively PGK1 inhibition by CBR-470-1 protects SH-SY5Y cells from MPP+ via activation of the Keap1-Nrf2 cascade.
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Penehyclidine hydrochloride inhibits renal ischemia/reperfusion-induced acute lung injury by activating the Nrf2 pathway

Zhaohui Liu, Yan Li, Lili Yu, Yulin Chang, Jingui Yu,

https://doi.org/10.18632/aging.103444 pp 13400—13421

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Liu Z, Li Y, Yu L, Chang Y, Yu J, . Penehyclidine hydrochloride inhibits renal ischemia/reperfusion-induced acute lung injury by activating the Nrf2 pathway. . 12:13400-13421. https://doi.org/10.18632/aging.103444

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                TY  - JOUR
                AU  - Liu, Zhaohui 
                AU  - Li, Yan 
                AU  - Yu, Lili 
                AU  - Chang, Yulin 
                AU  - Yu, Jingui 
                TI  - Penehyclidine hydrochloride inhibits renal ischemia/reperfusion-induced acute lung injury by activating the Nrf2 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103444
                DO  - 10.18632/aging.103444
                SP  - 13400
                EP  - 13421
                PY  - 
                AB  - The nuclear factor (NF)-&#x3BA;B and NOD-like receptor protein 3 (NLRP3) pathways promote inflammatory signaling that injures the kidneys, whereas the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway promotes anti-inflammatory signaling that inhibits oxidative damage. Penehyclidine hydrochloride (PHC) inhibits NF-&#x3BA;B and activates Nrf2 signaling. We investigated whether PHC induces communication between the Nrf2 and NF-&#x3BA;B/NLRP3 pathways, thereby protecting against renal ischemia/reperfusion (rI/R)-induced lung inflammation. Rat alveolar macrophages (NR8383 cells) were stimulated for 24 h with PHC with or without brusatol (a Nrf2 antagonist), after which they were treated for 4 h with tert-butyl hydroperoxide (10 mM). PHC Nrf2-dependently alleviated tert-butyl hydroperoxide-induced reactive oxygen species production in alveolar macrophages. Additionally, wild-type and Nrf2&#x2212;/&#x2212; rats were each divided into four groups: (1) sham, (2) PHC (1 mg/kg), (3) rI/R and (4) rI/R + PHC (1 mg/kg). PHC markedly induced the Nrf2 and adenosine monophosphate-activated protein kinase pathways and suppressed rI/R-induced NF-&#x3BA;B and NLRP3 activation in the lungs. Nrf2 deficiency diminished the ability of PHC to ameliorate rI/R-induced histopathological alterations and reactive oxygen species release in the lungs; however, PHC inhibited NLRP3 signaling Nrf2-dependently, while it inhibited NF-&#x3BA;B signaling Nrf2-independently. Our findings demonstrate the beneficial effects of PHC on rI/R-induced lung inflammation.
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Codonopsis pilosula polysaccharide attenuates Aβ toxicity and cognitive defects in APP/PS1 mice

Lu Wan, Qing Zhang, Hongbin Luo, Zhendong Xu, Sheng Huang, Fumin Yang, Yi Liu, Yacoubou Abdoul Razak Mahaman, Dan Ke, Qun Wang, Rong Liu, Jian-Zhi Wang, Xiji Shu, Xiaochuan Wang,

https://doi.org/10.18632/aging.103445 pp 13422—13436

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Wan L, Zhang Q, Luo H, Xu Z, Huang S, Yang F, Liu Y, Mahaman YAR, Ke D, Wang Q, Liu R, Wang J, Shu X, et al, . Codonopsis pilosula polysaccharide attenuates Aβ toxicity and cognitive defects in APP/PS1 mice. . 12:13422-13436. https://doi.org/10.18632/aging.103445

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Provider: 
 TY - JOUR
 AU - Wan, Lu 
 AU - Zhang, Qing 
 AU - Luo, Hongbin 
 AU - Xu, Zhendong 
 AU - Huang, Sheng 
 AU - Yang, Fumin 
 AU - Liu, Yi 
 AU - Mahaman, Yacoubou Abdoul Razak 
 AU - Ke, Dan 
 AU - Wang, Qun 
 AU - Liu, Rong 
 AU - Wang, Jian-Zhi 
 AU - Shu, Xiji 
 AU - Wang, Xiaochuan 
 TI - Codonopsis pilosula polysaccharide attenuates Aβ toxicity and cognitive defects in APP/PS1 mice
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103445
 DO - 10.18632/aging.103445
 SP - 13422
 EP - 13436
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Wan, Lu 
 AU - Zhang, Qing 
 AU - Luo, Hongbin 
 AU - Xu, Zhendong 
 AU - Huang, Sheng 
 AU - Yang, Fumin 
 AU - Liu, Yi 
 AU - Mahaman, Yacoubou Abdoul Razak 
 AU - Ke, Dan 
 AU - Wang, Qun 
 AU - Liu, Rong 
 AU - Wang, Jian-Zhi 
 AU - Shu, Xiji 
 AU - Wang, Xiaochuan 
 TI - Codonopsis pilosula polysaccharide attenuates Aβ toxicity and cognitive defects in APP/PS1 mice
 JO - 
 JA - 
 VL - 12
 IS - 13
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103445
 DO - 10.18632/aging.103445
 SP - 13422
 EP - 13436
 PY - 
 AB - Codonopsis pilosula Polysaccharides (CPPs), a traditional Chinese medicine used for thousands of years, is a potential neuroprotective polysaccharide via a relatively poorly understood mechanism. We previously reported that CPPs attenuated tau pathology in hTau transfected mice and therefore in the current work investigated the effect of CPPs on A&#x3B2; toxicity and cognitive defects in APP/PS1 mice model. It was found that one-month intragastric administration of CPPs significantly ameliorated cognitive defects in APP/PS1 mice. In addition, CPPs treatment mitigated the loss of the synaptic plasticity and increased the synaptic proteins including synaptotagmin and PSD95. The expression of A&#x3B2;42 and A&#x3B2;40 was remarkably decreased in the hippocampus of APP/PS1 mice after CPPs treatment. We also found that CPPs coincubation significantly reduced the amount of APP&#x3B2; and A&#x3B2;42 expression in cells. Intriguingly, the activity of BACE1 was decreased following CPPs treatment in both the hippocampus of APP/PS1 mice and in vitro experiments. Collectively, these results indicated that CPPs attenuated A&#x3B2; pathology in APP/PS1 mice, and down-regulating BACE1 might be the underlaying mechanism which could be a therapeutic target for alleviating cognitive defects in AD pathology.
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Loss of β-catenin via activated GSK3β causes diabetic retinal neurodegeneration by instigating a vicious cycle of oxidative stress-driven mitochondrial impairment

Xing-Sheng Shu, Huazhang Zhu, Xiaoyan Huang, Yangfan Yang, Dandan Wang, Yiling Zhang, Weizhen Zhang, Ying Ying,

https://doi.org/10.18632/aging.103446 pp 13437—13462

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Shu X, Zhu H, Huang X, Yang Y, Wang D, Zhang Y, Zhang W, Ying Y, . Loss of β-catenin via activated GSK3β causes diabetic retinal neurodegeneration by instigating a vicious cycle of oxidative stress-driven mitochondrial impairment. . 12:13437-13462. https://doi.org/10.18632/aging.103446

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                TY  - JOUR
                AU  - Shu, Xing-Sheng 
                AU  - Zhu, Huazhang 
                AU  - Huang, Xiaoyan 
                AU  - Yang, Yangfan 
                AU  - Wang, Dandan 
                AU  - Zhang, Yiling 
                AU  - Zhang, Weizhen 
                AU  - Ying, Ying 
                TI  - Loss of β-catenin via activated GSK3β causes diabetic retinal neurodegeneration by instigating a vicious cycle of oxidative stress-driven mitochondrial impairment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103446
                DO  - 10.18632/aging.103446
                SP  - 13437
                EP  - 13462
                PY  - 
                AB  - Synaptic neurodegeneration of retinal ganglion cells (RGCs) is the earliest event in the pathogenesis of diabetic retinopathy. Our previous study proposed that impairment of mitochondrial trafficking by hyperphosphorylated tau is a potential contributor to RGCs synapse degeneration. However, other molecular mechanisms underlying mitochondrial defect in diabetic retinal neurodegeneration remain to be elucidated. Here, using a high-fat diet (HFD)-induced diabetic mouse model, we showed for the first time that downregulation of active &#x3B2;-catenin due to abnormal GSK3&#x3B2; activation caused synaptic neurodegeneration of RGCs by inhibiting ROS scavenging enzymes, thus triggering oxidative stress-driven mitochondrial impairment in HFD-induced diabetes. Rescue of &#x3B2;-catenin via ectopic expression of &#x3B2;-catenin with a recombinant adenoviral vector, or via GSK3&#x3B2; inhibition by a targeted si-GSK3&#x3B2;, through intravitreal administration, abrogated the oxidative stress-derived mitochondrial defect and synaptic neurodegeneration in diabetic RGCs. By contrast, ablation of &#x3B2;-catenin by si-&#x3B2;-catenin abolished the protective effect of GSK3&#x3B2; inhibition on diabetic RGCs by suppression of antioxidant scavengers and augmentation of oxidative stress-driven mitochondrial lesion. Thus, our data identify &#x3B2;-catenin as a part of an endogenous protective system in diabetic RGCs and a promising target to develop intervention strategies that protect RGCs from neurodegeneration at early onset of diabetic retinopathy.
                ER  -

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Mechanistic study of mtROS-JNK-SOD2 signaling in bupivacaine-induced neuron oxidative stress

Zhongjie Liu, Shiyuan Xu, Zhonghua Ji, Huali Xu, Wei Zhao, Zhengyuan Xia, Rui Xu,

https://doi.org/10.18632/aging.103447 pp 13463—13476

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Liu Z, Xu S, Ji Z, Xu H, Zhao W, Xia Z, Xu R, . Mechanistic study of mtROS-JNK-SOD2 signaling in bupivacaine-induced neuron oxidative stress. . 12:13463-13476. https://doi.org/10.18632/aging.103447

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                TY  - JOUR
                AU  - Liu, Zhongjie 
                AU  - Xu, Shiyuan 
                AU  - Ji, Zhonghua 
                AU  - Xu, Huali 
                AU  - Zhao, Wei 
                AU  - Xia, Zhengyuan 
                AU  - Xu, Rui 
                TI  - Mechanistic study of mtROS-JNK-SOD2 signaling in bupivacaine-induced neuron oxidative stress
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103447
                DO  - 10.18632/aging.103447
                SP  - 13463
                EP  - 13476
                PY  - 
                AB  - Manganese superoxide dismutase (SOD2) is a key enzyme to scavenge free radical superoxide in the mitochondrion. SOD2 deficiency leads to oxidative injury in cells. Bupivacaine, a local anesthetic commonly used in clinic, could induce neurotoxic injury via oxidative stress. The role and the mechanism of SOD2 regulation in bupivacaine-induced oxidative stress remains unclear. Here, bupivacaine was used to treat Sprague-Dawley rats with intrathecal injection and culture human neuroblastoma cells for developing vivo injury model and vitro injury model. The results showed that bupivacaine caused the over-production of mitochondrial reactive oxygen species (mtROS), the activation of C-Jun N-terminal kinase (JNK), and the elevation of SOD2 transcription. Decrease of mtROS with N-acetyl-L-cysteine attenuated the activation of JNK and the increase of SOD2 transcription. Inhibition of JNK signaling with a small interfering RNA (siRNA) or with sp600125 down-regulated the increase of SOD2 transcription. SOD2 gene knock-down exacerbated bupivacaine-induced mtROS generation and neurotoxic injury but had no effect on JNK phosphorylation. Mito-TEMPO (a mitochondria-targeted antioxidant) could protect neuron against bupivacaine-induced toxic injury. Collectively, our results confirm that mtROS stimulates the transcription of SOD2 via activating JNK signaling in bupivacaine-induced oxidative stress. Enhancing antioxidant ability of SOD2 might be crucial in combating bupivacaine-induced neurotoxic injury.
                ER  -

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Hydrostatic pressure induces osteogenic differentiation of adipose-derived mesenchymal stem cells through increasing lncRNA-PAGBC

Jiangying Ru, Lieping Guo, Yinjun Ji, Yunfei Niu,

https://doi.org/10.18632/aging.103448 pp 13477—13487

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Ru J, Guo L, Ji Y, Niu Y, . Hydrostatic pressure induces osteogenic differentiation of adipose-derived mesenchymal stem cells through increasing lncRNA-PAGBC. . 12:13477-13487. https://doi.org/10.18632/aging.103448

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                TY  - JOUR
                AU  - Ru, Jiangying 
                AU  - Guo, Lieping 
                AU  - Ji, Yinjun 
                AU  - Niu, Yunfei 
                TI  - Hydrostatic pressure induces osteogenic differentiation of adipose-derived mesenchymal stem cells through increasing lncRNA-PAGBC
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103448
                DO  - 10.18632/aging.103448
                SP  - 13477
                EP  - 13487
                PY  - 
                AB  - Induced osteogenesis of adipose-derived mesenchymal stem cells (AMSCs) has been used to facilitate bone regeneration. Specifically, hydrostatic pressure (HP) has been implicated as a key regulator of AMSC differentiation, whereas the mechanisms that underlie the effects of HP on osteogenesis of AMSCs are not fully understood. Long noncoding RNAs (lncRNAs) are emerging regulators for osteogenic differentiation from AMSCs. In the current study, we found that lncRNA-PAGBC was a specific lncRNA that significantly upregulated during osteogenic differentiation of AMSCs based on published database. HP increased lncRNA-PAGBC, which is a competitive endogenous RNA (ceRNA) that binds to the osteogenesis-inhibitory microRNA, miR-133b, to regulate osteogenic differentiation of AMSCs. Moreover, a key osteogenesis-trigger gene, runt-related transcription factor 2 (RUNX2), was identified as a target gene for miR-133b. Suppression of RUNX2 by miR-133b caused impaired osteogenic differentiation of AMSCs. Furthermore, lncRNA-PAGBC overexpression upregulated, whereas lncRNA-PAGBC silencing decreased the expression of RUNX2 through miR-133b. Together, these data suggest that HP induces osteogenic differentiation of AMSCs through increasing lncRNA-PAGBC.
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TRIM29 mediates lung squamous cell carcinoma cell metastasis by regulating autophagic degradation of E-cadherin

Weifeng Xu, Beibei Chen, Dianshan Ke, Xiaobing Chen,

https://doi.org/10.18632/aging.103451 pp 13488—13501

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Xu W, Chen B, Ke D, Chen X, . TRIM29 mediates lung squamous cell carcinoma cell metastasis by regulating autophagic degradation of E-cadherin. . 12:13488-13501. https://doi.org/10.18632/aging.103451

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                TY  - JOUR
                AU  - Xu, Weifeng 
                AU  - Chen, Beibei 
                AU  - Ke, Dianshan 
                AU  - Chen, Xiaobing 
                TI  - TRIM29 mediates lung squamous cell carcinoma cell metastasis by regulating autophagic degradation of E-cadherin
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103451
                DO  - 10.18632/aging.103451
                SP  - 13488
                EP  - 13501
                PY  - 
                AB  - Lung squamous cell carcinoma (LSCC) is the most common histological type of primary lung cancer. In this study, we had tested the biological role of TRIM29 in LSCC cells. TRIM29 abundance, the relationships between TRIM29 and E-cadherin and autophagy degradation related proteins in clinical tissues and six cell lines were studied with quantitative real-time PCR test (qRT-PCR) and western blot. TRIM29 overexpression treated HTB-182 cells and knockdown treated NCL-H1915 cells was used for studying cell proliferation, colony formation, migration, invasion, and the expression of epithelial mesenchymal transformation (EMT) associated biomarkers. The relationships between TRIM29 and BECN1 were investigated with western blot. TRIM29 was profoundly overexpressed in LSCC tissues and cells compared with human normal bronchial epithelial cells (HNBE). High TRIM29 expression was closely related to overall survival (OS). TRIM29 overexpression and knockdown affected LSCC activity and the expression of EMT associated biomarkers. TRIM29 can regulate the degradation of E-cadherin and autophagy of LSCC through BECN1 gene, and promote autophagy in HTB-182 and NCL-H1915 cells. Our results revealed that TRIM29 could promote the proliferation, migration, and invasion of LSCC via E-cadherin autophagy degradation. The results are useful for further study in LSCC.
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Weighted correlation gene network analysis reveals a new stemness index-related survival model for prognostic prediction in hepatocellular carcinoma

Qiujing Zhang, Jia Wang, Menghan Liu, Qingqing Zhu, Qiang Li, Chao Xie, Congcong Han, Yali Wang, Min Gao, Jie Liu,

https://doi.org/10.18632/aging.103454 pp 13502—13517

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Zhang Q, Wang J, Liu M, Zhu Q, Li Q, Xie C, Han C, Wang Y, Gao M, Liu J, . Weighted correlation gene network analysis reveals a new stemness index-related survival model for prognostic prediction in hepatocellular carcinoma. . 12:13502-13517. https://doi.org/10.18632/aging.103454

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Provider: 
                TY  - JOUR
                AU  - Zhang, Qiujing 
                AU  - Wang, Jia 
                AU  - Liu, Menghan 
                AU  - Zhu, Qingqing 
                AU  - Li, Qiang 
                AU  - Xie, Chao 
                AU  - Han, Congcong 
                AU  - Wang, Yali 
                AU  - Gao, Min 
                AU  - Liu, Jie 
                TI  - Weighted correlation gene network analysis reveals a new stemness index-related survival model for prognostic prediction in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103454
                DO  - 10.18632/aging.103454
                SP  - 13502
                EP  - 13517
                PY  - 
                AB  - In this study, we constructed a new survival model using mRNA expression-based stemness index (mRNAsi) for prognostic prediction in hepatocellular carcinoma (HCC). Weighted correlation network analysis (WGCNA) of HCC transcriptome data (374 HCC and 50 normal liver tissue samples) from the TCGA database revealed 7498 differentially expressed genes (DEGs) that clustered into seven gene modules. LASSO regression analysis of the top two gene modules identified ANGPT2, EMCN, GLDN, USHBP1 and ZNF532 as the top five mRNAsi-related genes. We constructed our survival model with these five genes and tested its performance using 243 HCC and 202 normal liver samples from the ICGC database. Kaplan-Meier survival curve and receive operating characteristic curve analyses showed that the survival model accurately predicted the prognosis and survival of high- and low-risk HCC patients with high sensitivity and specificity. The expression of these five genes was significantly higher in the HCC tissues from the TCGA, ICGC, and GEO datasets (GSE25097 and GSE14520) than in normal liver tissues. These findings demonstrate that a new survival model derived from five strongly correlating mRNAsi-related genes provides highly accurate prognoses for HCC patients.
                ER  -

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Association of the serum microRNA-29 family with cognitive impairment in Parkinson's disease

Linlin Han, Yilin Tang, Xiaochen Bai, Xiaoniu Liang, Yun Fan, Yan Shen, Fang Huang, Jian Wang,

https://doi.org/10.18632/aging.103458 pp 13518—13528

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Han L, Tang Y, Bai X, Liang X, Fan Y, Shen Y, Huang F, Wang J, . Association of the serum microRNA-29 family with cognitive impairment in Parkinson's disease. . 12:13518-13528. https://doi.org/10.18632/aging.103458

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                TY  - JOUR
                AU  - Han, Linlin 
                AU  - Tang, Yilin 
                AU  - Bai, Xiaochen 
                AU  - Liang, Xiaoniu 
                AU  - Fan, Yun 
                AU  - Shen, Yan 
                AU  - Huang, Fang 
                AU  - Wang, Jian 
                TI  - Association of the serum microRNA-29 family with cognitive impairment in Parkinson's disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103458
                DO  - 10.18632/aging.103458
                SP  - 13518
                EP  - 13528
                PY  - 
                AB  - We aimed to examine whether miRNA-29s (miR-29s) in serum are associated with cognitive impairment in Parkinson&#x2019;s disease (PD). Thirty-nine PD patients with normal cognition (PD-NC), 37 PD patients with mild cognitive impairment (PD-MCI), 22 PD patients with dementia (PDD) and 40 healthy controls were recruited. Detailed clinical evaluations and a schedule of neuropsychological tests were administered to all patients. MiR-29s expression in serum samples was assessed using reverse-transcription quantitative real-time PCR. We found that the levels of all three miR-29s in the PDD group were significantly lower than those in the PD-NC group (p &lt; 0.05). In addition, the miR-29b level was downregulated in the PD-MCI group with respect to that in the PD-NC group (p &lt; 0.05). After adjusting for years of education and the UPDRS-III subscore using a multivariate model, miR-29s showed significant associations with PDD. MiR-29b levels were shown to be associated with different subsets of PD cognition and could accurately discriminate PDD from non-PDD (area under the curve (AUC) = 0.859; 95% CI, 0.7817-0.9372). Further analysis of the cognitive domains found that the miR-29s levels were all associated with memory performance in PD patients. In summary, miR-29s are associated with cognitive impairment in PD.
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Quantitative proteomics analysis of young and elderly skin with DIA mass spectrometry reveals new skin aging-related proteins

Jing Ma, Mengting Liu, Yaochi Wang, Cong Xin, Hui Zhang, Shirui Chen, Xiaodong Zheng, Xuejun Zhang, Fengli Xiao, Sen Yang,

https://doi.org/10.18632/aging.103461 pp 13529—13554

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Ma J, Liu M, Wang Y, Xin C, Zhang H, Chen S, Zheng X, Zhang X, Xiao F, Yang S, . Quantitative proteomics analysis of young and elderly skin with DIA mass spectrometry reveals new skin aging-related proteins. . 12:13529-13554. https://doi.org/10.18632/aging.103461

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                TY  - JOUR
                AU  - Ma, Jing 
                AU  - Liu, Mengting 
                AU  - Wang, Yaochi 
                AU  - Xin, Cong 
                AU  - Zhang, Hui 
                AU  - Chen, Shirui 
                AU  - Zheng, Xiaodong 
                AU  - Zhang, Xuejun 
                AU  - Xiao, Fengli 
                AU  - Yang, Sen 
                TI  - Quantitative proteomics analysis of young and elderly skin with DIA mass spectrometry reveals new skin aging-related proteins
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103461
                DO  - 10.18632/aging.103461
                SP  - 13529
                EP  - 13554
                PY  - 
                AB  - Skin aging is a specific manifestation of the physiological aging process that occurs in virtually all organisms. In this study, we used data independent acquisition mass spectrometry to perform a comparative analysis of protein expression in volar forearm skin samples from of 20 healthy young and elderly Chinese individuals. Our quantitative proteomic analysis identified a total of 95 differentially expressed proteins (DEPs) in aged skin compared to young skin. Enrichment analyses of these DEPs (57 upregulated and 38 downregulated proteins) based on the GO, KEGG, and KOG databases revealed functional clusters associated with immunity and inflammation, oxidative stress, biosynthesis and metabolism, proteases, cell proliferation, cell differentiation, and apoptosis. We also found that GAPDH, which was downregulated in aged skin samples, was the top hub gene in a protein-protein interaction network analysis. Some of the DEPs identified herein had been previously correlated with aging of the skin and other organs, while others may represent novel age-related entities. Our non-invasive proteomics analysis of human epidermal proteins may guide future research on skin aging to help develop treatments for age-related skin conditions and rejuvenation.
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Plasma acylcarnitine levels increase with healthy aging

Zachery R. Jarrell, M. Ryan Smith, Xin Hu, Michael Orr, Ken H. Liu, Arshed A. Quyyumi, Dean P. Jones, Young-Mi Go,

https://doi.org/10.18632/aging.103462 pp 13555—13570

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Jarrell ZR, Smith MR, Hu X, Orr M, Liu KH, Quyyumi AA, Jones DP, Go Y, . Plasma acylcarnitine levels increase with healthy aging. . 12:13555-13570. https://doi.org/10.18632/aging.103462

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                TY  - JOUR
                AU  - Jarrell, Zachery R. 
                AU  - Smith, M. Ryan 
                AU  - Hu, Xin 
                AU  - Orr, Michael 
                AU  - Liu, Ken H. 
                AU  - Quyyumi, Arshed A. 
                AU  - Jones, Dean P. 
                AU  - Go, Young-Mi 
                TI  - Plasma acylcarnitine levels increase with healthy aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103462
                DO  - 10.18632/aging.103462
                SP  - 13555
                EP  - 13570
                PY  - 
                AB  - Acylcarnitines transport fatty acids into mitochondria and are essential for &#x3B2;-oxidation and energy metabolism. Decreased mitochondrial activity results in increased plasma acylcarnitines, and increased acylcarnitines activate proinflammatory signaling and associate with age-related disease. Changes in acylcarnitines associated with healthy aging, however, are not well characterized. In the present study, we examined the associations of plasma acylcarnitines with age (range: 20-90) in 163 healthy, non-diseased individuals from the predictive medicine research cohort (NCT00336570) and tested for gender-specific differences. The results show that long-chain and very long-chain acylcarnitines increased with age, while many odd-chain acylcarnitines decreased with age. Gender-specific differences were observed for several acylcarnitines, e.g., eicosadienoylcarnitine varied with age in males, and hydroxystearoylcarnitine varied in females. Metabolome-wide association study (MWAS) of age-associated acylcarnitines with all untargeted metabolic features showed little overlap between genders. These results show that plasma concentrations of acylcarnitines vary with age and gender in individuals selected for criteria of health. Whether these variations reflect mitochondrial dysfunction with aging, mitochondrial reprogramming in response to chronic environmental exposures, early pre-disease change, or an adaptive response to healthy aging, is unclear. The results highlight a potential utility for untargeted metabolomics research to elucidate gender-specific mechanisms of aging and age-related disease.
                ER  -

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Altered complexity of resting-state BOLD activity in Alzheimer’s disease-related neurodegeneration: a multiscale entropy analysis

Ping Ren, Manxiu Ma, Guohua Xie, Zhiwei Wu, Donghui Wu, The Alzheimer's Disease Neuroimaging Initiative,

https://doi.org/10.18632/aging.103463 pp 13571—13582

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Ren P, Ma M, Xie G, Wu Z, Wu D, , . Altered complexity of resting-state BOLD activity in Alzheimer’s disease-related neurodegeneration: a multiscale entropy analysis. . 12:13571-13582. https://doi.org/10.18632/aging.103463

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                TY  - JOUR
                AU  - Ren, Ping 
                AU  - Ma, Manxiu 
                AU  - Xie, Guohua 
                AU  - Wu, Zhiwei 
                AU  - Wu, Donghui 
                AU  - ,  
                TI  - Altered complexity of resting-state BOLD activity in Alzheimer’s disease-related neurodegeneration: a multiscale entropy analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103463
                DO  - 10.18632/aging.103463
                SP  - 13571
                EP  - 13582
                PY  - 
                AB  - Brain complexity, which reflects the ability of the brain to adapt to a changing environment, has been found to be significantly changed with age. However, there is less evidence on the alterations of brain complexity in neurodegenerative disorders such as Alzheimer&#x2019;s disease (AD). Here we investigated the altered complexity of resting-state blood oxygen level-dependent signals in AD-related neurodegeneration using multiscale entropy (MSE) analysis. All participants were recruited from the Alzheimer&#x2019;s Disease Neuroimaging Initiative, including healthy controls (HC, n=62), amnestic mild cognitive impairment (aMCI, n =81) patients, and Alzheimer&#x2019;s disease (AD, n=25) patients. Our results showed time scale-dependent MSE differences across the three groups. In scale=1, significantly changed MSE patterns (HC&gt;aMCI&gt;AD) were found in four brain regions, including the hippocampus, middle frontal gyrus, intraparietal lobe, and superior frontal gyrus. In scale=4, reversed MSE patterns (HC&lt;aMCI&lt;AD) were found in the middle frontal gyrus and middle occipital gyrus. Furthermore, the values of regional entropy were significantly associated with cognitive functions positively on the short time scale, while negatively on the longer time scale. Our findings suggest that MSE could be a reliable measure for characterizing brain deterioration in AD, and may provide insights into the neural mechanism of AD-related neurodegeneration.
                ER  -

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Super elderly patients with intertrochanteric fractures do not predict worse outcomes and higher mortality than elderly patients: a propensity score matched analysis

Junfei Guo, Zhiqian Wang, Mingming Fu, Jun Di, Junpu Zha, Junchuan Liu, Guolei Zhang, Qingxian Wang, Hua Chen, Peifu Tang, Zhiyong Hou, Yingze Zhang,

https://doi.org/10.18632/aging.103466 pp 13583—13593

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Guo J, Wang Z, Fu M, Di J, Zha J, Liu J, Zhang G, Wang Q, Chen H, Tang P, Hou Z, Zhang Y, . Super elderly patients with intertrochanteric fractures do not predict worse outcomes and higher mortality than elderly patients: a propensity score matched analysis. . 12:13583-13593. https://doi.org/10.18632/aging.103466

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                TY  - JOUR
                AU  - Guo, Junfei 
                AU  - Wang, Zhiqian 
                AU  - Fu, Mingming 
                AU  - Di, Jun 
                AU  - Zha, Junpu 
                AU  - Liu, Junchuan 
                AU  - Zhang, Guolei 
                AU  - Wang, Qingxian 
                AU  - Chen, Hua 
                AU  - Tang, Peifu 
                AU  - Hou, Zhiyong 
                AU  - Zhang, Yingze 
                TI  - Super elderly patients with intertrochanteric fractures do not predict worse outcomes and higher mortality than elderly patients: a propensity score matched analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103466
                DO  - 10.18632/aging.103466
                SP  - 13583
                EP  - 13593
                PY  - 
                AB  - We aimed to investigate whether super elderly patients aged over 90 years had significantly worse functional outcomes, perioperative complications, and survival rates. Among 3560 patients aged over 65 years presenting with intertrochanteric fractures and treated surgically between Jan 2014 and Jan 2019, 2242 patients were included, including 206 in super elderly group and 2036 in elderly group. After using propensity score matching to minimize the effects of possible confounding variables, 192 remained in each group. No significant difference was observed in functional outcomes, perioperative complications, or 30-day, 90-day, and 1-year mortality after propensity score matching and McNemar&#x2019;s tests (p&gt;0.05). After an average follow-up of 37 months, the Kaplan-Meier survival curve showed no significant difference between the two groups in terms of cumulative survival rate (p=0.081, log-rank). Our data demonstrated progressive increases in mortality and poor outcomes with increasing Elixhauser comorbidity scores, which represented the severity index of patients preoperatively. Our study also found that there were weak correlations between five characteristics and the patient age. These results all suggested that it is not the advanced age itself but other concomitant factors, that appear to be responsible for the adverse functional outcomes, perioperative complications, and mortality in super elderly patients.
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The transcription factor CREB acts as an important regulator mediating oxidative stress-induced apoptosis by suppressing αB-crystallin expression

Ling Wang, Qian Nie, Meng Gao, Lan Yang, Jia-Wen Xiang, Yuan Xiao, Fang-Yuan Liu, Xiao-Dong Gong, Jia-Ling Fu, Yan Wang, Quan Dong Nguyen, Yizhi Liu, Mugen Liu, David Wan-Cheng Li,

https://doi.org/10.18632/aging.103474 pp 13594—13617

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Wang L, Nie Q, Gao M, Yang L, Xiang J, Xiao Y, Liu F, Gong X, Fu J, Wang Y, Nguyen QD, Liu Y, Liu M, et al, . The transcription factor CREB acts as an important regulator mediating oxidative stress-induced apoptosis by suppressing αB-crystallin expression. . 12:13594-13617. https://doi.org/10.18632/aging.103474

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                TY  - JOUR
                AU  - Wang, Ling 
                AU  - Nie, Qian 
                AU  - Gao, Meng 
                AU  - Yang, Lan 
                AU  - Xiang, Jia-Wen 
                AU  - Xiao, Yuan 
                AU  - Liu, Fang-Yuan 
                AU  - Gong, Xiao-Dong 
                AU  - Fu, Jia-Ling 
                AU  - Wang, Yan 
                AU  - Nguyen, Quan Dong 
                AU  - Liu, Yizhi 
                AU  - Liu, Mugen 
                AU  - Li, David Wan-Cheng 
                TI  - The transcription factor CREB acts as an important regulator mediating oxidative stress-induced apoptosis by suppressing αB-crystallin expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103474
                DO  - 10.18632/aging.103474
                SP  - 13594
                EP  - 13617
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wang, Ling 
                AU  - Nie, Qian 
                AU  - Gao, Meng 
                AU  - Yang, Lan 
                AU  - Xiang, Jia-Wen 
                AU  - Xiao, Yuan 
                AU  - Liu, Fang-Yuan 
                AU  - Gong, Xiao-Dong 
                AU  - Fu, Jia-Ling 
                AU  - Wang, Yan 
                AU  - Nguyen, Quan Dong 
                AU  - Liu, Yizhi 
                AU  - Liu, Mugen 
                AU  - Li, David Wan-Cheng 
                TI  - The transcription factor CREB acts as an important regulator mediating oxidative stress-induced apoptosis by suppressing αB-crystallin expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103474
                DO  - 10.18632/aging.103474
                SP  - 13594
                EP  - 13617
                PY  - 
                AB  - The general transcription factor, CREB has been shown to play an essential role in promoting cell proliferation, neuronal survival and synaptic plasticity in the nervous system. However, its function in stress response remains to be elusive. In the present study, we demonstrated that CREB plays a major role in mediating stress response. In both rat lens organ culture and mouse lens epithelial cells (MLECs), CREB promotes oxidative stress-induced apoptosis. To confirm that CREB is a major player mediating the above stress response, we established stable lines of MLECs stably expressing CREB and found that they are also very sensitive to oxidative stress-induced apoptosis. To define the underlying mechanism, RNAseq analysis was conducted. It was found that CREB significantly suppressed expression of the &#x3B1;B-crystallin gene to sensitize CREB-expressing cells undergoing oxidative stress-induced apoptosis. CREB knockdown via CRISPR/CAS9 technology led to upregulation of &#x3B1;B-crystallin and enhanced resistance against oxidative stress-induced apoptosis. Moreover, overexpression of exogenous human &#x3B1;B-crystallin can restore the resistance against oxidative stress-induced apoptosis. Finally, we provided first evidence that CREB directly regulates &#x3B1;B-crystallin gene. Together, our results demonstrate that CREB is an important transcription factor mediating stress response, and it promotes oxidative stress-induced apoptosis by suppressing &#x3B1;B-crystallin expression.
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The YAP/SERCA2a signaling pathway protects cardiomyocytes against reperfusion-induced apoptosis

Jiankai Zhong, Haichun Ouyang, Sulin Zheng, Zhongzhou Guo, Yuying Chen, Yuanlin Zhong, Wenhao Zhong, Liuer Zuo, Jianhua Lu,

https://doi.org/10.18632/aging.103481 pp 13618—13632

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Zhong J, Ouyang H, Zheng S, Guo Z, Chen Y, Zhong Y, Zhong W, Zuo L, Lu J, . The YAP/SERCA2a signaling pathway protects cardiomyocytes against reperfusion-induced apoptosis. . 12:13618-13632. https://doi.org/10.18632/aging.103481

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                TY  - JOUR
                AU  - Zhong, Jiankai 
                AU  - Ouyang, Haichun 
                AU  - Zheng, Sulin 
                AU  - Guo, Zhongzhou 
                AU  - Chen, Yuying 
                AU  - Zhong, Yuanlin 
                AU  - Zhong, Wenhao 
                AU  - Zuo, Liuer 
                AU  - Lu, Jianhua 
                TI  - The YAP/SERCA2a signaling pathway protects cardiomyocytes against reperfusion-induced apoptosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103481
                DO  - 10.18632/aging.103481
                SP  - 13618
                EP  - 13632
                PY  - 
                AB  - Mitochondria and the endoplasmic reticulum (ER) are known to promote cardiac ischemia/reperfusion (I/R) injury. Overexpression of yes-associated protein (YAP) and/or sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) has been shown to protect cardiomyocytes against I/R-induced injury. Here, we show that activation of the YAP/SERCA2a pathway attenuated mitochondrial damage and ER stress (ERS) to maintain cardiomyocyte viability in the setting of I/R injury. Our results demonstrate that I/R treatment reduced the transcription and expression of YAP and SERCA2a, along with a decline in cardiomyocyte viability. The overexpression of YAP promoted SERCA2a transcription, whereas SERCA2a upregulation did not affect the YAP transcription, suggesting that YAP functions upstream of SERCA2a. Activation of the YAP/SERCA2a pathway suppressed mitochondrial damage by sustaining the mitochondrial redox balance and restoring mitochondrial bioenergetics. Additionally, its activation repressed ERS, reduced calcium overload, and eventually blocked caspase activation. The knockdown of SERCA2a suppressed the protective effects of YAP overexpression on mitochondrial damage and ERS. Overall, our findings reveal that the YAP/SERCA2a pathway attenuates the mitochondrial damage and ERS in response to cardiac I/R injury by regulating the mitochondria&#x2013;ER communication.
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Melatonin protects against apoptosis of megakaryocytic cells via its receptors and the AKT/mitochondrial/caspase pathway

Mo Yang, Liang Li, Shichao Chen, Suyi Li, Bo Wang, Changhua Zhang, Youpeng Chen, Liuming Yang, Hongwu Xin, Chun Chen, Xiaojun Xu, Qing Zhang, Yulong He, Jieyu Ye,

https://doi.org/10.18632/aging.103483 pp 13633—13646

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Yang M, Li L, Chen S, Li S, Wang B, Zhang C, Chen Y, Yang L, Xin H, Chen C, Xu X, Zhang Q, He Y, et al, . Melatonin protects against apoptosis of megakaryocytic cells via its receptors and the AKT/mitochondrial/caspase pathway. . 12:13633-13646. https://doi.org/10.18632/aging.103483

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                TY  - JOUR
                AU  - Yang, Mo 
                AU  - Li, Liang 
                AU  - Chen, Shichao 
                AU  - Li, Suyi 
                AU  - Wang, Bo 
                AU  - Zhang, Changhua 
                AU  - Chen, Youpeng 
                AU  - Yang, Liuming 
                AU  - Xin, Hongwu 
                AU  - Chen, Chun 
                AU  - Xu, Xiaojun 
                AU  - Zhang, Qing 
                AU  - He, Yulong 
                AU  - Ye, Jieyu 
                TI  - Melatonin protects against apoptosis of megakaryocytic cells via its receptors and the AKT/mitochondrial/caspase pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103483
                DO  - 10.18632/aging.103483
                SP  - 13633
                EP  - 13646
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Yang, Mo 
                AU  - Li, Liang 
                AU  - Chen, Shichao 
                AU  - Li, Suyi 
                AU  - Wang, Bo 
                AU  - Zhang, Changhua 
                AU  - Chen, Youpeng 
                AU  - Yang, Liuming 
                AU  - Xin, Hongwu 
                AU  - Chen, Chun 
                AU  - Xu, Xiaojun 
                AU  - Zhang, Qing 
                AU  - He, Yulong 
                AU  - Ye, Jieyu 
                TI  - Melatonin protects against apoptosis of megakaryocytic cells via its receptors and the AKT/mitochondrial/caspase pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103483
                DO  - 10.18632/aging.103483
                SP  - 13633
                EP  - 13646
                PY  - 
                AB  - Clinical studies have shown that melatonin lowers the frequency of thrombocytopenia in patients with cancer undergoing radiotherapy or chemotherapy. Here, we investigated the mechanisms by which melatonin promotes platelet formation and survival. Our results show that melatonin exerted protective effects on serum-free induced apoptosis of CHRF megakaryocytes (MKs). Melatonin promoted the formation of MK colony forming units (CFUs) in a dose-dependent manner. Using doxorubicin-treated CHRF cells, we found that melatonin rescued G2/M cell cycle arrest and cell apoptosis induced by doxorubicin. The expression of p-AKT was increased by melatonin treatment, an effect that was abolished by melatonin receptor blocker. In addition, we demonstrated that melatonin enhanced the recovery of platelets in an irradiated mouse model. Megakaryopoiesis was largely preserved in melatonin-treated mice. We obtained the same results in vivo from bone marrow histology and CFU-MK formation assays. Melatonin may exert these protective effects by directly stimulating megakaryopoiesis and inhibiting megakaryocyte apoptosis through activation of its receptors and AKT signaling.
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MiR-146b-5p suppresses the malignancy of GSC/MSC fusion cells by targeting SMARCA5

Haiyang Wang, Liping Tan, Xuchen Dong, Liang Liu, Qianqian Jiang, Haoran Li, Jia Shi, Xuejun Yang, Xingliang Dai, Zhiyuan Qian, Jun Dong,

https://doi.org/10.18632/aging.103489 pp 13647—13667

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Wang H, Tan L, Dong X, Liu L, Jiang Q, Li H, Shi J, Yang X, Dai X, Qian Z, Dong J, . MiR-146b-5p suppresses the malignancy of GSC/MSC fusion cells by targeting SMARCA5. . 12:13647-13667. https://doi.org/10.18632/aging.103489

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                TY  - JOUR
                AU  - Wang, Haiyang 
                AU  - Tan, Liping 
                AU  - Dong, Xuchen 
                AU  - Liu, Liang 
                AU  - Jiang, Qianqian 
                AU  - Li, Haoran 
                AU  - Shi, Jia 
                AU  - Yang, Xuejun 
                AU  - Dai, Xingliang 
                AU  - Qian, Zhiyuan 
                AU  - Dong, Jun 
                TI  - MiR-146b-5p suppresses the malignancy of GSC/MSC fusion cells by targeting SMARCA5
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103489
                DO  - 10.18632/aging.103489
                SP  - 13647
                EP  - 13667
                PY  - 
                AB  - Recent studies have confirmed that both cancer-associated bone marrow mesenchymal stem cells (BM-MSCs, MSCs) and glioma stem-like cells (GSCs) contribute to malignant progression of gliomas through their mutual interactions within the tumor microenvironment. However, the exact ways and relevant mechanisms involved in the actions of GSCs and MSCs within the glioma microenvironment are not fully understood. Using a dual-color fluorescence tracing model, our studies revealed that GSCs are able to spontaneously fuse with MSCs, yielding GSC/MSC fusion cells, which exhibited markedly enhanced proliferation and invasiveness. MiR-146b-5p was downregulated in the GSC/MSC fusion cells, and its overexpression suppressed proliferation, migration and invasion by the fusion cells. SMARCA5, which is highly expressed in high-grade gliomas, was a direct downstream target of miR-146b-5p in the GSC/MSC fusion cells. miR-146b-5p inhibited SMARCA5 expression and inactivated a TGF-&#x3B2; pathway, thereby decreasing GSC/MSC fusion cell proliferation, migration and invasion. Collectively, these findings demonstrate that miR-146b-5p suppresses the malignant phenotype of GSC/MSC fusion cells in the glioma microenvironment by targeting a SMARCA5-regulated TGF-&#x3B2; pathway.
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CAMKIIγ is a targetable driver of multiple myeloma through CaMKIIγ/ Stat3 axis

Linlin Yang, Bowen Wu, Zhaoxing Wu, Ying Xu, Ping Wang, Mengyuan Li, Rongzhen Xu, Yun Liang,

https://doi.org/10.18632/aging.103490 pp 13668—13683

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Yang L, Wu B, Wu Z, Xu Y, Wang P, Li M, Xu R, Liang Y, . CAMKIIγ is a targetable driver of multiple myeloma through CaMKIIγ/ Stat3 axis. . 12:13668-13683. https://doi.org/10.18632/aging.103490

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                TY  - JOUR
                AU  - Yang, Linlin 
                AU  - Wu, Bowen 
                AU  - Wu, Zhaoxing 
                AU  - Xu, Ying 
                AU  - Wang, Ping 
                AU  - Li, Mengyuan 
                AU  - Xu, Rongzhen 
                AU  - Liang, Yun 
                TI  - CAMKIIγ is a targetable driver of multiple myeloma through CaMKIIγ/ Stat3 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103490
                DO  - 10.18632/aging.103490
                SP  - 13668
                EP  - 13683
                PY  - 
                AB  - Aberrant activation of CAMKII&#x3B3; has been linked to leukemia and T-cell lymphoma, but not multiple myeloma (MM). The purpose of this study was to explore the role of CaMKII&#x3B3; in the pathogenesis and therapy of MM. In this study, we found that CaMKII&#x3B3; was aberrantly activated in human MM and its expression level was positively correlated with malignant progression and poor prognosis. Ectopic expression of CaMKII&#x3B3; promoted cell growth, colony formation, cell cycle progress and inhibited apoptosis of MM cell lines, whereas, knockdown of CAMKII&#x3B3; expression suppressed MM cell growth in vitro and in vivo. Mechanically, we observed that CaMKII&#x3B3; overexpression upregulated p-ERK and p-Stat3 levels and suppression of CaMKII&#x3B3; had opposite effects. CaMKII&#x3B3; is frequently dysregulated in MM and plays a critical role in maintaining MM cell growth through upregulating STAT3 signaling pathway. Furthermore, our preclinical studies suggest that CaMKII&#x3B3; is a potential therapeutic target in MM, and could be intervened pharmacologically by small-molecule berbamine analogues.
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Genome-wide analyses of the prognosis-related mRNA alternative splicing landscape and novel splicing factors based on large-scale low grade glioma cohort

Wang-Rui Liu, Chuan-Yu Li, Wen-Hao Xu, Xiao-Juan Liu, Hai-Dan Tang, Hai-Neng Huang,

https://doi.org/10.18632/aging.103491 pp 13684—13700

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Liu W, Li C, Xu W, Liu X, Tang H, Huang H, . Genome-wide analyses of the prognosis-related mRNA alternative splicing landscape and novel splicing factors based on large-scale low grade glioma cohort. . 12:13684-13700. https://doi.org/10.18632/aging.103491

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                TY  - JOUR
                AU  - Liu, Wang-Rui 
                AU  - Li, Chuan-Yu 
                AU  - Xu, Wen-Hao 
                AU  - Liu, Xiao-Juan 
                AU  - Tang, Hai-Dan 
                AU  - Huang, Hai-Neng 
                TI  - Genome-wide analyses of the prognosis-related mRNA alternative splicing landscape and novel splicing factors based on large-scale low grade glioma cohort
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103491
                DO  - 10.18632/aging.103491
                SP  - 13684
                EP  - 13700
                PY  - 
                AB  - Alternative splicing (AS) changes are considered to be critical in predicting treatment response. Our study aimed to investigate differential splicing patterns and to elucidate the role of splicing factor (SF) as prognostic markers of low-grade glioma (LGG). We downloaded RNA-seq data from a cohort of 516 LGG tumors in The Cancer Genome Atlas and analyzed independent prognostic factors using LASSO regression and Cox proportional regression to build a network based on the correlation between SF-related survival AS events. We collected 100 patients from our center for immunohistochemistry and analyzed survival using &#x3C7;2 test and Cox and Kaplan-Meier analyses. A total of 9,616 AS events related to LGG were screened and identified as well as established related models. Through analyzing specific splicing patterns in LGG, we screened 16 genes to construct a prognostic model to stratify the risk of LGG patients. Validation revealed that the expression level of the prognostic model in LGG tissue was increased, and patients with high expression showed worse prognosis. In summary, we demonstrated the role of SFs and AS events in the progression of LGG, which may provide insights into the clinical significance and aid the future exploration of LGG-associated AS.
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Exome sequencing identifies somatic mutations in novel driver genes in non-small cell lung cancer

Manman Zhang, Lele Zhang, Yan Li, Feng Sun, Ya Fang, Ruijia Zhang, Jin Wu, Guanbiao Zhou, Huaidong Song, Liqiong Xue, Bing Han, Cuixia Zheng,

https://doi.org/10.18632/aging.103500 pp 13701—13715

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Zhang M, Zhang L, Li Y, Sun F, Fang Y, Zhang R, Wu J, Zhou G, Song H, Xue L, Han B, Zheng C, . Exome sequencing identifies somatic mutations in novel driver genes in non-small cell lung cancer. . 12:13701-13715. https://doi.org/10.18632/aging.103500

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                TY  - JOUR
                AU  - Zhang, Manman 
                AU  - Zhang, Lele 
                AU  - Li, Yan 
                AU  - Sun, Feng 
                AU  - Fang, Ya 
                AU  - Zhang, Ruijia 
                AU  - Wu, Jin 
                AU  - Zhou, Guanbiao 
                AU  - Song, Huaidong 
                AU  - Xue, Liqiong 
                AU  - Han, Bing 
                AU  - Zheng, Cuixia 
                TI  - Exome sequencing identifies somatic mutations in novel driver genes in non-small cell lung cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103500
                DO  - 10.18632/aging.103500
                SP  - 13701
                EP  - 13715
                PY  - 
                AB  - Lung cancer is the leading cause of cancer death worldwide and accounts for more than one-third of all newly diagnosed cancer cases in China. Therefore, it is of great clinical significance to explore new driver gene mutations in non-small-cell lung cancer (NSCLC). Using an initial bioinformatic analysis, we identified somatic gene mutations in 13 patients with NSCLC and confirmed these mutations by targeted sequencing in an extended validation group of 88 patients. Recurrent mutations were detected in UNC5D (7.9%), PREX1 (5.0%), HECW1 (4.0%), DACH1 (2.0%), and GPC5 (2.0%). A functional study was also performed in UNC5D mutants. Mutations in UNC5D promoted tumorigenesis by abolishing the tumor suppressor function of the encoded protein. Additionally, in ten patients with lung squamous cell carcinoma, we identified mutations in KEAP1/NFE2L2 that influenced the expression of target genes in vivo and in vitro. Overall, the results of our study expanded the known spectrum of driver mutations involved in the pathogenesis of NSCLC.
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Spermine and spermidine modulate T-cell function in older adults with and without cognitive decline ex vivo

Maximilian Fischer, Johanna Ruhnau, Juliane Schulze, Daniela Obst, Agnes Flöel, Antje Vogelgesang,

https://doi.org/10.18632/aging.103527 pp 13716—13739

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Fischer M, Ruhnau J, Schulze J, Obst D, Flöel A, Vogelgesang A, . Spermine and spermidine modulate T-cell function in older adults with and without cognitive decline ex vivo. . 12:13716-13739. https://doi.org/10.18632/aging.103527

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                TY  - JOUR
                AU  - Fischer, Maximilian 
                AU  - Ruhnau, Johanna 
                AU  - Schulze, Juliane 
                AU  - Obst, Daniela 
                AU  - Flöel, Agnes 
                AU  - Vogelgesang, Antje 
                TI  - Spermine and spermidine modulate T-cell function in older adults with and without cognitive decline ex vivo
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103527
                DO  - 10.18632/aging.103527
                SP  - 13716
                EP  - 13739
                PY  - 
                AB  - The global increase in neurodegenerative disorders is one of the most crucial public health issues. Oral polyamine intake was shown to improve memory performance which is thought to be mediated at least in part via increased autophagy induced in brain cells. In Alzheimer&#x2019;s Disease, T-cells were identified as important mediators of disease pathology. Since autophagy is a central regulator of cell activation and cytokine production, we investigated the influence of polyamines on T-cell activation, autophagy, and the release of Th1/Th2 cytokines from blood samples of patients (n=22) with cognitive impairment or dementia in comparison to healthy controls (n=12) ex vivo. We found that spermine downregulated all investigated cytokines in a dose-dependent manner. Spermidine led to an upregulation of some cytokines for lower dosages, while high dosages downregulated all cytokines apart from upregulated IL-17A. Autophagy and T-cell activation increased in a dose-dependent manner by incubation with either polyamine. Although effects in patients were seen in lower concentrations, alterations were similar to controls.We provide novel evidence that supplementation of polyamines alters the function of T-cells. Given their important role in dementia, these data indicate a possible mechanism by which polyamines would help to prevent structural and cognitive decline in aging.
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Cognitive enhancement of healthy older adults using hyperbaric oxygen: a randomized controlled trial

Amir Hadanny, Malka Daniel-Kotovsky, Gil Suzin, Rahav Boussi-Gross, Merav Catalogna, Kobi Dagan, Yafit Hachmo, Ramzia Abu Hamed, Efrat Sasson, Gregory Fishlev, Erez Lang, Nir Polak, Keren Doenyas, Mony Friedman, Sigal Tal, Yonatan Zemel, Yair Bechor, Shai Efrati,

https://doi.org/10.18632/aging.103571 pp 13740—13761

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Hadanny A, Daniel-Kotovsky M, Suzin G, Boussi-Gross R, Catalogna M, Dagan K, Hachmo Y, Abu Hamed R, Sasson E, Fishlev G, Lang E, Polak N, Doenyas K, et al, . Cognitive enhancement of healthy older adults using hyperbaric oxygen: a randomized controlled trial. . 12:13740-13761. https://doi.org/10.18632/aging.103571

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                TY  - JOUR
                AU  - Hadanny, Amir 
                AU  - Daniel-Kotovsky, Malka 
                AU  - Suzin, Gil 
                AU  - Boussi-Gross, Rahav 
                AU  - Catalogna, Merav 
                AU  - Dagan, Kobi 
                AU  - Hachmo, Yafit 
                AU  - Abu Hamed, Ramzia 
                AU  - Sasson, Efrat 
                AU  - Fishlev, Gregory 
                AU  - Lang, Erez 
                AU  - Polak, Nir 
                AU  - Doenyas, Keren 
                AU  - Friedman, Mony 
                AU  - Tal, Sigal 
                AU  - Zemel, Yonatan 
                AU  - Bechor, Yair 
                AU  - Efrati, Shai 
                TI  - Cognitive enhancement of healthy older adults using hyperbaric oxygen: a randomized controlled trial
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103571
                DO  - 10.18632/aging.103571
                SP  - 13740
                EP  - 13761
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Hadanny, Amir 
                AU  - Daniel-Kotovsky, Malka 
                AU  - Suzin, Gil 
                AU  - Boussi-Gross, Rahav 
                AU  - Catalogna, Merav 
                AU  - Dagan, Kobi 
                AU  - Hachmo, Yafit 
                AU  - Abu Hamed, Ramzia 
                AU  - Sasson, Efrat 
                AU  - Fishlev, Gregory 
                AU  - Lang, Erez 
                AU  - Polak, Nir 
                AU  - Doenyas, Keren 
                AU  - Friedman, Mony 
                AU  - Tal, Sigal 
                AU  - Zemel, Yonatan 
                AU  - Bechor, Yair 
                AU  - Efrati, Shai 
                TI  - Cognitive enhancement of healthy older adults using hyperbaric oxygen: a randomized controlled trial
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103571
                DO  - 10.18632/aging.103571
                SP  - 13740
                EP  - 13761
                PY  - 
                AB  - More than half of community-dwelling individuals sixty years and older express concern about declining cognitive abilities. The current study&#x2019;s aim was to evaluate hyperbaric oxygen therapy (HBOT) effect on cognitive functions in healthy aging adults.A randomized controlled clinical trial randomized 63 healthy adults (&gt;64) either to HBOT(n=33) or control arms(n=30) for three months. Primary endpoint included the general cognitive function measured post intervention/control. Cerebral blood flow (CBF) was evaluated by perfusion magnetic resonance imaging.There was a significant group-by-time interaction in global cognitive function post-HBOT compared to control (p=0.0017). The most striking improvements were in attention (net effect size=0.745) and information processing speed (net effect size=0.788).Voxel-based analysis showed significant cerebral blood flow increases in the HBOT group compared to the control group in the right superior medial frontal gyrus (BA10), right and left supplementary motor area (BA6), right middle frontal gyrus (BA6), left middle frontal gyrus (BA9), left superior frontal gyrus (BA8) and the right superior parietal gyrus (BA7).In this study, HBOT was shown to induce cognitive enhancements in healthy aging adults via mechanisms involving regional changes in CBF. The main improvements include attention, information processing speed and executive functions, which normally decline with aging.
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Aging affects sex- and organ-specific trace element profiles in mice

Kristina Lossow, Johannes F. Kopp, Maria Schwarz, Hannah Finke, Nicola Winkelbeiner, Kostja Renko, Xheni Meçi, Christiane Ott, Wiebke Alker, Julian Hackler, Tilman Grune, Lutz Schomburg, Hajo Haase, Tanja Schwerdtle, Anna P. Kipp,

https://doi.org/10.18632/aging.103572 pp 13762—13790

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Lossow K, Kopp JF, Schwarz M, Finke H, Winkelbeiner N, Renko K, Meçi X, Ott C, Alker W, Hackler J, Grune T, Schomburg L, Haase H, et al, . Aging affects sex- and organ-specific trace element profiles in mice. . 12:13762-13790. https://doi.org/10.18632/aging.103572

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                TY  - JOUR
                AU  - Lossow, Kristina 
                AU  - Kopp, Johannes F. 
                AU  - Schwarz, Maria 
                AU  - Finke, Hannah 
                AU  - Winkelbeiner, Nicola 
                AU  - Renko, Kostja 
                AU  - Meçi, Xheni 
                AU  - Ott, Christiane 
                AU  - Alker, Wiebke 
                AU  - Hackler, Julian 
                AU  - Grune, Tilman 
                AU  - Schomburg, Lutz 
                AU  - Haase, Hajo 
                AU  - Schwerdtle, Tanja 
                AU  - Kipp, Anna P. 
                TI  - Aging affects sex- and organ-specific trace element profiles in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103572
                DO  - 10.18632/aging.103572
                SP  - 13762
                EP  - 13790
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Lossow, Kristina 
                AU  - Kopp, Johannes F. 
                AU  - Schwarz, Maria 
                AU  - Finke, Hannah 
                AU  - Winkelbeiner, Nicola 
                AU  - Renko, Kostja 
                AU  - Meçi, Xheni 
                AU  - Ott, Christiane 
                AU  - Alker, Wiebke 
                AU  - Hackler, Julian 
                AU  - Grune, Tilman 
                AU  - Schomburg, Lutz 
                AU  - Haase, Hajo 
                AU  - Schwerdtle, Tanja 
                AU  - Kipp, Anna P. 
                TI  - Aging affects sex- and organ-specific trace element profiles in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103572
                DO  - 10.18632/aging.103572
                SP  - 13762
                EP  - 13790
                PY  - 
                AB  - A decline of immune responses and dynamic modulation of the redox status are observed during aging and are influenced by trace elements such as copper, iodine, iron, manganese, selenium, and zinc. So far, analytical studies have focused mainly on single trace elements. Therefore, we aimed to characterize age-specific profiles of several trace elements simultaneously in serum and organs of adult and old mice. This allows for correlating multiple trace element levels and to identify potential patterns of age-dependent alterations. In serum, copper and iodine concentrations were increased and zinc concentration was decreased in old as compared to adult mice. In parallel, decreased copper and elevated iron concentrations were observed in liver. The age-related reduction of hepatic copper levels was associated with reduced expression of copper transporters, whereas the increased hepatic iron concentrations correlated positively with proinflammatory mediators and Nrf2-induced ferritin H levels. Interestingly, the age-dependent inverse regulation of copper and iron was unique for the liver and not observed in any other organ. The physiological importance of alterations in the iron/copper ratio for liver function and the aging process needs to be addressed in further studies.
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COVID-19
Pathophysiology of SARS-CoV-2 infection in patients with intracerebral hemorrhage

Sisi Dong, Peipei Liu, Yuhan Luo, Ying Cui, Lilong Song, Yingzhu Chen,

https://doi.org/10.18632/aging.103511 pp 13791—13802

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Dong S, Liu P, Luo Y, Cui Y, Song L, Chen Y, . Pathophysiology of SARS-CoV-2 infection in patients with intracerebral hemorrhage. . 12:13791-13802. https://doi.org/10.18632/aging.103511

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                TY  - JOUR
                AU  - Dong, Sisi 
                AU  - Liu, Peipei 
                AU  - Luo, Yuhan 
                AU  - Cui, Ying 
                AU  - Song, Lilong 
                AU  - Chen, Yingzhu 
                TI  - Pathophysiology of SARS-CoV-2 infection in patients with intracerebral hemorrhage
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103511
                DO  - 10.18632/aging.103511
                SP  - 13791
                EP  - 13802
                PY  - 
                AB  - Intracerebral hemorrhage (ICH) is associated with old age and underlying conditions such as hypertension and diabetes. ICH patients are vulnerable to SARS-CoV-2 infection and develop serious complications as a result of infection. The pathophysiology of ICH patients with SARS-CoV-2 infection includes viral invasion, dysfunction of the ACE2&#x2013;Ang (1&#x2013;7)&#x2013;MasR and ACE&#x2013;Ang II&#x2013;AT1R axes, overactive immune response, cytokine storm, and excessive oxidative stress. These patients have high morbidity and mortality due to hyaline membrane formation, respiratory failure, neurologic deficits, and multiple organ failure.
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Physical activity, a modulator of aging through effects on telomere biology

Maria Donatella Semeraro, Cassandra Smith, Melanie Kaiser, Itamar Levinger, Gustavo Duque, Hans-Juergen Gruber, Markus Herrmann,

https://doi.org/10.18632/aging.103504 pp 13803—13823

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Semeraro MD, Smith C, Kaiser M, Levinger I, Duque G, Gruber H, Herrmann M, . Physical activity, a modulator of aging through effects on telomere biology. . 12:13803-13823. https://doi.org/10.18632/aging.103504

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                TY  - JOUR
                AU  - Semeraro, Maria Donatella 
                AU  - Smith, Cassandra 
                AU  - Kaiser, Melanie 
                AU  - Levinger, Itamar 
                AU  - Duque, Gustavo 
                AU  - Gruber, Hans-Juergen 
                AU  - Herrmann, Markus 
                TI  - Physical activity, a modulator of aging through effects on telomere biology
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103504
                DO  - 10.18632/aging.103504
                SP  - 13803
                EP  - 13823
                PY  - 
                AB  - Aging is a complex process that is not well understood but involves finite changes at the genetic and epigenetic level. Physical activity is a well-documented modulator of the physiological process of aging. It has been suggested that the beneficial health effects of regular exercise are at least partly mediated through its effects on telomeres and associated regulatory pathways. Telomeres, the region of repetitive nucleotide sequences functioning as a &#x201C;cap&#x201D; at the chromosomal ends, play an important role to protect genomic DNA from degradation. Telomeres of dividing cells progressively shorten with age. Leucocyte telomere length (TL) has been associated with age-related diseases. Epidemiologic evidence indicates a strong relationship between physical activity and TL. In addition, TL has also been shown to predict all-cause and cardiovascular mortality. Experimental studies support a functional link between aerobic exercise and telomere preservation through activation of telomerase, an enzyme that adds nucleotides to the telomeric ends. However, unresolved questions regarding exercise modalities, pathomechanistic aspects and analytical issues limit the interpretability of available data. This review provides an overview about the current knowledge in the area of telomere biology, aging and physical activity. Finally, the capabilities and limitations of available analytical methods are addressed.
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Vitamin D deficiency as a potential risk factor for accelerated aging, impaired hippocampal neurogenesis and cognitive decline: a role for Wnt/β-catenin signaling

Ricardo Gómez-Oliva, Noelia Geribaldi-Doldán, Samuel Domínguez-García, Livia Carrascal, Cristina Verástegui, Pedro Nunez-Abades, Carmen Castro,

https://doi.org/10.18632/aging.103510 pp 13824—13844

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Gómez-Oliva R, Geribaldi-Doldán N, Domínguez-García S, Carrascal L, Verástegui C, Nunez-Abades P, Castro C, . Vitamin D deficiency as a potential risk factor for accelerated aging, impaired hippocampal neurogenesis and cognitive decline: a role for Wnt/β-catenin signaling. . 12:13824-13844. https://doi.org/10.18632/aging.103510

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                TY  - JOUR
                AU  - Gómez-Oliva, Ricardo 
                AU  - Geribaldi-Doldán, Noelia 
                AU  - Domínguez-García, Samuel 
                AU  - Carrascal, Livia 
                AU  - Verástegui, Cristina 
                AU  - Nunez-Abades, Pedro 
                AU  - Castro, Carmen 
                TI  - Vitamin D deficiency as a potential risk factor for accelerated aging, impaired hippocampal neurogenesis and cognitive decline: a role for Wnt/β-catenin signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 13
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103510
                DO  - 10.18632/aging.103510
                SP  - 13824
                EP  - 13844
                PY  - 
                AB  - Vitamin D is an essential fat-soluble vitamin that participates in several homeostatic functions in mammalian organisms. Lower levels of vitamin D are produced in the older population, vitamin D deficiency being an accelerating factor for the progression of the aging process. In this review, we focus on the effect that vitamin D exerts in the aged brain paying special attention to the neurogenic process. Neurogenesis occurs in the adult brain in neurogenic regions, such as the dentate gyrus of the hippocampus (DG). This region generates new neurons that participate in cognitive tasks. The neurogenic rate in the DG is reduced in the aged brain because of a reduction in the number of neural stem cells (NSC). Homeostatic mechanisms controlled by the Wnt signaling pathway protect this pool of NSC from being depleted. We discuss in here the crosstalk between Wnt signaling and vitamin D, and hypothesize that hypovitaminosis might cause failure in the control of the neurogenic homeostatic mechanisms in the old brain leading to cognitive impairment. Understanding the relationship between vitamin D, neurogenesis and cognitive performance in the aged brain may facilitate prevention of cognitive decline and it can open a door into new therapeutic fields by perspectives in the elderly.
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Volume 12, Issue 13

About the Cover

Priority Research Papers

COVID-19 Serum IgM against SARS-CoV-2 correlates with in-hospital mortality in severe/critical patients with COVID-19 in Wuhan, China

Xintian Liu, Xuan Zheng, Bo Liu, Mingxiang Wu, Zhenlu Zhang, Gangcheng Zhang, Xi Su,

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Franny Jongbloed, Ron W.F. de Bruin, Harry Van Steeg, Piet Beekhof, Paul Wackers, Dennis A. Hesselink, Jan H.J. Hoeijmakers, Martijn E.T. Dollé, Jan N.M. IJzermans,

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Research Papers

COVID-19 Questionnaire assessment helps the self-management of patients with inflammatory bowel disease during the outbreak of Coronavirus Disease 2019

Meiping Yu, Zhenghao Ye, Yu Chen, Tingting Qin, Jiguang Kou, De’an Tian, Fang Xiao,

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COVID-19 A qualitative study of the vocational and psychological perceptions and issues of transdisciplinary nurses during the COVID-19 outbreak

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