Volume 12, Issue 8

COVID-19
Biomarkers of biological age as predictors of COVID-19 disease severity

Gordan Lauc, David Sinclair,

https://doi.org/10.18632/aging.103052 pp 6490—6491

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Lauc G, Sinclair D, . Biomarkers of biological age as predictors of COVID-19 disease severity. . 12:6490-6491. https://doi.org/10.18632/aging.103052

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COVID-19
Geroprotective and senoremediative strategies to reduce the comorbidity, infection rates, severity, and lethality in gerophilic and gerolavic infections

Alex Zhavoronkov,

https://doi.org/10.18632/aging.102988 pp 6492—6510

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Zhavoronkov A, . Geroprotective and senoremediative strategies to reduce the comorbidity, infection rates, severity, and lethality in gerophilic and gerolavic infections. . 12:6492-6510. https://doi.org/10.18632/aging.102988

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                TY  - JOUR
                AU  - Zhavoronkov, Alex 
                TI  - Geroprotective and senoremediative strategies to reduce the comorbidity, infection rates, severity, and lethality in gerophilic and gerolavic infections
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102988
                DO  - 10.18632/aging.102988
                SP  - 6492
                EP  - 6510
                PY  - 
                AB  - The recently identified SARS-CoV-2 betacoronavirus responsible for the COVID-19 pandemic has uncovered the age-associated vulnerability in the burden of disease and put aging research in the spotlight. The limited data available indicates that COVID-19 should be referred to as a gerolavic (from Greek, g&#xE9;ros &#x201C;old man&#x201D; and epilav&#xED;s, &#x201C;harmful&#x201D;) infection because the infection rates, severity, and lethality are substantially higher in the population aged 60 and older. This is primarily due to comorbidity but may be partially due to immunosenescence, decreased immune function in the elderly, and general loss of function, fitness, and increased frailty associated with aging. Immunosenescence is a major factor affecting vaccination response, as well as the severity and lethality of infectious diseases. While vaccination reduces infection rates, and therapeutic interventions reduce the severity and lethality of infections, these interventions have limitations. Previous studies showed that postulated geroprotectors, such as sirolimus (rapamycin) and its close derivative rapalog everolimus (RAD001), decreased infection rates in a small sample of elderly patients. This article presents a review of the limited literature available on geroprotective and senoremediative interventions that may be investigated to decrease the disease burden of gerolavic infections. This article also highlights a need for rigorous clinical validation of deep aging clocks as surrogate markers of biological age. These could be used to assess the need for, and efficacy of, geroprotective and senoremediative interventions and provide better protection for elderly populations from gerolavic infections. This article does not represent medical advice and the medications described are not yet licensed or recommended as immune system boosters, as they have not undergone clinical evaluation for this purpose.
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COVID-19
COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?

Camillo Sargiacomo, Federica Sotgia, Michael P. Lisanti,

https://doi.org/10.18632/aging.103001 pp 6511—6517

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Sargiacomo C, Sotgia F, Lisanti MP, . COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?. . 12:6511-6517. https://doi.org/10.18632/aging.103001

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                TY  - JOUR
                AU  - Sargiacomo, Camillo 
                AU  - Sotgia, Federica 
                AU  - Lisanti, Michael P. 
                TI  - COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103001
                DO  - 10.18632/aging.103001
                SP  - 6511
                EP  - 6517
                PY  - 
                AB  - COVID-19, also known as SARS-CoV-2, is a new emerging zoonotic corona virus of the SARS (Severe Acute Respiratory Syndrome) and the MERS (Middle East Respiratory Syndrome) family. COVID-19 originated in China and spread world-wide, resulting in the pandemic of 2020. For some reason, COVID-19 shows a considerably higher mortality rate in patients with advanced chronological age. This begs the question as to whether there is a functional association between COVID-19 infection and the process of chronological aging. Two host receptors have been proposed for COVID-19. One is CD26 and the other is ACE-2 (angiotensin-converting enzyme 2). Interestingly, both CD26 and the angiotensin system show associations with senescence. Similarly, two proposed therapeutics for the treatment of COVID-19 infection are Azithromycin and Quercetin, both drugs with significant senolytic activity. Also, Chloroquine-related compounds inhibit the induction of the well-known senescence marker, Beta-galactosidase. Other anti-aging drugs should also be considered, such as Rapamycin and Doxycycline, as they behave as inhibitors of protein synthesis, blocking both SASP and viral replication. Therefore, we wish to speculate that the fight against COVID-19 disease should involve testing the hypothesis that senolytics and other anti-aging drugs may have a prominent role in preventing the transmission of the virus, as well as aid in its treatment. Thus, we propose that new clinical trials may be warranted, as several senolytic and anti-aging therapeutics are existing FDA-approved drugs, with excellent safety profiles, and would be readily available for drug repurposing efforts. As Azithromycin and Doxycycline are both commonly used antibiotics that inhibit viral replication and IL-6 production, we may want to consider this general class of antibiotics that functionally inhibits cellular protein synthesis as a side-effect, for the treatment and prevention of COVID-19 disease.
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COVID-19
ACE2 correlated with immune infiltration serves as a prognostic biomarker in endometrial carcinoma and renal papillary cell carcinoma: implication for COVID-19

Jing Yang, Hongxia Li, Shengda Hu, Yafeng Zhou,

https://doi.org/10.18632/aging.103100 pp 6518—6535

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Yang J, Li H, Hu S, Zhou Y, . ACE2 correlated with immune infiltration serves as a prognostic biomarker in endometrial carcinoma and renal papillary cell carcinoma: implication for COVID-19. . 12:6518-6535. https://doi.org/10.18632/aging.103100

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                TY  - JOUR
                AU  - Yang, Jing 
                AU  - Li, Hongxia 
                AU  - Hu, Shengda 
                AU  - Zhou, Yafeng 
                TI  - ACE2 correlated with immune infiltration serves as a prognostic biomarker in endometrial carcinoma and renal papillary cell carcinoma: implication for COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103100
                DO  - 10.18632/aging.103100
                SP  - 6518
                EP  - 6535
                PY  - 
                AB  - Angiotensin-converting enzyme 2 (ACE2) is a member of the renin-angiotension system, however, the correlation between ACE2 and prognosis in UCEC (Uterine Corpus Endometrial Carcinoma) and KIRP (Kidney Renal Papillary Cell Carcinoma) is not clear. We analyzed the expression levels of ACE2 in the Oncomine and TIMER databases, the correlation between ACE2 and overall survival in the PrognoScan, GEPIA and Kaplan-Meier plotter databases. The correlation between ACE2 and immune infiltration level and the type markers of immune cells was investigated in TIMER database. A prognosis analysis based on the expression levels of ACE2 was further performed in related immune cells subgroup. The ACE2 promoter methylation profile was tested in the UALCAN database. In addition, we used GSE30589 and GSE52920 databases to elucidate the changes of ACE2 expression in vivo and in vitro after SARS-CoV infection. ACE2 was elevated in UCEC and KIRP, and high ACE2 had a favorable prognosis. The expression of ACE2 was positively correlated with the level of immune infiltration of macrophage in KIRP, B cell, CD4+T cell, neutrophil and dendritic cell immune infiltration levels in UCEC. ACE2 was significantly positively correlated with the type markers of B cells and neutrophils, macrophages in UCEC, while ACE2 in KIRP was positively correlated with the type markers of macrophages. High ACE2 expression level had a favorable prognosis in different enriched immune cells subgroups in UCEC and KIRP. And the promoter methylation levels of ACE2 in UCEC and KIRP were significantly reduced. What&#x2019;s more, we found that the expression of ACE2 decreased in vivo and in vitro after SARS-CoV infection. In conclusion, ACE2 expression increased significantly in UCEC and KIRP, elevated ACE2 was positively correlated with immune infiltration and prognosis. Moreover, tumor tissues may be more susceptible to SARS-CoV-2 infection in COVID-19 patients with UCEC and KIRP, which may worsen the prognosis.
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COVID-19
Anti-SARS-CoV-2 virus antibody levels in convalescent plasma of six donors who have recovered from COVID-19

Libo Zhang, Rongrong Pang, Xiang Xue, Jingjing Bao, Sheng Ye, Yudong Dai, Yishan Zheng, Qiang Fu, Zhiliang Hu, Yongxiang Yi,

https://doi.org/10.18632/aging.103102 pp 6536—6542

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Zhang L, Pang R, Xue X, Bao J, Ye S, Dai Y, Zheng Y, Fu Q, Hu Z, Yi Y, . Anti-SARS-CoV-2 virus antibody levels in convalescent plasma of six donors who have recovered from COVID-19. . 12:6536-6542. https://doi.org/10.18632/aging.103102

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                TY  - JOUR
                AU  - Zhang, Libo 
                AU  - Pang, Rongrong 
                AU  - Xue, Xiang 
                AU  - Bao, Jingjing 
                AU  - Ye, Sheng 
                AU  - Dai, Yudong 
                AU  - Zheng, Yishan 
                AU  - Fu, Qiang 
                AU  - Hu, Zhiliang 
                AU  - Yi, Yongxiang 
                TI  - Anti-SARS-CoV-2 virus antibody levels in convalescent plasma of six donors who have recovered from COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103102
                DO  - 10.18632/aging.103102
                SP  - 6536
                EP  - 6542
                PY  - 
                AB  - Background: Anti-SARS-CoV-2 virus antibody levels in convalescent plasma (CP), which may be useful in severe Anti-SARS-CoV-2 virus infections, have been rarely reported.Results: A total of eight donors were considered for enrollment; two of them were excluded because of ineligible routine check. Of the six remaining participants, five samples were tested weakly positive by the IgM ELISA. Meanwhile, high titers of IgG were observed in five samples. The patient treated with CP did not require mechanical ventilation 11 days after plasma transfusion, and was then transferred to a general ward.Conclusions: Our serological findings in convalescent plasma from recovered patients may help facilitate understanding of the SARS-CoV-2 infection and establish CP donor screening protocol in COVID-19 outbreak.Methods: Anti-SARS-CoV-2 antibodies including IgM and IgG were measured by two enzyme-linked immunosorbent assays (ELISA) in convalescent plasma from six donors who have recovered from coronavirus disease 2019 (COVID-19) in Nanjing, China. CP was also utilized for the treatment of one severe COVID-19 patient.
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Long non-coding RNA ANRIL alleviates H₂O₂-induced injury by up-regulating microRNA-21 in human lens epithelial cells

Shanshan Du, Jingzhi Shao, Ying Qi, Xuhui Liu, Jingjing Liu, Fengyan Zhang,

https://doi.org/10.18632/aging.102800 pp 6543—6557

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Du S, Shao J, Qi Y, Liu X, Liu J, Zhang F, . Long non-coding RNA ANRIL alleviates H₂O₂-induced injury by up-regulating microRNA-21 in human lens epithelial cells. . 12:6543-6557. https://doi.org/10.18632/aging.102800

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 TY - JOUR
 AU - Du, Shanshan 
 AU - Shao, Jingzhi 
 AU - Qi, Ying 
 AU - Liu, Xuhui 
 AU - Liu, Jingjing 
 AU - Zhang, Fengyan 
 TI - Long non-coding RNA ANRIL alleviates H2O2-induced injury by up-regulating microRNA-21 in human lens epithelial cells
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102800
 DO - 10.18632/aging.102800
 SP - 6543
 EP - 6557
 PY - 
 AB - The accurate role of ANRIL in cataract is poorly understood. We aimed to reveal the effects of ANRIL on H2O2-treated HLECs, SRA01/04, as well as the regulatory mechanisms. Oxidative stress model of HLECs was induced by H2O2. Cell injury was evaluated according to cell proliferation, apoptosis and DNA damage using CCK-8 assay/flow cytometry and TUNEL assays/&#x3B3;H2AX staining. Expressions of ANRIL and miR-21 in HLECs were determined by RT-qPCR. The effects of miR-21, miR-34a and miR-122-5p inhibition as well as AMPK and &#x3B2;-catenin on HLECs with ANRIL overexpression and H2O2 stimulation were analyzed. In vivo experiment was performed via RT-qPCR. H2O2 repressed proliferation and induced apoptosis or DNA damage in HLECs. Those alterations induced by H2O2 were attenuated by ANRIL overexpression. MiR-21 was positively regulated by ANRIL, and both of them were repressed in H2O2-induced HLECs and cataract patient tissues. Inhibition of miR-21 but not miR-34a or miR-122-5p reversed the effects of ANRIL on H2O2-treated HLECs. Phosphorylation of AMPK and expression of &#x3B2;-catenin were increased by ANRIL via regulating miR-21. AMPK and &#x3B2;-catenin affected beneficial function of ANRIL-miR-21 axis.Therefore, lncRNA ANRIL attenuated H2O2-induced cell injury in HELCs via up-regulating miR-21 via the activation of AMPK and &#x3B2;-catenin.
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Epigenetic modulation of macrophage polarization prevents lumbar disc degeneration

Yang Hou, Guodong Shi, Yongfei Guo, Jiangang Shi,

https://doi.org/10.18632/aging.102909 pp 6558—6569

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Hou Y, Shi G, Guo Y, Shi J, . Epigenetic modulation of macrophage polarization prevents lumbar disc degeneration. . 12:6558-6569. https://doi.org/10.18632/aging.102909

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                TY  - JOUR
                AU  - Hou, Yang 
                AU  - Shi, Guodong 
                AU  - Guo, Yongfei 
                AU  - Shi, Jiangang 
                TI  - Epigenetic modulation of macrophage polarization prevents lumbar disc degeneration
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102909
                DO  - 10.18632/aging.102909
                SP  - 6558
                EP  - 6569
                PY  - 
                AB  - Inflammation plays an essential role in the development of lumbar disc degeneration (LDD), although the exact effects of macrophage subtypes on LDD remain unclear. Based on previous studies, we hypothesized that M2-polarization of local macrophages and simultaneous suppression of their production of fibrotic transforming growth factor beta 1 (TGF&#x3B2;1) could inhibit progression of LDD. Thus, we applied an orthotopic injection of adeno-associated virus (AAV) carrying shRNA for DNA Methyltransferase 1 (DNMT1) and/or shRNA for TGF&#x3B2;1 under a macrophage-specific CD68 promoter to specifically target local macrophages in a mouse model for LDD. We found that shDNMT1 significantly reduced levels of the pro-inflammatory cytokines TNF&#x3B1;, IL-1&#x3B2; and IL-6, significantly increased levels of the anti-inflammatory cytokines IL-4 and IL-10, significantly increased M2 macrophage polarization, significantly reduced cell apoptosis in the disc degeneration zone and significantly reduced LDD-associated pain. The anti-apoptotic and anti-pain effects were further strengthened by co-application of shTGF&#x3B2;1. Together, these data suggest that M2 polarization of macrophages induced by both epigenetic modulation and suppressed production and release of TGF&#x3B2;1 from polarized M2 macrophages, may have a demonstrable therapeutic effect on LDD.
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Long non-coding RNA MALAT1 exacerbates acute respiratory distress syndrome by upregulating ICAM-1 expression via microRNA-150-5p downregulation

Meng-Ying Yao, Wei-Hong Zhang, Wen-Tao Ma, Qiu-Hong Liu, Li-Hua Xing, Gao-Feng Zhao,

https://doi.org/10.18632/aging.102953 pp 6570—6585

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Yao M, Zhang W, Ma W, Liu Q, Xing L, Zhao G, . Long non-coding RNA MALAT1 exacerbates acute respiratory distress syndrome by upregulating ICAM-1 expression via microRNA-150-5p downregulation. . 12:6570-6585. https://doi.org/10.18632/aging.102953

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                TY  - JOUR
                AU  - Yao, Meng-Ying 
                AU  - Zhang, Wei-Hong 
                AU  - Ma, Wen-Tao 
                AU  - Liu, Qiu-Hong 
                AU  - Xing, Li-Hua 
                AU  - Zhao, Gao-Feng 
                TI  - Long non-coding RNA MALAT1 exacerbates acute respiratory distress syndrome by upregulating ICAM-1 expression via microRNA-150-5p downregulation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102953
                DO  - 10.18632/aging.102953
                SP  - 6570
                EP  - 6585
                PY  - 
                AB  - Acute respiratory distress syndrome (ARDS) is a severe form of acute lung injury in which severe inflammatory responses induce cell apoptosis, necrosis, and fibrosis. This study investigated the role of lung adenocarcinoma transcript 1 (MALAT1) in ARDS and the underlying mechanism involved. The expression of MALAT1, microRNA-150-5p (miR-150-5p), and intercellular adhesion molecule-1 (ICAM-1) was determined in ARDS patients and lipopolysaccharide (LPS)-treated human pulmonary microvascular endothelial cells (HPMECs). Next, the interactions among MALAT1, miR-150-5p, and ICAM-1 were explored. Gain- or loss-of-function experiments in HPMECs were employed to determine cell apoptosis and inflammation. Furthermore, a mouse xenograft model of ARDS was established in order to verify the function of MALAT1 in vivo. MALAT1 and ICAM-1 were upregulated, while miR-150-5p was downregulated in both ARDS patients and LPS-treated HPMECs. MALAT1 upregulated ICAM-1 expression by competitively binding to miR-150-5p. MALAT1 silencing or miR-150-5p overexpression was shown to suppress HPMEC apoptosis, decrease the expressions of pro-inflammatory cytokines (IL-6, IL-1&#x3B2; and TNF-&#x3B1;) and E-selectin in HPMECs, as well as alleviated lung injury in nude mice. These findings demonstrated that MALAT1 silencing can potentially suppress HPMEC apoptosis and alleviate lung injury in ARDS via miR-150-5p-targeted ICAM-1, suggestive of a novel therapeutic target for ARDS.
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The expression of PDGF-BB predicts curative effect in locally advanced esophageal squamous cell carcinoma treated by radiotherapy

Puchun Er, Dong Qian, Wencheng Zhang, Baozhong Zhang, Hui Wei, Tian Zhang, Xi Chen, Yuwen Wang, Jingjing Zhao, Qi Wang, Qingsong Pang, Ping Wang,

https://doi.org/10.18632/aging.102993 pp 6586—6599

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Er P, Qian D, Zhang W, Zhang B, Wei H, Zhang T, Chen X, Wang Y, Zhao J, Wang Q, Pang Q, Wang P, . The expression of PDGF-BB predicts curative effect in locally advanced esophageal squamous cell carcinoma treated by radiotherapy. . 12:6586-6599. https://doi.org/10.18632/aging.102993

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                TY  - JOUR
                AU  - Er, Puchun 
                AU  - Qian, Dong 
                AU  - Zhang, Wencheng 
                AU  - Zhang, Baozhong 
                AU  - Wei, Hui 
                AU  - Zhang, Tian 
                AU  - Chen, Xi 
                AU  - Wang, Yuwen 
                AU  - Zhao, Jingjing 
                AU  - Wang, Qi 
                AU  - Pang, Qingsong 
                AU  - Wang, Ping 
                TI  - The expression of PDGF-BB predicts curative effect in locally advanced esophageal squamous cell carcinoma treated by radiotherapy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102993
                DO  - 10.18632/aging.102993
                SP  - 6586
                EP  - 6599
                PY  - 
                AB  - Radiotherapy is the major approach and is well tolerated in locally advanced esophageal squamous cell carcinoma (ESCC). And nowadays, no effective biological markers have been identified for predicting the prognosis of patients with ESCC. Platelet-derived growth factor (PDGF) is associated with a poor prognosis of various malignancies. The present study aimed to assess the effect of PDGF-BB on radiotherapeutic responses of ESCC and the underlying mechanisms of its roles in ESCC. Serum from 68 cases that received neoadjuvant or radical radiotherapy was obtained before and during radiotherapy. Gene expression analyses were validated by enzyme linked immunosorbent assay. The prognosis of patients with significantly reduced PDGF-BB was probably better than that of the others found in the progression-free survival and overall survival groups. Depletion of PDGFB significantly suppressed the proliferation, invasion and migration of cancer cells. Inhibiting PDGFB induced cellular apoptosis and promoted the sensitivity to ionizing radiation (IR). Furthermore, IR inhibited PDGF-BB-induced migration by blocking the PI3K/AKT pathway in ESCC cells. We found that the expression of PDGF-BB provided a possible model for predicting ESCC radiotherapy. It can also be used as a prognostic indicator for locally advanced ESCC that was treated by radiotherapy.
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PHTF2 regulates lipids metabolism in gastric cancer

Yuhua Chi, Haiyan Wang, Fengsong Wang, Mingcui Ding,

https://doi.org/10.18632/aging.102995 pp 6600—6610

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Chi Y, Wang H, Wang F, Ding M, . PHTF2 regulates lipids metabolism in gastric cancer. . 12:6600-6610. https://doi.org/10.18632/aging.102995

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                TY  - JOUR
                AU  - Chi, Yuhua 
                AU  - Wang, Haiyan 
                AU  - Wang, Fengsong 
                AU  - Ding, Mingcui 
                TI  - PHTF2 regulates lipids metabolism in gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102995
                DO  - 10.18632/aging.102995
                SP  - 6600
                EP  - 6610
                PY  - 
                AB  - Identification of hub genes and key pathways of gastric cancer was recognized to be essential to elucidate the tumorigenesis of GC. This study was aimed to identify the differentially expressed genes (DEGs) in GC via bioinformatics methods and their related pathways involved in the pathological process of GC. Gene expression profile datasets acquired by microarray chips or RNA-seq were downloaded from GEO dataset and TCGA, and 298 differentially expressed genes was identified. The Gene Ontology (GO) and Kyoto Gene and Genomic Encyclopedia (KEGG) pathways of DEGs were then analyzed by the DAVID database to elucidate the potential molecular functions of DEGs. The protein-protein interaction (PPI) network of DEGs was further analyzed with the STRING database and PHTF2 was identified as a hub gene in the PPI network. Subsequently, PHTF2 was found to be highly expressed in different subtypes of gastric cancer tissues obtained from TCGA database or clinical patients, resulting with a poor prognosis. By GSEA, PHTF2 was found to significantly enrich the fatty acid metabolism pathway in gastric cancer. Moreover, PHTF2-regulated lipids metabolism significantly affected the tumorigenesis of GC cells. In summary, this work identified a new mechanism by which PHTF2 precipitated in the pathological process of GC by regulating cellular lipid metabolism.
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Heme oxygenase-1 inhibition mediates Gas6 to enhance bortezomib-sensitivity in multiple myeloma via ERK/STAT3 axis

Zhaoyuan Zhang, Weili Wang, Dan Ma, Jie Xiong, Xingyi Kuang, Siyu Zhang, Qin Fang, Jishi Wang,

https://doi.org/10.18632/aging.102996 pp 6611—6629

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Zhang Z, Wang W, Ma D, Xiong J, Kuang X, Zhang S, Fang Q, Wang J, . Heme oxygenase-1 inhibition mediates Gas6 to enhance bortezomib-sensitivity in multiple myeloma via ERK/STAT3 axis. . 12:6611-6629. https://doi.org/10.18632/aging.102996

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                TY  - JOUR
                AU  - Zhang, Zhaoyuan 
                AU  - Wang, Weili 
                AU  - Ma, Dan 
                AU  - Xiong, Jie 
                AU  - Kuang, Xingyi 
                AU  - Zhang, Siyu 
                AU  - Fang, Qin 
                AU  - Wang, Jishi 
                TI  - Heme oxygenase-1 inhibition mediates Gas6 to enhance bortezomib-sensitivity in multiple myeloma via ERK/STAT3 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102996
                DO  - 10.18632/aging.102996
                SP  - 6611
                EP  - 6629
                PY  - 
                AB  - Chemoresistance is still a critical challenge for efficient treatment of multiple myeloma (MM) during the bortezomib-based chemotherapy. Recent studies have suggested that heme oxygenase-1 (HO-1) is involved in apoptosis, proliferation and chemoresistance in cancer cells. Here we aim to investigate the role and mechanism of HO-1 in bortezomib-sensitivity to myeloma cells. In the study population, we found that HO-1 was highly expressed in CD138+ primary myeloma cells, which was positively associated with Gas6 expression and Gas6 plasma levels in MM patients. Downregulation of HO-1 using pharmacological inhibitor ZnPPIX or siRNA knockdown significantly enhanced myeloma cell sensitivity to bortezomib in human primary CD138+ cells, U266 and RPMI8226 cell lines. Mechanistically, HO-1 regulated Gas6 production via ERK/STAT3 axis. Combination with HO-1 inhibition increased bortezomib-induced apoptosis and antiproliferative effects via suppressing Gas6 production. These findings suggest that combination of bortezomib and HO-1 inhibitor may serve as a promising therapeutic target against bortezomib-resistant MM.
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γ-Mangostin isolated from Garcinia mangostana L. suppresses inflammation and alleviates symptoms of osteoarthritis via modulating miR-124-3p/IL-6/NF-κB signaling

Yen-Shuo Chiu, Jia-Lin Wu, Chi-Tai Yeh, Vijesh Kumar Yadav, Hsu-Shan Huang, Liang-Shun Wang,

https://doi.org/10.18632/aging.103003 pp 6630—6643

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Chiu Y, Wu J, Yeh C, Yadav VK, Huang H, Wang L, . γ-Mangostin isolated from Garcinia mangostana L. suppresses inflammation and alleviates symptoms of osteoarthritis via modulating miR-124-3p/IL-6/NF-κB signaling. . 12:6630-6643. https://doi.org/10.18632/aging.103003

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 TY - JOUR
 AU - Chiu, Yen-Shuo 
 AU - Wu, Jia-Lin 
 AU - Yeh, Chi-Tai 
 AU - Yadav, Vijesh Kumar 
 AU - Huang, Hsu-Shan 
 AU - Wang, Liang-Shun 
 TI - γ-Mangostin isolated from Garcinia mangostana L. suppresses inflammation and alleviates symptoms of osteoarthritis via modulating miR-124-3p/IL-6/NF-κB signaling
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103003
 DO - 10.18632/aging.103003
 SP - 6630
 EP - 6643
 PY - 
 AB - Osteoarthritis (OA) a disease associated with joints and become severe with age, due to softening, inflammation and degradation of cartilage in joints. The agents that can target OA is needed, specifically without any side effects. Garcinia mangostana L. (Mangosteen) a tropical fruit used to treat many skin and stomach associated ailments. &#x3B3;- Mangostin (&#x3B3;-MS) a key bioactive substance present in mangosteen. Here, we aimed to explore &#x3B3;-MS potential in targeting the pro-inflammatory cytokine, factors and miRs in OA progression. Significantly, &#x3B3;-MS suppresses the inflammatory cytokines (IL-6, TNF-&#x3B1;, and INF- &#x3B3;) and factors (NF-&#x3BA;B, STAT3, and COX-2) which regulates/participate in the catabolic process of cartilage destruction. Result of Hematoxylin-eosin (H&amp;E) staining of tissue sections of OA joints of &#x3B3;-MS treated and non-treated mice confirm &#x3B3;-MS improves the signs of injuries, and maintains the structural integrity of the articular cartilage (epiphyseal disk joints and bone marrow) and reduces inflammation. Mechanistically, &#x3B3;-MS targets miR-98-5p and miR-124-3p which are found to suppress the expression IL-6 and NF-&#x3BA;B, respectively. But in OA these miRs are inhibited, especially miR-124-3p which regulates not only NF-&#x3BA;B but also TNF-&#x3B1;, IL-6 and MMP7. With a further investigation underway, &#x3B3;-MS represents an important source for treating and managing OA.
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LncRNA Sox2OT-V7 promotes doxorubicin-induced autophagy and chemoresistance in osteosarcoma via tumor-suppressive miR-142/miR-22

Kewei Zhu, Yang Yuan, Jie Wen, Ding Chen, Weihong Zhu, Zhengxiao Ouyang, Wanchun Wang,

https://doi.org/10.18632/aging.103004 pp 6644—6666

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Zhu K, Yuan Y, Wen J, Chen D, Zhu W, Ouyang Z, Wang W, . LncRNA Sox2OT-V7 promotes doxorubicin-induced autophagy and chemoresistance in osteosarcoma via tumor-suppressive miR-142/miR-22. . 12:6644-6666. https://doi.org/10.18632/aging.103004

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                TY  - JOUR
                AU  - Zhu, Kewei 
                AU  - Yuan, Yang 
                AU  - Wen, Jie 
                AU  - Chen, Ding 
                AU  - Zhu, Weihong 
                AU  - Ouyang, Zhengxiao 
                AU  - Wang, Wanchun 
                TI  - LncRNA Sox2OT-V7 promotes doxorubicin-induced autophagy and chemoresistance in osteosarcoma via tumor-suppressive miR-142/miR-22
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103004
                DO  - 10.18632/aging.103004
                SP  - 6644
                EP  - 6666
                PY  - 
                AB  - Doxorubicin (Dox) is one of the most commonly used chemotherapeutic drugs for osteosarcoma (OS) treatment. In the present study, we attempted to investigate the mechanism by which Sox2OT-V7 dysregulation affects Dox chemoresistance to provide a novel experimental basis for developing neoadjuvant therapy. Sox2OT-V7 expression is upregulated in OS tissues, particularly in chemoresistant OS tissues, and in OS cell lines compared to controls. Dox treatment induces autophagy and Sox2OT-V7 expression in U2OS cells, and Dox-induced autophagy is partially attenuated by Sox2OT-V7 silencing. Knocking down Sox2OT-V7 or blocking autophagy in Dox-resistant U2OS/Dox cells resensitizes the cells to Dox treatment in vitro. Moreover, Sox2OT-V7 directly targets miR-142/miR-22 to inhibit their expression, and the effect of Sox2OT-V7 silencing on U2OS cell autophagy and U2OS/Dox cell sensitivity to Dox can be reversed by miR-142/miR-22 inhibition. Sox2OT-V7 silencing enhances the suppressive effects of Dox on U2OS/Dox cell-derived tumor growth in vivo, while miR-22 inhibition or miR-142 inhibition reverses the effects of Sox2OT-V7 silencing on Dox-induced suppression on tumor growth. Finally, miR-142 directly targets ULK1, ATG4A, and ATG5, while miR-22 directly targets ULK1 to inhibit the expression of the target gene; The Sox2OT-V7/miR-142/miR-22 axis modulates autophagy in OS cells by regulating ULK1, ATG4A, and ATG5.
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Ultraconserved element uc.333 increases insulin sensitivity by binding to miR-223

Yang Zhang, Jingyu Sun, He Yao, Yajun Lin, Jie Wei, Gang Hu, Jun Guo, Jian Li,

https://doi.org/10.18632/aging.103020 pp 6667—6679

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Zhang Y, Sun J, Yao H, Lin Y, Wei J, Hu G, Guo J, Li J, . Ultraconserved element uc.333 increases insulin sensitivity by binding to miR-223. . 12:6667-6679. https://doi.org/10.18632/aging.103020

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                TY  - JOUR
                AU  - Zhang, Yang 
                AU  - Sun, Jingyu 
                AU  - Yao, He 
                AU  - Lin, Yajun 
                AU  - Wei, Jie 
                AU  - Hu, Gang 
                AU  - Guo, Jun 
                AU  - Li, Jian 
                TI  - Ultraconserved element uc.333 increases insulin sensitivity by binding to miR-223
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103020
                DO  - 10.18632/aging.103020
                SP  - 6667
                EP  - 6679
                PY  - 
                AB  - Insulin resistance (IR) contributes to diabetes and aging. Ultraconserved elements (UCEs) are a class of long noncoding RNAs (lncRNAs) that are 100% conserved in humans, mice, and rats. We identified the lncRNA uc.333 using an lncRNA microarray and then used quantitative real-time polymerase chain reaction to analyze its expression in the livers of nonalcoholic fatty liver disease (NAFLD) patients, db/db mice, high-fat diet&#x2013;fed mice, IL-6-treated mice, and TNF-&#x3B1;-treated mice. The underlying mechanisms of uc.333 in IR were investigated using fluorescence in situ hybridization, Western blot, and miRNA microarray analyses. The results revealed that uc.333 expression was decreased in liver tissues from NAFLD patients and treated mice. Furthermore, overexpression of uc.333 decreased IR, whereas knocking down uc.333 increased IR. We also confirmed that uc.333 binds to miR-223 and that the levels of miR-223 were increased in the livers of patients and treated mice. These findings showed that uc.333 improves IR by binding to miR-223; thus, uc.333 may be a useful target for the treatment and prevention of IR.
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Long intergenic non-protein coding RNA 324 prevents breast cancer progression by modulating miR-10b-5p

Bo Wang, Yangyang Zhang, Haitian Zhang, Faquan Lin, Qixin Tan, Qinghong Qin, Wei Bao, Yi Liu, Jiaying Xie, Qiyan Zeng,

https://doi.org/10.18632/aging.103021 pp 6680—6699

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Wang B, Zhang Y, Zhang H, Lin F, Tan Q, Qin Q, Bao W, Liu Y, Xie J, Zeng Q, . Long intergenic non-protein coding RNA 324 prevents breast cancer progression by modulating miR-10b-5p. . 12:6680-6699. https://doi.org/10.18632/aging.103021

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                TY  - JOUR
                AU  - Wang, Bo 
                AU  - Zhang, Yangyang 
                AU  - Zhang, Haitian 
                AU  - Lin, Faquan 
                AU  - Tan, Qixin 
                AU  - Qin, Qinghong 
                AU  - Bao, Wei 
                AU  - Liu, Yi 
                AU  - Xie, Jiaying 
                AU  - Zeng, Qiyan 
                TI  - Long intergenic non-protein coding RNA 324 prevents breast cancer progression by modulating miR-10b-5p
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103021
                DO  - 10.18632/aging.103021
                SP  - 6680
                EP  - 6699
                PY  - 
                AB  - Mounting evidence suggests that long noncoding RNAs serve as specific biomarkers and potent modulators of multiple cancers. Long intergenic non-protein coding RNA 324 (LINC00324) is ubiquitously expressed in various tissues, including breast cancer. The biological function of LINC00324 in the development and progression of breast cancer remains unknown. Here, we fully elucidate the relation between LINC00324 expression and breast cancer, and suggest a potential mechanism of action. We found that decreased expression of LINC00324 was dramatically correlated with malignancy of breast cancer, both in breast cancer tissues and in cell lines. Overexpression of LINC00324 in MDA-MB-231 cells resulted in a decrease in cell proliferation, invasion, and migration, while increasing cells apoptosis. On the other hand, loss-of-function experiments indicated that deficiency of LINC00324 promoted malignant phenotypes in breast cancer cells. Mechanically, we found that LINC00324 is mainly distributed in the cytoplasm, fostering the expression of E-cadherin by sponging miR-10b-5p. Taken together, these findings suggest that LINC00324 plays a critical role in breast cancer progression by directly interacting with miR-10b-5p. LINC00324 can thus potentially act as an early diagnostic marker and a novel therapeutic agent for breast cancer.
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Mitochondrial nucleoid remodeling and biogenesis are regulated by the p53-p21^WAF1-PKCζ pathway in p16^INK4a-silenced cells

Yun Yeong Lee, Yeon Seung Choi, Do Wan Kim, Jae Youn Cheong, Kye Yong Song, Min Sook Ryu, In Kyoung Lim,

https://doi.org/10.18632/aging.103029 pp 6700—6732

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Lee YY, Choi YS, Kim DW, Cheong JY, Song KY, Ryu MS, Lim IK, . Mitochondrial nucleoid remodeling and biogenesis are regulated by the p53-p21^WAF1-PKCζ pathway in p16^INK4a-silenced cells. . 12:6700-6732. https://doi.org/10.18632/aging.103029

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Provider: 
 TY - JOUR
 AU - Lee, Yun Yeong 
 AU - Choi, Yeon Seung 
 AU - Kim, Do Wan 
 AU - Cheong, Jae Youn 
 AU - Song, Kye Yong 
 AU - Ryu, Min Sook 
 AU - Lim, In Kyoung 
 TI - Mitochondrial nucleoid remodeling and biogenesis are regulated by the p53-p21WAF1-PKCζ pathway in p16INK4a-silenced cells
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103029
 DO - 10.18632/aging.103029
 SP - 6700
 EP - 6732
 PY - 
 AB - Mitochondrial dysfunction is linked to age-related senescence phenotypes. We report here the pathway increasing nucleoid remodeling and biogenesis in mitochondria during the senescence of foreskin human diploid fibroblasts (fs-HDF) and WI-38 cells. Replicative senescence in fs-HDF cells increased mitochondrial nucleoid remodeling as indicated by 5-bromo-2&apos;-deoxyuridine (BrdU) incorporation and mitochondrial transcription factor A (TFAM) expression in enlarged and fused mitochondria. Mitochondrial nucleoid remodeling was accompanied by mitochondrial biogenesis in old cells, and the expression levels of OXPHOS complex-I, -IV and -V subunits, PGC-1&#x3B1; and NRF1 were greatly increased compared to young cells. Activated protein kinase C zeta (PKC&#x3B6;) increased mitochondrial activity and expressed phenotypes of delayed senescence in fs-HDF cells, but not in WI-38 cells. The findings were reproduced in the doxorubicin-induced senescence of young fs-HDF and WI-38 cells via the PKC&#x3B6;-LKB1-AMPK signaling pathway, which was regulated by the p53-p21WAF1 pathway when p16INK4a was silenced. The signaling enhanced PGC-1&#x3B1;-NRF1-TFAM axis in mitochondria, which was demonstrated by Ingenuity Pathway Analysis of young and old fs-HDF cells. Activation of the p53-p21WAF1 pathway and silencing of p16INK4a are responsible for mitochondrial reprogramming in senescent cells, which may be a compensatory mechanism to promote cell survival under senescence stress.
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Carnitine palmitoyltransferase 1C contributes to progressive cellular senescence

Yongtao Wang, Tao Yu, Yanying Zhou, Shike Wang, Xunian Zhou, Limin Wang, Tianmiao Ou, Yixin Chen, Yawen Zhou, Huizhen Zhang, Ying Wang, Xiaomei Fan, Pan Chen, Frank J. Gonzalez, Aiming Yu, Peng Huang, Min Huang, Huichang Bi,

https://doi.org/10.18632/aging.103033 pp 6733—6755

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Wang Y, Yu T, Zhou Y, Wang S, Zhou X, Wang L, Ou T, Chen Y, Zhou Y, Zhang H, Wang Y, Fan X, Chen P, et al, . Carnitine palmitoyltransferase 1C contributes to progressive cellular senescence. . 12:6733-6755. https://doi.org/10.18632/aging.103033

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                TY  - JOUR
                AU  - Wang, Yongtao 
                AU  - Yu, Tao 
                AU  - Zhou, Yanying 
                AU  - Wang, Shike 
                AU  - Zhou, Xunian 
                AU  - Wang, Limin 
                AU  - Ou, Tianmiao 
                AU  - Chen, Yixin 
                AU  - Zhou, Yawen 
                AU  - Zhang, Huizhen 
                AU  - Wang, Ying 
                AU  - Fan, Xiaomei 
                AU  - Chen, Pan 
                AU  - Gonzalez, Frank J. 
                AU  - Yu, Aiming 
                AU  - Huang, Peng 
                AU  - Huang, Min 
                AU  - Bi, Huichang 
                TI  - Carnitine palmitoyltransferase 1C contributes to progressive cellular senescence
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103033
                DO  - 10.18632/aging.103033
                SP  - 6733
                EP  - 6755
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wang, Yongtao 
                AU  - Yu, Tao 
                AU  - Zhou, Yanying 
                AU  - Wang, Shike 
                AU  - Zhou, Xunian 
                AU  - Wang, Limin 
                AU  - Ou, Tianmiao 
                AU  - Chen, Yixin 
                AU  - Zhou, Yawen 
                AU  - Zhang, Huizhen 
                AU  - Wang, Ying 
                AU  - Fan, Xiaomei 
                AU  - Chen, Pan 
                AU  - Gonzalez, Frank J. 
                AU  - Yu, Aiming 
                AU  - Huang, Peng 
                AU  - Huang, Min 
                AU  - Bi, Huichang 
                TI  - Carnitine palmitoyltransferase 1C contributes to progressive cellular senescence
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103033
                DO  - 10.18632/aging.103033
                SP  - 6733
                EP  - 6755
                PY  - 
                AB  - Stable transfection manipulation with antibiotic selection and passaging induces progressive cellular senescence phenotypes. However, the underlying mechanisms remain poorly understood. This study demonstrated that stable transfection of the empty vector induced PANC-1 cells into cellular senescence. Metabolomics revealed several acylcarnitines and their upstream regulatory gene, carnitine palmitoyltransferase 1C (CPT1C) involved in fatty acid &#x3B2;-oxidation in mitochondria, were strikingly decreased in senescent PANC-1 cells. Low CPT1C expression triggered mitochondrial dysfunction, inhibited telomere elongation, impaired cell survival under metabolic stress, and hindered the malignance and tumorigenesis of senescent cells. On the contrary, mitochondrial activity was restored by CPT1C gain-of-function in senescent vector PANC-1 cells. PPAR&#x3B1; and TP53/CDKN1A, crucial signaling components in cellular senescence, were downregulated in senescent PANC-1 cells. This study identifies CPT1C as a key regulator of stable transfection-induced progressive PANC-1 cell senescence that inhibits mitochondrial function-associated metabolic reprogramming. These findings confirm the need to identify cell culture alterations after stable transfection, particularly when cells are used for metabolomics and mitochondria-associated studies, and suggest inhibition of CPT1C could be a promising target to intervene pancreatic tumorigenesis.
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Exosomal miR-200c suppresses chemoresistance of docetaxel in tongue squamous cell carcinoma by suppressing TUBB3 and PPP2R1B

Jun Cui, Haiyan Wang, Xiaohe Zhang, Xiaodong Sun, Jin Zhang, Jinji Ma,

https://doi.org/10.18632/aging.103036 pp 6756—6773

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Cui J, Wang H, Zhang X, Sun X, Zhang J, Ma J, . Exosomal miR-200c suppresses chemoresistance of docetaxel in tongue squamous cell carcinoma by suppressing TUBB3 and PPP2R1B. . 12:6756-6773. https://doi.org/10.18632/aging.103036

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                TY  - JOUR
                AU  - Cui, Jun 
                AU  - Wang, Haiyan 
                AU  - Zhang, Xiaohe 
                AU  - Sun, Xiaodong 
                AU  - Zhang, Jin 
                AU  - Ma, Jinji 
                TI  - Exosomal miR-200c suppresses chemoresistance of docetaxel in tongue squamous cell carcinoma by suppressing TUBB3 and PPP2R1B
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103036
                DO  - 10.18632/aging.103036
                SP  - 6756
                EP  - 6773
                PY  - 
                AB  - Background: Chemoresistance is the main challenge for treating tongue squamous cell carcinoma (TSCC). MiR-200c is an important regulator of chemoresistance. Exosomes are a promising molecule-delivery system for cancer treatment. Thus, this study aimed to investigate the role of miR-200c in chemoresistance of TSCC and whether exosomes could effectively deliver miR-200c to chemo-resistant cells and regulate cellular activities.Results: The results showed that the downregulation of miR-200c increased resistance to DTX, migration, and invasion and decreased apoptosis, which was reversed by the overexpression of miR-200c. The NTECs-derived exosomes transported miR-200c to HSC-3DR, increasing the sensitivity to DTX in vitro and in vivo. Also, epithelial-to-mesenchymal transition (EMT) and DNA damage responses were involved in DTX resistance. Furthermore, miR-200c regulated DTX resistance by targeting TUBB3 and PPP2R1B.Conclusion: Exosome-mediated miR-200c delivery may be an effective and promising strategy to treat chemoresistance in TSCC.Methods: Docetaxel (DTX) resistant HSC-3 cells (HSC-3DR) were transfected with miR-200c lentivirus and cocultured with exosomes derived from normal tongue epithelial cells (NTECs) that were overexpressed with miR-200c. The roles of miR-200c and exosomal miR-200c in vitro and in vivo were determined by RNA-Seq, qRT-PCR, western blots, transmission electron microscopy, and flow cytometry, fluorescence, CCK8, Transwell, and wound healing assays.
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circTNFRSF21, a newly identified circular RNA promotes endometrial carcinoma pathogenesis through regulating miR-1227-MAPK13/ATF2 axis

Yun Liu, Yue Chang, Yixuan Cai,

https://doi.org/10.18632/aging.103037 pp 6774—6792

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Liu Y, Chang Y, Cai Y, . circTNFRSF21, a newly identified circular RNA promotes endometrial carcinoma pathogenesis through regulating miR-1227-MAPK13/ATF2 axis. . 12:6774-6792. https://doi.org/10.18632/aging.103037

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                TY  - JOUR
                AU  - Liu, Yun 
                AU  - Chang, Yue 
                AU  - Cai, Yixuan 
                TI  - circTNFRSF21, a newly identified circular RNA promotes endometrial carcinoma pathogenesis through regulating miR-1227-MAPK13/ATF2 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103037
                DO  - 10.18632/aging.103037
                SP  - 6774
                EP  - 6792
                PY  - 
                AB  - Background: Circular RNA is a type of non-coding RNA with great potential in regulating gene expression and associated with disease progression. However, the role of circular RNA in endometrial carcinoma (EC) remains largely unknown.Results: In this study, we found that circTNFRSF21 was highly expressed in EC cells and tumor tissues. In vitro and in vivo results showed that circTNFRSF21 was linked to increased EC cell growth and EC xenografts formation in nude mice. Mechanically, we showed that circTNFRSF21 acts as a sponge of miR-1227 in EC cells to rescue MAPK13/ATF2 signaling pathway activity.Conclusions: Our studies suggested that in the EC, circTNFRSF21 promotes EC formation through downregulating miR-1227 expression and activating MAPK13/ATF2 signaling pathway. These findings provide strong evidence that circTNFRSF21-miR-1227-MAPK13/ATF2 axis is a promising target for EC treatment.Methods: qRT-PCR was used to detect circTNFRSF21expression in EC patients and EC cell lines. Cell growth, cell colony formation, cell apoptosis, cell cycle progression, and in vivo tumor formation assays were used to evaluate the roles of circTNFRSF21 in EC. Western blot, luciferase assay, RNA pull-down, siRNA knockdown, and CRISPR gene knock out assays were applied to study the mechanisms through which circTNFRSF21 regulates EC formation.
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LINC00514 drives osteosarcoma progression through sponging microRNA-708 and consequently increases URGCP expression

Dapeng Yu, Xiangyan Xu, Sufen Li, Kai Zhang,

https://doi.org/10.18632/aging.103043 pp 6793—6807

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Yu D, Xu X, Li S, Zhang K, . LINC00514 drives osteosarcoma progression through sponging microRNA-708 and consequently increases URGCP expression. . 12:6793-6807. https://doi.org/10.18632/aging.103043

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                TY  - JOUR
                AU  - Yu, Dapeng 
                AU  - Xu, Xiangyan 
                AU  - Li, Sufen 
                AU  - Zhang, Kai 
                TI  - LINC00514 drives osteosarcoma progression through sponging microRNA-708 and consequently increases URGCP expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103043
                DO  - 10.18632/aging.103043
                SP  - 6793
                EP  - 6807
                PY  - 
                AB  - Long intergenic nonprotein-coding RNA 00514 (LINC00514) is upregulated in papillary thyroid cancer and contributes to its aggressiveness. In this study, we thoroughly explored the expression profile, specific functions, and relevant molecular mechanism of LINC00514 in osteosarcoma (OS). Herein, LINC00514 was significantly upregulated in OS tissues and cells, and increased LINC00514 expression was closely correlated with tumor size, TNM stage, and distant metastasis. OS patients with high LINC00514 expression had shorter overall survival than those with low LINC00514 expression. LINC00514 interference inhibited OS cell proliferation, colony formation, migration, and invasion in vitro but promoted cell apoptosis and G0/G1 cell cycle arrest. LINC00514 downregulation hindered OS tumor growth in vivo. Mechanistically, LINC00514 functioned as a competing endogenous RNA by directly interacting with microRNA-708-5p (miR-708) and consequently increasing the expression of upregulator of cell proliferation (URGCP). Both miR-708 knockdown and URGCP restoration partially neutralized anticancer activities of LINC00514 silencing in OS cells. LINC00514 increases URGCP expression by acting as a competing endogenous RNA for miR-708, thus exerting oncogenic roles in OS progression. In conclusion, the LINC00514/miR-708/URGCP pathway may be a promising target for drug discovery in the future.
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FAM84B, amplified in pancreatic ductal adenocarcinoma, promotes tumorigenesis through the Wnt/β-catenin pathway

Xin Zhang, Jiapeng Xu, Ronglin Yan, Yu Zhang, Zunqi Hu, Hongbing Fu, Qing You, Qingping Cai, Dejun Yang,

https://doi.org/10.18632/aging.103044 pp 6808—6822

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Zhang X, Xu J, Yan R, Zhang Y, Hu Z, Fu H, You Q, Cai Q, Yang D, . FAM84B, amplified in pancreatic ductal adenocarcinoma, promotes tumorigenesis through the Wnt/β-catenin pathway. . 12:6808-6822. https://doi.org/10.18632/aging.103044

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Provider: 
                TY  - JOUR
                AU  - Zhang, Xin 
                AU  - Xu, Jiapeng 
                AU  - Yan, Ronglin 
                AU  - Zhang, Yu 
                AU  - Hu, Zunqi 
                AU  - Fu, Hongbing 
                AU  - You, Qing 
                AU  - Cai, Qingping 
                AU  - Yang, Dejun 
                TI  - FAM84B, amplified in pancreatic ductal adenocarcinoma, promotes tumorigenesis through the Wnt/β-catenin pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103044
                DO  - 10.18632/aging.103044
                SP  - 6808
                EP  - 6822
                PY  - 
                AB  - Altered expression of family with sequence similarity 84, member B (FAM84B) has been found in various human cancers. However, the expression and function of FAM84B in pancreatic ductal adenocarcinoma (PDAC) has not been studied. Here, by analyzing The Cancer Genome Atlas cohort, we found that FAM84B amplification was observed in 11% of 141 PDAC patients, and FAM84B amplification was correlated with higher mRNA expression of FAM84B. FAM84B amplification and overexpression was significantly correlated with poor overall survival. Moreover, knockdown of FAM84B in PDAC cell lines suppressed cell proliferation and induced apoptosis. FAM84B knockdown also suppressed mitochondrial function and glycolysis of PDAC cells. Interestingly, knockdown of FAM84B decreased the nuclear accumulation of &#x3B2;-catenin, and the expression of c-Myc and lactate dehydrogenase A, but enhanced the expression of Survivin. On the contrary, FAM84B overexpression displayed reversed effects in cell proliferation, apoptosis, mitochondrial function, and glycolysis, which was blocked by the Wnt/&#x3B2;-catenin pathway inhibitor (XAV939). In addition, PDAC cells with lower expression of FAM84B were more sensitive to gemcitabine-induced cell proliferation inhibition both in vitro and in vivo. In conclusion, FAM84B plays an important role in aerobic glycolysis and tumorigenesis in PDAC and Wnt/&#x3B2;-catenin may be involved in this process.
                ER  -

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Intracellular Insulin-like growth factor binding protein 2 (IGFBP2) contributes to the senescence of keratinocytes in psoriasis by stabilizing cytoplasmic p21

Laura Mercurio, Daniela Lulli, Francesca Mascia, Elena Dellambra, Claudia Scarponi, Martina Morelli, Carola Valente, Maria Luigia Carbone, Sabatino Pallotta, Giampiero Girolomoni, Cristina Albanesi, Saveria Pastore, Stefania Madonna,

https://doi.org/10.18632/aging.103045 pp 6823—6851

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Mercurio L, Lulli D, Mascia F, Dellambra E, Scarponi C, Morelli M, Valente C, Carbone ML, Pallotta S, Girolomoni G, Albanesi C, Pastore S, Madonna S, . Intracellular Insulin-like growth factor binding protein 2 (IGFBP2) contributes to the senescence of keratinocytes in psoriasis by stabilizing cytoplasmic p21. . 12:6823-6851. https://doi.org/10.18632/aging.103045

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                TY  - JOUR
                AU  - Mercurio, Laura 
                AU  - Lulli, Daniela 
                AU  - Mascia, Francesca 
                AU  - Dellambra, Elena 
                AU  - Scarponi, Claudia 
                AU  - Morelli, Martina 
                AU  - Valente, Carola 
                AU  - Carbone, Maria Luigia 
                AU  - Pallotta, Sabatino 
                AU  - Girolomoni, Giampiero 
                AU  - Albanesi, Cristina 
                AU  - Pastore, Saveria 
                AU  - Madonna, Stefania 
                TI  - Intracellular Insulin-like growth factor binding protein 2 (IGFBP2) contributes to the senescence of keratinocytes in psoriasis by stabilizing cytoplasmic p21
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103045
                DO  - 10.18632/aging.103045
                SP  - 6823
                EP  - 6851
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Mercurio, Laura 
                AU  - Lulli, Daniela 
                AU  - Mascia, Francesca 
                AU  - Dellambra, Elena 
                AU  - Scarponi, Claudia 
                AU  - Morelli, Martina 
                AU  - Valente, Carola 
                AU  - Carbone, Maria Luigia 
                AU  - Pallotta, Sabatino 
                AU  - Girolomoni, Giampiero 
                AU  - Albanesi, Cristina 
                AU  - Pastore, Saveria 
                AU  - Madonna, Stefania 
                TI  - Intracellular Insulin-like growth factor binding protein 2 (IGFBP2) contributes to the senescence of keratinocytes in psoriasis by stabilizing cytoplasmic p21
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103045
                DO  - 10.18632/aging.103045
                SP  - 6823
                EP  - 6851
                PY  - 
                AB  - Psoriasis is a chronic Th1/Th17 lymphocytes-mediated inflammatory skin disease, in which epidermal keratinocytes exhibit a peculiar senescent state, resistance to apoptosis and the acquisition of senescence-associated secretory phenotype (SASP). SASP consists of the release of soluble factors, including IGFBPs, that exert extracellular and intracellular functions in IGF-dependent or independent manner.In this report, we investigated the expression and function of IGFBP2 in senescent keratinocytes isolated from the skin of patients with plaque psoriasis. We found that IGFBP2 is aberrantly expressed and released by these cells in vivo, as well as in vitro in keratinocyte cultures undergoing progressive senescence, and it associates with the cyclin-dependent kinase inhibitors p21 and p16 expression. For the first time, we provide evidence for a dual action of IGFBP2 in psoriatic keratinocytes during growth and senescence processes. While extracellular IGFBP2 counter-regulates IGF-induced keratinocyte hyper-proliferation, intracellular IGFBP2 inhibits apoptosis by interacting with p21 and protecting it from ubiquitin-dependent degradation. Indeed, we found that cytoplasmic p21 sustains anti-apoptotic processes, by inhibiting pro-caspase 3 cleavage and JNK phosphorylation in senescent psoriatic keratinocytes. As a consequence, abrogation of p21, as well as that of IGFBP2, found to stabilize cytoplasmic p21 levels, lead to the restoration of apoptosis mechanisms in psoriatic keratinocytes, commonly observed in healthy cells.
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Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus

Jing-Ying Lin, Wei-Wen Kuo, Rathinasamy Baskaran, Chia-Hua Kuo, Yun-An Chen, William Shao-Tsu Chen, Tsung-Jung Ho, Cecilia Hsuan Day, B. Mahalakshmi, Chih-Yang Huang,

https://doi.org/10.18632/aging.103046 pp 6852—6864

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Lin J, Kuo W, Baskaran R, Kuo C, Chen Y, Chen WS, Ho T, Day CH, Mahalakshmi B, Huang C, . Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus. . 12:6852-6864. https://doi.org/10.18632/aging.103046

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                TY  - JOUR
                AU  - Lin, Jing-Ying 
                AU  - Kuo, Wei-Wen 
                AU  - Baskaran, Rathinasamy 
                AU  - Kuo, Chia-Hua 
                AU  - Chen, Yun-An 
                AU  - Chen, William Shao-Tsu 
                AU  - Ho, Tsung-Jung 
                AU  - Day, Cecilia Hsuan 
                AU  - Mahalakshmi, B. 
                AU  - Huang, Chih-Yang 
                TI  - Swimming exercise stimulates IGF1/ PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103046
                DO  - 10.18632/aging.103046
                SP  - 6852
                EP  - 6864
                PY  - 
                AB  - Hippocampus is one of the most vulnerable brain regions in terms of age-related pathological change. Exercise is presumed to delay the aging process and promote health because it seems to improve the function of most of the aging mechanisms. The purpose of this study is to evaluate the effects of swimming exercise training on brain inflammation, apoptotic and survival pathways in the hippocampus of D-galactose-induced aging in SD rats. The rats were allocated to the following groups: (1) control; (2) swimming exercise; (3) induced-aging by injecting D-galactose; (4) induced-aging rats with swimming exercise. The longevity-related AMPK/SIRT1/PGC-1&#x3B1; signaling pathway and brain IGF1/PI3K/Akt survival pathway were significantly reduced in D-galactose-induced aging group compared to non-aging control group and increased after exercise training. The inflammation pathway markers were over-expressed in induced-aging hippocampus, exercise significantly inhibited the inflammatory signaling activity. Fas-dependent and mitochondrial-dependent apoptotic pathways were significantly increased in the induced-aging group relative to the control group whereas they were decreased in the aging-exercise group. This study demonstrated that swimming exercise not only reduced aging-induced brain apoptosis and inflammatory signaling activity, but also enhanced the survival pathways in the hippocampus, which provides one of the new beneficial effects for exercise training in aging brain.
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Circular RNA circRGNEF promotes bladder cancer progression via miR-548/KIF2C axis regulation

Chen Yang, Qiong Li, Xinan Chen, Zheyu Zhang, Zezhong Mou, Fangdie Ye, Shengming Jin, Xiang Jun, Feng Tang, Haowen Jiang,

https://doi.org/10.18632/aging.103047 pp 6865—6879

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Yang C, Li Q, Chen X, Zhang Z, Mou Z, Ye F, Jin S, Jun X, Tang F, Jiang H, . Circular RNA circRGNEF promotes bladder cancer progression via miR-548/KIF2C axis regulation. . 12:6865-6879. https://doi.org/10.18632/aging.103047

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                TY  - JOUR
                AU  - Yang, Chen 
                AU  - Li, Qiong 
                AU  - Chen, Xinan 
                AU  - Zhang, Zheyu 
                AU  - Mou, Zezhong 
                AU  - Ye, Fangdie 
                AU  - Jin, Shengming 
                AU  - Jun, Xiang 
                AU  - Tang, Feng 
                AU  - Jiang, Haowen 
                TI  - Circular RNA circRGNEF promotes bladder cancer progression via miR-548/KIF2C axis regulation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103047
                DO  - 10.18632/aging.103047
                SP  - 6865
                EP  - 6879
                PY  - 
                AB  - Circular RNAs (circRNAs) play an important role in bladder cancer (BC). Though circRNA involvement in BC has been reported, the underlying regulatory mechanisms are unknown. In this study, we performed EdU, CCK8, colony formation and Transwell assays to establish the role of circRGNEF in BC cell migration, proliferation, and invasion. We used bioinformatics and luciferase reporter experiments to investigate the regulatory mechanism. Nude mice xenografts and live imaging were used to explore the role of circRGNEF in tumor metastasis and growth. Expression profile analysis of human circRNAs in BC revealed that circRGNEF was upregulated significantly. High circRGNEF expression was correlated with aggressive BC phenotypes. The downregulation of circRGNEF suppressed BC cell metastasis and proliferation by targeting the miR-548/KIF2C axis in vitro and in vivo; these results were verified with luciferase reporter assays. Our results show that miR-548 downregulation or KIF2C overexpression restored BC cell proliferation, migration, and invasion following silencing of circRGNEF. KIF2C overexpression reversed miR-548-induced cell invasion and migration as well as growth inhibition in vitro. In summary, the data illustrate that circRGNEF suppresses BC progression by functioning as a miR-548 sponge to enhance KIF2C expression. Therefore, circRGNEF might be a candidate BC treatment target.
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PP2A subunit PPP2R2C is downregulated in the brains of Alzheimer’s transgenic mice

Waiian Leong, Wei Xu, Bo Wang, Shuaiyun Gao, Xiuyun Zhai, Cuicui Wang, Eric Gilson, Jing Ye, Yiming Lu,

https://doi.org/10.18632/aging.103048 pp 6880—6890

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Leong W, Xu W, Wang B, Gao S, Zhai X, Wang C, Gilson E, Ye J, Lu Y, . PP2A subunit PPP2R2C is downregulated in the brains of Alzheimer’s transgenic mice. . 12:6880-6890. https://doi.org/10.18632/aging.103048

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                TY  - JOUR
                AU  - Leong, Waiian 
                AU  - Xu, Wei 
                AU  - Wang, Bo 
                AU  - Gao, Shuaiyun 
                AU  - Zhai, Xiuyun 
                AU  - Wang, Cuicui 
                AU  - Gilson, Eric 
                AU  - Ye, Jing 
                AU  - Lu, Yiming 
                TI  - PP2A subunit PPP2R2C is downregulated in the brains of Alzheimer’s transgenic mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103048
                DO  - 10.18632/aging.103048
                SP  - 6880
                EP  - 6890
                PY  - 
                AB  - Targeting of PP2A suggests a close link to tau-related cognitive and functional declines. However, little is known about how the expression of PP2A subunits and PP2A activity are dysregulated in the course of AD, precluding any specific targeting strategy for restoring PP2A in AD patients. Although the PP2A heterotrimer containing the regulatory subunit PR55/B&#x3B1; (encoded by the PPP2R2A gene) is the major tau phosphatase, the involvement of other brain-specific PP2A regulatory subunits in tau dephosphorylation remains unknown. PR55/B&#x3B3; (encoded by the PPP2R2C gene) is a pivotal phosphatase in the brain, and single-nucleotide polymorphisms (SNPs) of PPP2R2C are involved in several mental disorders. By measuring the differential spatiotemporal expression patterns of PPP2R2C in Wt and transgenic AD mice, we revealed that PPP2R2C expression is downregulated in the aged AD mouse brain as compared to the Wt mouse brain. In cultured cells, PPP2R2C expression regulates PP2A activity and tau dephosphorylation. These results suggest that dysregulation of PPP2R2C expression may be involved in the onset of AD and that specifically targeting PPP2R2C expression or activity is a promising strategy against brain dementia disorders, including AD and other tauopathies.
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Hypoxia-induced let-7f-5p/TARBP2 feedback loop regulates osteosarcoma cell proliferation and invasion by inhibiting the Wnt signaling pathway

Guangnan Chen, Huijie Gu, Tingting Fang, Kaifeng Zhou, Jun Xu, Xiaofan Yin,

https://doi.org/10.18632/aging.103049 pp 6891—6903

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Chen G, Gu H, Fang T, Zhou K, Xu J, Yin X, . Hypoxia-induced let-7f-5p/TARBP2 feedback loop regulates osteosarcoma cell proliferation and invasion by inhibiting the Wnt signaling pathway. . 12:6891-6903. https://doi.org/10.18632/aging.103049

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                TY  - JOUR
                AU  - Chen, Guangnan 
                AU  - Gu, Huijie 
                AU  - Fang, Tingting 
                AU  - Zhou, Kaifeng 
                AU  - Xu, Jun 
                AU  - Yin, Xiaofan 
                TI  - Hypoxia-induced let-7f-5p/TARBP2 feedback loop regulates osteosarcoma cell proliferation and invasion by inhibiting the Wnt signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103049
                DO  - 10.18632/aging.103049
                SP  - 6891
                EP  - 6903
                PY  - 
                AB  - Osteosarcoma (OS) is the most common bone tumor in children and adolescents and is characterized by high metastatic and recurrence rates. In the past, it has been shown that microRNAs may play critical roles in hypoxia-related OS proliferation and invasion. However, the mechanisms by which OS cells acquire this malignant phenotype have remained largely unknown. In the present study, we report that let-7f-5p and TARBP2 were expressed in lower amounts in human OS cell lines when compared with the hFOB normal human osteoblastic cell line; however, both types of cells were repressed by hypoxia. let-7f-5p and TARBP2 significantly inhibited the proliferation and invasion of OS cells. Furthermore, TARBP2 as a downstream and functional target of let-7f-5p regulated the expression of let-7f-5p, and there was a regulatory feedback loop between let-7f-5p and TARBP2. This loop reduced the expression of let-7f-5p and TARBP2 in OS cells to a very low level, which was induced by hypoxia. Furthermore, the hypoxia-induced let-7f-5p/TARBP2 feedback loop contributed to activation of the Wnt signaling pathway. Taken together, our data clearly showed that the feedback loop between let-7f-5p and TARBP2 induced by the hypoxia-promoted OS cell malignant phenotype increased with activation of the Wnt signaling pathway.
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Identification of UAP1L1 as tumor promotor in gastric cancer through regulation of CDK6

Jing Qi, Sheng Liu, Weihang Liu, Gaoqiang Cai, Guoqing Liao,

https://doi.org/10.18632/aging.103050 pp 6904—6927

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Qi J, Liu S, Liu W, Cai G, Liao G, . Identification of UAP1L1 as tumor promotor in gastric cancer through regulation of CDK6. . 12:6904-6927. https://doi.org/10.18632/aging.103050

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                TY  - JOUR
                AU  - Qi, Jing 
                AU  - Liu, Sheng 
                AU  - Liu, Weihang 
                AU  - Cai, Gaoqiang 
                AU  - Liao, Guoqing 
                TI  - Identification of UAP1L1 as tumor promotor in gastric cancer through regulation of CDK6
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103050
                DO  - 10.18632/aging.103050
                SP  - 6904
                EP  - 6927
                PY  - 
                AB  - Gastric cancer (GC) is one of the most commonly diagnosed malignancies in digestive tract and its underlying molecular mechanism is still not clear, so we aimed to reveal the relationship between GC and UDP-GlcNAc pyrophosphorylase-1 like 1 (UAP1L1). The detection of UAP1L1 expression in GC tumor and normal tissues was accomplished by immunohistochemistry and demonstrated the upregulation of UAP1L1 in GC, which was statistically associated with tumor grade. GC cell models constructed via transfection of UAP1L1-silencing/overexpressing lentiviruses were employed for evaluating the effects of UAP1L1 knockdown/overexpression on GC in vitro and in vivo. The results indicated that UAP1L1 played important role in development of GC through regulating cell proliferation, colony formation, cell apoptosis and cell migration. Subsequently, CDK6 was identified as a potential target in UAP1L1 induced regulation of GC, downregulation of which exhibited similar inhibition effects on GC with UAP1L1. Moreover, it was demonstrated that the promotion of GC by UAP1L1 overexpression could be significantly attenuated or even reversed by simultaneously silencing CDK6. In conclusion, UAP1L1 was reported to be a tumor promotor in the development and progression of GC which may exert its role through regulating CDK6 and may act as a candidate of therapeutic target in treatment.
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AKT3 deficiency in M2 macrophages impairs cutaneous wound healing by disrupting tissue remodeling

Song Gu, Hanhao Dai, Xilian Zhao, Chang Gui, Jianchao Gui,

https://doi.org/10.18632/aging.103051 pp 6928—6946

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Gu S, Dai H, Zhao X, Gui C, Gui J, . AKT3 deficiency in M2 macrophages impairs cutaneous wound healing by disrupting tissue remodeling. . 12:6928-6946. https://doi.org/10.18632/aging.103051

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                TY  - JOUR
                AU  - Gu, Song 
                AU  - Dai, Hanhao 
                AU  - Zhao, Xilian 
                AU  - Gui, Chang 
                AU  - Gui, Jianchao 
                TI  - AKT3 deficiency in M2 macrophages impairs cutaneous wound healing by disrupting tissue remodeling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103051
                DO  - 10.18632/aging.103051
                SP  - 6928
                EP  - 6946
                PY  - 
                AB  - AKT signaling and M2 macrophage-guided tissue repair are key factors in cutaneous wound healing. A delay in this process threatens human health worldwide. However, the role of AKT3 in delayed cutaneous wound healing is largely unknown. In this study, histological staining and transcriptomics demonstrated that prolonged tissue remodeling delayed wound healing. This delay was accompanied by defects in AKT3, collagen alpha-1(I) chain (COL1A1), and collagen alpha-1(XI) chain (COL11A1) expression and AKT signaling. The defect in AKT3 expression was M2 macrophage-specific, and decreased AKT3 protein levels were observed in CD68/CD206-positive macrophages from delayed wound tissue. Downregulation of AKT3 in M2 macrophages did not influence cell polarization but impaired collagen organization by inhibiting COL1A1 and COL11A1 expression in human skin fibroblasts (HSFs). Moreover, a co-culture model revealed that the downregulation of AKT3 in the human monocytic cell line (THP-1)-derived M2 macrophages impaired HSF proliferation and migration. Finally, cutaneous wound healing in AKT3-/- mice was much slower than that of AKT3+/+ mice, and F4/80 macrophages from the AKT3-/- mice had an impaired ability to promote wound healing. Thus, the downregulation of AKT3 in M2 macrophages prolonged tissue remodeling and delayed cutaneous wound healing.
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Diabetes-induced glucolipotoxicity impairs wound healing ability of adipose-derived stem cells-through the miR-1248/CITED2/HIF-1α pathway

Shune Xiao, Dan Zhang, Zhiyuan Liu, Wenhu Jin, Guangtao Huang, Zairong Wei, Dali Wang, Chengliang Deng,

https://doi.org/10.18632/aging.103053 pp 6947—6965

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Xiao S, Zhang D, Liu Z, Jin W, Huang G, Wei Z, Wang D, Deng C, . Diabetes-induced glucolipotoxicity impairs wound healing ability of adipose-derived stem cells-through the miR-1248/CITED2/HIF-1α pathway. . 12:6947-6965. https://doi.org/10.18632/aging.103053

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                TY  - JOUR
                AU  - Xiao, Shune 
                AU  - Zhang, Dan 
                AU  - Liu, Zhiyuan 
                AU  - Jin, Wenhu 
                AU  - Huang, Guangtao 
                AU  - Wei, Zairong 
                AU  - Wang, Dali 
                AU  - Deng, Chengliang 
                TI  - Diabetes-induced glucolipotoxicity impairs wound healing ability of adipose-derived stem cells-through the miR-1248/CITED2/HIF-1α pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103053
                DO  - 10.18632/aging.103053
                SP  - 6947
                EP  - 6965
                PY  - 
                AB  - Despite being an attractive cell type for mesenchymal stem cell (MSC) transplantation therapy for wound healing, human adipose-derived stem cells (hADSCs) from diabetes mellitus (DM) patients result in remarkable retention of stem cell activity due to diabetes-induced glucolipotoxicity. We explored the effect of diabetes and medium containing AGEs on the cell activity, phenotype, multipotency, angiogenic potential, and the therapeutic effect of hADSCs. Then, miRNA-1248 was selected by miRNA microarray analysis to further study the core molecular pathways that regulate the wound healing ability of hADSCs. hADSCs isolated from DM patients or cultured in medium containing AGEs in vitro exhibited decreased effectiveness in stem cell therapy. The expression of miRNA-1248 was decreased in the hADSCs of DM patients and hence failed to positively regulate stem cell activity, differentiation functions, and angiogenesis promotion effect. This concomitantly increased the expression of CITED2, an inhibitor of HIF-1&#x3B1;, thus influencing growth factors that promote angiogenesis, cellular proliferation, and wound healing. Overall, our data demonstrated that the glucolipotoxicity-impaired wound healing ability of hADSCs might occur through the miR-1248/CITED2/HIF-1&#x3B1; pathway. MiRNA-1248 may have potential to be used as a novel therapeutic target for wound healing in DM patients or restoring the wound healing ability of diabetic hADSCs.
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A novel immune-related genes prognosis biomarker for melanoma: associated with tumor microenvironment

Rongzhi Huang, Min Mao, Yunxin Lu, Qingliang Yu, Liang Liao,

https://doi.org/10.18632/aging.103054 pp 6966—6980

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Huang R, Mao M, Lu Y, Yu Q, Liao L, . A novel immune-related genes prognosis biomarker for melanoma: associated with tumor microenvironment. . 12:6966-6980. https://doi.org/10.18632/aging.103054

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                TY  - JOUR
                AU  - Huang, Rongzhi 
                AU  - Mao, Min 
                AU  - Lu, Yunxin 
                AU  - Yu, Qingliang 
                AU  - Liao, Liang 
                TI  - A novel immune-related genes prognosis biomarker for melanoma: associated with tumor microenvironment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103054
                DO  - 10.18632/aging.103054
                SP  - 6966
                EP  - 6980
                PY  - 
                AB  - Background: Melanoma is a cancer of the skin with potential to spread to other organs and is responsible for most deaths due to skin cancer. It is imperative to identify immune biomarkers for early melanoma diagnosis and treatment.Results: 63 immune-related genes of the total 1039 unique IRGs retrieved were associated with overall survival of melanoma. A multi-IRGs classifier constructed using eight IRGs showed a powerful predictive ability. The classifier had better predictive power compared with the current clinical data. GSEA analysis showed multiple signaling differences between high and low risk score group. Furthermore, biomarker was associated with multiple immune cells and immune infiltration in tumor microenvironment.Conclusions: The immune-related genes prognosis biomarker is an effective potential prognostic classifier in the immunotherapies and surveillance of melanoma.Methods: Melanoma samples of genes were retrieved from TCGA and GEO databases while the immune-related genes (IRGs) were retrieved from the ImmPort database. WGCNA, Cox regression analysis and LASSO analysis were used to classify melanoma prognosis. ESTIMATE and CIBERSORT algorithms were used to explore the relationship between risk score and tumor immune microenvironment. GSEA analysis was performed to explore the biological signaling pathway.
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Blastocyst-stage embryos provide better frozen-thawed embryo transfer outcomes for young patients with previous fresh embryo transfer failure

Lanlan Fang, Jingyan He, Yang Yan, Qiongqiong Jia, Yiping Yu, Ruizhe Zhang, Jung-Chien Cheng, Ying-Pu Sun,

https://doi.org/10.18632/aging.103055 pp 6981—6989

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Fang L, He J, Yan Y, Jia Q, Yu Y, Zhang R, Cheng J, Sun Y, . Blastocyst-stage embryos provide better frozen-thawed embryo transfer outcomes for young patients with previous fresh embryo transfer failure. . 12:6981-6989. https://doi.org/10.18632/aging.103055

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                TY  - JOUR
                AU  - Fang, Lanlan 
                AU  - He, Jingyan 
                AU  - Yan, Yang 
                AU  - Jia, Qiongqiong 
                AU  - Yu, Yiping 
                AU  - Zhang, Ruizhe 
                AU  - Cheng, Jung-Chien 
                AU  - Sun, Ying-Pu 
                TI  - Blastocyst-stage embryos provide better frozen-thawed embryo transfer outcomes for young patients with previous fresh embryo transfer failure
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103055
                DO  - 10.18632/aging.103055
                SP  - 6981
                EP  - 6989
                PY  - 
                AB  - Older patients or patients with a reduced ovarian response have a low number of embryos, which limits the opportunity for embryo selection. However, for young patients undergoing frozen-thawed embryo transfer (ET), it remains unclear whether embryo stage affects pregnancy outcomes. In the present study, a total of 2952 patients undergoing their first frozen-thawed ET were divided into two groups: patients who had experienced one failed fresh ET (Group A) and patients who had not received fresh ET because of the high risk of ovarian hyperstimulation syndrome (OHSS) (Group B). Our results show that Group B patients had a significantly higher clinical pregnancy rate (CPR) and live birth rate (LBR) than Group A patients. However, Group A patients who underwent blastocyst-stage frozen-thawed ET had a significantly higher CPR and LBR and a lower ectopic pregnancy rate (ePR) than did those who underwent cleavage-stage frozen-thawed ET. In Group B, CPR, ePR, LBR and spontaneous abortion rate (sAR) were similar with blastocyst-stage and cleavage-stage frozen-thawed ET. These results suggest that blastocyst-stage frozen-thawed ET is more appropriate for young patients who had previously undergone one failed fresh ET cycle.
                ER  -

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USP22 promotes development of lung adenocarcinoma through ubiquitination and immunosuppression

Bing Han, Yue Sun, Dongdong Yang, Huijuan Zhang, Steven Mo, Xuesong Chen, Hailing Lu, Xueyan Mao, Jing Hu,

https://doi.org/10.18632/aging.103056 pp 6990—7005

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Han B, Sun Y, Yang D, Zhang H, Mo S, Chen X, Lu H, Mao X, Hu J, . USP22 promotes development of lung adenocarcinoma through ubiquitination and immunosuppression. . 12:6990-7005. https://doi.org/10.18632/aging.103056

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                TY  - JOUR
                AU  - Han, Bing 
                AU  - Sun, Yue 
                AU  - Yang, Dongdong 
                AU  - Zhang, Huijuan 
                AU  - Mo, Steven 
                AU  - Chen, Xuesong 
                AU  - Lu, Hailing 
                AU  - Mao, Xueyan 
                AU  - Hu, Jing 
                TI  - USP22 promotes development of lung adenocarcinoma through ubiquitination and immunosuppression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103056
                DO  - 10.18632/aging.103056
                SP  - 6990
                EP  - 7005
                PY  - 
                AB  - Ubiquitin-specific protease 22 (USP22) expresses highly in lung adenocarcinoma (LUAD), which are associated with poor overall survival (OS). Microarray processing was performed to determine gene expression profiling, in which it was found that knocking down USP22 resulted in abnormal expression of a large number of genes. Differentially expressed genes (DEGs)-based protein-protein interaction (PPI) network was organized into 9 functional modules. These functional modules participated significantly in protein modification-related biological process and were involved in cancer-related pathways. The network was constructed to describe the global regulation of USP22-TF/pivot-module-pathway. It suggested that knocking down USP22 may up-regulate the expression of UBC to promote the pathways of cell cycle and ubiquitin-mediated proteolysis in the development of LUAD. More than that, knocking down USP22 can up-regulate STAT1 to activate JAK1-STAT1-caspase pathway, and promote apoptosis of tumor cell. Receiver operating characteristic (ROC) curve analysis suggested that E2F3, H2AFX, TFAP2A, PITX1, IRF7, and FOXM1 may be the potential diagnosis biomarkers for LUAD. On the other hand, BRCA1, FOXM1 and TFAP2A may be prognostic biomarkers of LUAD. In conclusion, we constructed a global regulation network to show that USP22 may promote the development of LUAD through ubiquitination and immunosuppression.
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Intra-operative hyperoxia and the risk of delirium in elderly patients after cardiac surgery

Anna Kupiec, Barbara Adamik, Katarzyna Forkasiewicz-Gardynik, Waldemar Goździk,

https://doi.org/10.18632/aging.103058 pp 7006—7014

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Kupiec A, Adamik B, Forkasiewicz-Gardynik K, Goździk W, . Intra-operative hyperoxia and the risk of delirium in elderly patients after cardiac surgery. . 12:7006-7014. https://doi.org/10.18632/aging.103058

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                TY  - JOUR
                AU  - Kupiec, Anna 
                AU  - Adamik, Barbara 
                AU  - Forkasiewicz-Gardynik, Katarzyna 
                AU  - Goździk, Waldemar 
                TI  - Intra-operative hyperoxia and the risk of delirium in elderly patients after cardiac surgery
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103058
                DO  - 10.18632/aging.103058
                SP  - 7006
                EP  - 7014
                PY  - 
                AB  - Delirium is a common complication after cardiac surgery. The aim of our study was to determine the impact of hyperoxia episodes occurring during cardiopulmonary bypass (CBP) on the rate of delirium episodes in the postoperative period. 93 patients, aged &#x2265; 65, who underwent elective cardiac surgery (CBP &lt;90 minutes) were enrolled. The occurrence of delirium episodes was examined every 12 hours for three days after surgery. Eleven patients (11.8%) developed postoperative delirium (POD (+)) and 83 did not (POD (-)). More incidences of severe hyperoxia (PaO2 &#x2265; 26.6kPa) during CBP were observed in the POD (+) group: 64% had &#x2265; 2 episodes of hyperoxia, 27% &#x2265; 3, and 18% &#x2265; 4, while in the POD (-) group: 42%, 13% and 1%, respectively (P=0.02). Patients in the POD (+) group had a higher maximum PaO2 during CBP than the POD (-) group (37 &#xB1; 5.8 vs 31.6 &#xB1; 6.6 kPa; P=0.01) and a higher mean PaO2 (30.1 &#xB1; 4.5 vs 26.1 &#xB1; 5.6 kPa; P=0.01). The optimal maximum PaO2 cut-off point for the occurrence of delirium was 33.2 kPa (AUC 0.72, P=0.001, sensitivity 75%, specificity 38%). We conclude that CBP hyperoxia episodes may be a risk factor associated with the occurrence of postoperative delirium.
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Quercetin ameliorates diabetic encephalopathy through SIRT1/ER stress pathway in db/db mice

Tian Hu, Jing-Jing Shi, Jiansong Fang, Qi Wang, Yun-Bo Chen, Shi-Jie Zhang,

https://doi.org/10.18632/aging.103059 pp 7015—7029

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Hu T, Shi J, Fang J, Wang Q, Chen Y, Zhang S, . Quercetin ameliorates diabetic encephalopathy through SIRT1/ER stress pathway in db/db mice. . 12:7015-7029. https://doi.org/10.18632/aging.103059

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                TY  - JOUR
                AU  - Hu, Tian 
                AU  - Shi, Jing-Jing 
                AU  - Fang, Jiansong 
                AU  - Wang, Qi 
                AU  - Chen, Yun-Bo 
                AU  - Zhang, Shi-Jie 
                TI  - Quercetin ameliorates diabetic encephalopathy through SIRT1/ER stress pathway in db/db mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103059
                DO  - 10.18632/aging.103059
                SP  - 7015
                EP  - 7029
                PY  - 
                AB  - Studies have shown that diabetes is an important risk factor for cognitive dysfunction, also called diabetic encephalopathy (DE). Quercetin has been reported to be effective in improving cognitive dysfunction in DE. But its detailed mechanism is still ambiguous. In this study, we used db/db mice to investigate whether quercetin could activate SIRT1 and inhibit ER pathways to improve DE. Behavioral tests (Morris water maze and new objects) showed that quercetin (70 mg/kg) can effectively improve the learning and memory ability in db/db mice. OGTT and ITT tests indicated that quercetin could alleviate impaired glucose tolerance and insulin resistance in db/db mice. Western blot analysis and Nissl staining showed that quercetin can improve the expression of nerve and synapse-associated proteins (PSD93, PSD95, NGF and BDNF) and inhibit neurodegeneration. Meanwhile, quercetin up-regulates SIRT1 protein expression and inhibits the expression of ER signaling pathway-related proteins (PERK, IRE-1&#x3B1;, ATF6, eIF2&#x3B1;, BIP and PDI). In addition, oxidative stress levels were significantly reduced after quercetin treatment. In conclusion, current experimental results indicated that SIRT1/ER stress is a promising mechanism involved in quercetin-treated diabetic encephalopathy.
                ER  -

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βig-h3 enhances chondrogenesis via promoting mesenchymal condensation in rat Achilles tendon heterotopic ossification model

Qiang Zhang, Yan Zhang, Meijun Yan, Kai Zhu, Qihang Su, Jie Pan, Mingjie Yang, Dong Zhou, Jun Tan,

https://doi.org/10.18632/aging.103060 pp 7030—7041

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Zhang Q, Zhang Y, Yan M, Zhu K, Su Q, Pan J, Yang M, Zhou D, Tan J, . βig-h3 enhances chondrogenesis via promoting mesenchymal condensation in rat Achilles tendon heterotopic ossification model. . 12:7030-7041. https://doi.org/10.18632/aging.103060

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                TY  - JOUR
                AU  - Zhang, Qiang 
                AU  - Zhang, Yan 
                AU  - Yan, Meijun 
                AU  - Zhu, Kai 
                AU  - Su, Qihang 
                AU  - Pan, Jie 
                AU  - Yang, Mingjie 
                AU  - Zhou, Dong 
                AU  - Tan, Jun 
                TI  - βig-h3 enhances chondrogenesis via promoting mesenchymal condensation in rat Achilles tendon heterotopic ossification model
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103060
                DO  - 10.18632/aging.103060
                SP  - 7030
                EP  - 7041
                PY  - 
                AB  - Heterotopic ossification (HO) is a poorly characterized disease with ectopic bone formation in the musculoskeletal soft tissues. HO is widely considered as a tissue repair process goes away, with endochondral ossification to be the major pathological basis. The molecular mechanism of how the resident/recruited progenitor cells for tissue regeneration error differentiated into the chondrocytes remains unknown. Here, we found Transforming Growth Factor B Induced Gene Human Clone 3 (&#x3B2;ig-h3) was highly expressed in the inflammation and chondrogenesis stages of a heterotopic ossification model after rat Achilles tendon injury, as well as upon chondrogenic differentiation conditions in vitro. &#x3B2;ig-h3 functioned as an extracellular matrix protein, which was induced by TGF&#x3B2; signaling, could bind to the injured tendon-derived stem cells (iTDSCs) and inhibit the attachment of iTDSCs to collagen I. Exogenous &#x3B2;ig-h3 was also found able to accelerate the process of mesenchymal condensation of cultured iTDSCs and promote chondrogenic differentiation in vitro, and additional injection of iTDSCs could promote endochondral ossification in Achilles tendon injury model. Taken together, &#x3B2;ig-h3 might function as an adhesion protein that inhibited the attachment of iTDSCs to collagen I (the injury site) but promoted the attachment of iTDSCs to each other, which resulted in promoting chondrogenic differentiation.
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SIRT1 regulates O-GlcNAcylation of tau through OGT

Shu Lu, Xiaomin Yin, Jia Wang, Qun Gu, Qin Huang, Nana Jin, Dandan Chu, Ziqi Xu, Fei Liu, Wei Qian,

https://doi.org/10.18632/aging.103062 pp 7042—7055

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Lu S, Yin X, Wang J, Gu Q, Huang Q, Jin N, Chu D, Xu Z, Liu F, Qian W, . SIRT1 regulates O-GlcNAcylation of tau through OGT. . 12:7042-7055. https://doi.org/10.18632/aging.103062

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                TY  - JOUR
                AU  - Lu, Shu 
                AU  - Yin, Xiaomin 
                AU  - Wang, Jia 
                AU  - Gu, Qun 
                AU  - Huang, Qin 
                AU  - Jin, Nana 
                AU  - Chu, Dandan 
                AU  - Xu, Ziqi 
                AU  - Liu, Fei 
                AU  - Qian, Wei 
                TI  - SIRT1 regulates O-GlcNAcylation of tau through OGT
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103062
                DO  - 10.18632/aging.103062
                SP  - 7042
                EP  - 7055
                PY  - 
                AB  - Tau is modified with O-GlcNAcylation extensively in human brain. The O-GlcNAcylation levels of tau are decreased in Alzheimer&#x2019;s disease (AD) brain. Sirtuin type 1 (SIRT1) is an enzyme that deacetylates proteins including transcriptional factors and associates with neurodegenerative diseases, such as AD. Aberrant SIRT1 expression levels in AD brain is in parallel with the accumulation of tau. cAMP response element binding protein (CREB), a cellular transcription factor, plays a critical role in learning and memory. In this present study, we found SIRT1 deacetylates CREB and inhibits phosphorylation of CREB at Ser133. The inactivated CREB suppresses OGT expression and therefore decreases the O-GlcNAcylation of tau and thus increases the phosphorylation of tau at specific sites. These findings suggest that SIRT1 may be a potential therapeutic target for treating tauopathies.
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CO₂ lattice laser reverses skin aging caused by UVB

Hongyi Wang, Bingyu Guo, Qiang Hui, Feng Lin, Kai Tao,

https://doi.org/10.18632/aging.103063 pp 7056—7065

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Wang H, Guo B, Hui Q, Lin F, Tao K, . CO₂ lattice laser reverses skin aging caused by UVB. . 12:7056-7065. https://doi.org/10.18632/aging.103063

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 TY - JOUR
 AU - Wang, Hongyi 
 AU - Guo, Bingyu 
 AU - Hui, Qiang 
 AU - Lin, Feng 
 AU - Tao, Kai 
 TI - CO2 lattice laser reverses skin aging caused by UVB
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103063
 DO - 10.18632/aging.103063
 SP - 7056
 EP - 7065
 PY - 
 AB - The carbon dioxide (CO2) lattice laser has been successfully used to treat facial skin photoaging induced by UV light. In this study, we analyzed the effect of CO2 lattice laser irradiation on skin photoaging, and investigated the underlying mechanisms. Our results demonstrate that the laser promoted collagen synthesis and proliferation of primary human skin fibroblasts, inhibited cell senescence, and induced expression of superoxide dismutase (SOD) and the signaling protein SMAD3. In addition, this laser reversed cell cycle arrest and fibroblast apoptosis induced by UVB irradiation, and restored fibroblast proliferation inhibited by SMAD3 silencing. Using a rat model of photoaging, our results show that the laser increased collagen expression and dermal thickness, demonstrating that the CO2 lattice laser has a profound therapeutic effect on photoaged skin. Together, our in vitro and in vivo data show that the CO2 lattice laser can reverse the skin aging caused by UVB, and indicate that this effect is mediated through SMAD3.
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Cutaneous wound healing in aged, high fat diet-induced obese female or male C57BL/6 mice

Marta Kopcewicz, Katarzyna Walendzik, Joanna Bukowska, Anna Kur-Piotrowska, Sylwia Machcinska, Jeffrey M. Gimble, Barbara Gawronska-Kozak,

https://doi.org/10.18632/aging.103064 pp 7066—7111

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Kopcewicz M, Walendzik K, Bukowska J, Kur-Piotrowska A, Machcinska S, Gimble JM, Gawronska-Kozak B, . Cutaneous wound healing in aged, high fat diet-induced obese female or male C57BL/6 mice. . 12:7066-7111. https://doi.org/10.18632/aging.103064

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                TY  - JOUR
                AU  - Kopcewicz, Marta 
                AU  - Walendzik, Katarzyna 
                AU  - Bukowska, Joanna 
                AU  - Kur-Piotrowska, Anna 
                AU  - Machcinska, Sylwia 
                AU  - Gimble, Jeffrey M. 
                AU  - Gawronska-Kozak, Barbara 
                TI  - Cutaneous wound healing in aged, high fat diet-induced obese female or male C57BL/6 mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103064
                DO  - 10.18632/aging.103064
                SP  - 7066
                EP  - 7111
                PY  - 
                AB  - Since there are limited studies analyzing the impact of age, sex and obesity on cutaneous repair, the current study evaluated excisional skin wound healing as a function of age, sex and diet in C57BL/6 mice subjected to either low (LFD) or high (HFD) fat diet. Older mice accumulated increased body fat relative to younger mice under HFD. Skin wound healing at particular stages was affected by age in the aspect of Tgf&#x3B2;-1, MCP-1, Mmp-9 and Mmp-13 expression. The most profound, cumulative effect was observed for the combination of two parameters: age and sex. While skin of younger males displayed extremely high collagen 1 and collagen 3 expression, younger females showed exceptionally high Mmp-13 expression at day 3 and 7 after injury. Diet as a single variable modified the thickness of dermis due to increased dermal White Adipose Tissue (dWAT) accumulation in mice fed HFD. The combination of age and diet affected the re-epithelialization and inflammatory response of injured skin. Overall, our data indicate that age has the most fundamental impact although all components (age, sex and diet) contribute to skin repair.
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Identification of immunologic subtype and prognosis of GBM based on TNFSF14 and immune checkpoint gene expression profiling

Shengrong Long, Mingdong Li, Jia Liu, Yi Yang, Guangyu Li,

https://doi.org/10.18632/aging.103065 pp 7112—7128

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Long S, Li M, Liu J, Yang Y, Li G, . Identification of immunologic subtype and prognosis of GBM based on TNFSF14 and immune checkpoint gene expression profiling. . 12:7112-7128. https://doi.org/10.18632/aging.103065

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                TY  - JOUR
                AU  - Long, Shengrong 
                AU  - Li, Mingdong 
                AU  - Liu, Jia 
                AU  - Yang, Yi 
                AU  - Li, Guangyu 
                TI  - Identification of immunologic subtype and prognosis of GBM based on TNFSF14 and immune checkpoint gene expression profiling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103065
                DO  - 10.18632/aging.103065
                SP  - 7112
                EP  - 7128
                PY  - 
                AB  - Immune-checkpoint therapy has failed to show significant benefit in glioblastoma (GBM) patients. Immunologic subtypes of GBM are necessary to identify patients who might benefit from immune-checkpoint therapy. This study reviewed 152 GBM samples from The Cancer Genome Atlas (TCGA) and 214 GBM samples from Chinese Glioma Genome Atlas (CGGA). Correlation analysis showed that immune checkpoint genes (ICGs) were mainly positively correlated. The prognostic analysis of the overall survival showed that there was a significant correlation between the overall survival (OS) and the prognosis of ICGs, in which the TNFSF14 gene was a significant adverse prognostic factor. Combined with TMB and neoantigens, we found that TNFSF9 and CD27 were significantly negatively correlated with TMB and neoantigens. The association between adaptive immune pathway genes and ICG expression showed that they were positively correlated with ICGs, indicating that adaptive immune pathway genes have a certain regulatory effect on the expression of ICGs. The analysis of clinical features of the samples showed that the higher the expression of ICGs, the more likely to be correlated with mutant isocitrate dehydrogenase (IDH), while the lower the expression level of IDH, the more likely to be significantly correlated with the primary GBM. Survival analysis showed that low expression of PD-L1, IDO1, or CTLA4 with TNFSF14 in the low expression group had the best prognosis, while high expression of IDO1 or CD274 with TNFSF14 in the high expression group and low expression of CTLA4 with TNFSF14 in the high expression group had the worst prognosis. We conclude that TNFSF14 is a biomarker to identify immunologic subtype and prognosis with other ICGs in GBM and may serve as a potential therapeutic target.
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Therapeutic options for advanced epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer: a Bayesian network secondary analysis

Xinmin Zeng, Xuan Wan, Jun Xu, Hui Wang, Hua Chen, Qinghua Zeng, Wenxiong Zhang, Binghao Zhao,

https://doi.org/10.18632/aging.103066 pp 7129—7162

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Zeng X, Wan X, Xu J, Wang H, Chen H, Zeng Q, Zhang W, Zhao B, . Therapeutic options for advanced epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer: a Bayesian network secondary analysis. . 12:7129-7162. https://doi.org/10.18632/aging.103066

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                TY  - JOUR
                AU  - Zeng, Xinmin 
                AU  - Wan, Xuan 
                AU  - Xu, Jun 
                AU  - Wang, Hui 
                AU  - Chen, Hua 
                AU  - Zeng, Qinghua 
                AU  - Zhang, Wenxiong 
                AU  - Zhao, Binghao 
                TI  - Therapeutic options for advanced epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer: a Bayesian network secondary analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103066
                DO  - 10.18632/aging.103066
                SP  - 7129
                EP  - 7162
                PY  - 
                AB  - The most favorable treatments for advanced EGFR-mutant NSCLC are less indicated. Forty-one studies were eligible for this Bayesian network secondary analysis. For PFS, erlotinib (Erlo)+bevacizumab (Bev) (HR 0.26, 95% CrI: 0.08-0.75 vs placebo), osimertinib (Osi) (HR 0.29, 0.11-0.70 vs placebo), and afatinib (Afa) were top-ranking individual treatments, while immunotherapy (IT)+anti-VEGFR (aVEGFR)+platinum-based therapy (Plat) (HR 0.42, 0.06-2.63 vs placebo), EGFR-TKI (ET)+aVEGFR (HR 0.35, 0.14-0.85 vs placebo), and ET+aVEGFR+Plat were top-ranking medication classes. For OS, Osi (HR 0.52, 0.10-2.00 vs placebo), cetuximab (Cet)+Bev+Plat (HR 0.51, 0.06-3.38 vs placebo), and cilengitide (Cil)+Cet+Plat were top-ranking individual treatments, while ET+aVEGFR+Plat, ET+Plat, and third-generation EGFR-TKI (3rd ET) were top-ranking medication classes. For PFS regarding the EGFR genomic aberration status, Erlo+Bev, Osi, and Afa were superior for exon 19 deletion status, whereas ET+Bev, Osi, and gefitinib (Gef)+pemetrexed (Peme) were excellent for exon 21 L858Arg mutation status. The results were consistent in terms of the ORR and DoR and remained robust across sensitivity analyses. However, Erlo + Bev had the most grade 3 or higher adverse events. Osi, Erlo+Bev, and Erlo+Bev+Plat are reasonably recommended to balance PFS and OS, but adverse events should be considered. IT+aVEGFR+Plat shows potential superiority, but more clinical evidence is needed.
                ER  -

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Association of common variation in ADD3 and GPC1 with biliary atresia susceptibility

Mei-Rong Bai, Wei-Bo Niu, Ying Zhou, Yi-Ming Gong, Yan-Jiao Lu, Xian-Xian Yu, Zhi-Liang Wei, Wenjie Wu, Huan-Lei Song, Wen-Wen Yu, Bei-Lin Gu, Wei Cai, Xun Chu,

https://doi.org/10.18632/aging.103067 pp 7163—7182

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Bai M, Niu W, Zhou Y, Gong Y, Lu Y, Yu X, Wei Z, Wu W, Song H, Yu W, Gu B, Cai W, Chu X, . Association of common variation in ADD3 and GPC1 with biliary atresia susceptibility. . 12:7163-7182. https://doi.org/10.18632/aging.103067

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 TY - JOUR
 AU - Bai, Mei-Rong 
 AU - Niu, Wei-Bo 
 AU - Zhou, Ying 
 AU - Gong, Yi-Ming 
 AU - Lu, Yan-Jiao 
 AU - Yu, Xian-Xian 
 AU - Wei, Zhi-Liang 
 AU - Wu, Wenjie 
 AU - Song, Huan-Lei 
 AU - Yu, Wen-Wen 
 AU - Gu, Bei-Lin 
 AU - Cai, Wei 
 AU - Chu, Xun 
 TI - Association of common variation in ADD3 and GPC1 with biliary atresia susceptibility
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103067
 DO - 10.18632/aging.103067
 SP - 7163
 EP - 7182
 PY - 
 AB - Biliary atresia (BA) is an idiopathic neonatal cholestatic disease. Recent genome-wide association study (GWAS) revealed that common variation of ADD3, GPC1, ARF6, and EFEMP1 gene was associated with BA susceptibility. We aimed to evaluate the association of these genes with BA in Chinese population. Twenty single nucleotide polymorphisms (SNPs) in these four genes were genotyped in 340 BA patients and 1,665 controls. Three SNPs in ADD3 were significantly associated with BA, and rs17095355 was the top SNP (PAllele = 3.23&#xD7;10-6). Meta-analysis of published data and current data indicated that rs17095355 was associated with BA susceptibility in Asians and Caucasians. Three associated SNPs were expression quantitative trait loci (eQTL) for ADD3. Two GPC1 SNPs in high linkage disequilibrium (LD) showed nominal association with BA susceptibility (PAllele = 0.03 for rs6707262 and PAllele = 0.04 for rs6750380), and were eQTL of GPC1. Haplotype harboring these two SNPs almost reached the study-wide significance (P = 0.0035). No association for ARF6 and EFEMP1 was found with BA risk in the current population. Our study validated associations of ADD3 and GPC1 SNPs with BA risk in Chinese population and provided evidence of epistatic contributions of genetic factors to BA susceptibility.
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Integrated data analysis reveals significant associations of KEAP1 mutations with DNA methylation alterations in lung adenocarcinomas

Mohamed Elshaer, Ahmed Islam ElManawy, Ahmed Hammad, Akhileshwar Namani, Xiu Jun Wang, Xiuwen Tang,

https://doi.org/10.18632/aging.103068 pp 7183—7206

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Elshaer M, ElManawy AI, Hammad A, Namani A, Wang XJ, Tang X, . Integrated data analysis reveals significant associations of KEAP1 mutations with DNA methylation alterations in lung adenocarcinomas. . 12:7183-7206. https://doi.org/10.18632/aging.103068

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 TY - JOUR
 AU - Elshaer, Mohamed 
 AU - ElManawy, Ahmed Islam 
 AU - Hammad, Ahmed 
 AU - Namani, Akhileshwar 
 AU - Wang, Xiu Jun 
 AU - Tang, Xiuwen 
 TI - Integrated data analysis reveals significant associations of KEAP1 mutations with DNA methylation alterations in lung adenocarcinomas
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103068
 DO - 10.18632/aging.103068
 SP - 7183
 EP - 7206
 PY - 
 AB - KEAP1 regulates the cytoprotection induced by NRF2 and has been reported to be a candidate tumor suppressor. Recent evidence has shown that mutations in several driver genes cause aberrant DNA methylation patterns, a hallmark of cancer. However, the correlation between KEAP1 mutations and DNA methylation in lung cancer has still not been investigated. In this study, we systematically carried out an integrated multi-omics analysis to explore the correlation between KEAP1 mutations and DNA methylation and its effect on gene expression in lung adenocarcinoma (LUAD). We found that most of the DNA aberrations associated with KEAP1 mutations in LAUD were hypomethylation. Surprisingly, we found several NRF2-regulated genes among the genes that showed differential DNA methylation. Moreover, we identified an 8-gene signature with altered DNA methylation pattern and elevated gene expression levels in LUAD patients with mutated KEAP1, and evaluated the prognostic value of this signature in various clinical datasets. These results establish that KEAP1 mutations are associated with DNA methylation changes capable of shaping regulatory network functions. Combining both epigenomic and transcriptomic changes along with KEAP1 mutations may provide a better understanding of the molecular mechanisms associated with the progression of lung cancer and may help to provide better therapeutic approaches.
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Dynamics of outcome after aneurysmal subarachnoid hemorrhage

Alexander Hammer, Gholamreza Ranaie, Eduard Yakubov, Frank Erbguth, Markus Holtmannspoetter, Hans-Herbert Steiner, Hendrik Janssen,

https://doi.org/10.18632/aging.103069 pp 7207—7217

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Hammer A, Ranaie G, Yakubov E, Erbguth F, Holtmannspoetter M, Steiner H, Janssen H, . Dynamics of outcome after aneurysmal subarachnoid hemorrhage. . 12:7207-7217. https://doi.org/10.18632/aging.103069

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                TY  - JOUR
                AU  - Hammer, Alexander 
                AU  - Ranaie, Gholamreza 
                AU  - Yakubov, Eduard 
                AU  - Erbguth, Frank 
                AU  - Holtmannspoetter, Markus 
                AU  - Steiner, Hans-Herbert 
                AU  - Janssen, Hendrik 
                TI  - Dynamics of outcome after aneurysmal subarachnoid hemorrhage
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103069
                DO  - 10.18632/aging.103069
                SP  - 7207
                EP  - 7217
                PY  - 
                AB  - In this observational study, we analyzed and described the dynamics of the outcome after aneurysmal subarachnoid hemorrhage (SAH) in a collective of 203 cases. We detected a significant improvement of the mean aggregate modified Rankin Score (mRS) in every time interval from discharge to 6 months and up to 1 year. Every forth to fifth patient with potential of recovery (mRS 1-5) at discharge improved by 1 mRS point in the time interval from 6 month to 1 year (22.6%). Patients with mRS 3 at discharge had a remarkable late recovery rate (73.3%, p = 0.000085). Multivariate analysis revealed age &#x2264; 65 years (odds ratio 4.93; p = 0.0045) and &#x201C;World Federation of Neurological Surgeons&#x201D; (WFNS) grades I and II (odds ratio 4.77; p = 0.0077) as significant predictors of early improvement (discharge to 6 months). Absence of a shunting procedure (odds ratio 8.32; p = 0.0049) was a significant predictor of late improvement (6 months to 1 year), but not age &#x2264; 65 years (p = 0.54) and WFNS grades I and II (p = 0.92). Thus, late recovery (6 month to 1 year) is significant and independent from age and WFNS grade.
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Prevalence of somatic-mental multimorbidity and its prospective association with disability among older adults in China

Haibin Li, Anxin Wang, Qi Gao, Xiaonan Wang, Yanxia Luo, Xinghua Yang, Xia Li, Wei Wang, Deqiang Zheng, Xiuhua Guo,

https://doi.org/10.18632/aging.103070 pp 7218—7231

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Li H, Wang A, Gao Q, Wang X, Luo Y, Yang X, Li X, Wang W, Zheng D, Guo X, . Prevalence of somatic-mental multimorbidity and its prospective association with disability among older adults in China. . 12:7218-7231. https://doi.org/10.18632/aging.103070

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                TY  - JOUR
                AU  - Li, Haibin 
                AU  - Wang, Anxin 
                AU  - Gao, Qi 
                AU  - Wang, Xiaonan 
                AU  - Luo, Yanxia 
                AU  - Yang, Xinghua 
                AU  - Li, Xia 
                AU  - Wang, Wei 
                AU  - Zheng, Deqiang 
                AU  - Guo, Xiuhua 
                TI  - Prevalence of somatic-mental multimorbidity and its prospective association with disability among older adults in China
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103070
                DO  - 10.18632/aging.103070
                SP  - 7218
                EP  - 7231
                PY  - 
                AB  - We aimed to identify prevalent somatic-mental multimorbidity (SMM) and examine its prospective association with disability among a nationally representative sample. A total of 6728 participants aged 60 years and older in the China Health and Retirement Longitudinal Study were included. A total of 14 somatic or mental conditions were assessed in 2013. SMM was defined as any combination of two or more conditions in which at least one condition was somatic and at least one condition was mental. Disability risk was measured using the combined Activities of Daily Living (ADL)-Instrumental Activities of Daily Living (IADL) index (range 0&#x2013;11; higher index indicates higher disability) in 2013 and 2015. Overall, the prevalence of SMM was 35.7% (95% confidence interval (CI): 34.1%-37.3%) in 2013. After adjustment for sociodemographic characteristics, lifestyles and baseline ADL-IADL index, over a maximum follow-up period of 2 years, SMM was associated with a 2.61 (95% CI: 2.12-3.22)-fold increase in ADL-IADL disability risk compared with that of healthy participants. In conclusion, SMM was prevalent in older Chinese adults, and it was associated with a higher risk of prospective disability.
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LncRNA XIST promotes myocardial infarction by regulating FOS through targeting miR-101a-3p

Bin Lin, Jing Xu, Feng Wang, Jiaxiang Wang, Hui Zhao, Deguang Feng,

https://doi.org/10.18632/aging.103072 pp 7232—7247

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Lin B, Xu J, Wang F, Wang J, Zhao H, Feng D, . LncRNA XIST promotes myocardial infarction by regulating FOS through targeting miR-101a-3p. . 12:7232-7247. https://doi.org/10.18632/aging.103072

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Provider: 
 TY - JOUR
 AU - Lin, Bin 
 AU - Xu, Jing 
 AU - Wang, Feng 
 AU - Wang, Jiaxiang 
 AU - Zhao, Hui 
 AU - Feng, Deguang 
 TI - LncRNA XIST promotes myocardial infarction by regulating FOS through targeting miR-101a-3p
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103072
 DO - 10.18632/aging.103072
 SP - 7232
 EP - 7247
 PY - 
 AB - The purpose of this study was to reveal the hypothesis that lncRNA X inactive specific transcript (XIST) can participate in the regulation of cardiomyocyte apoptosis in neonatal mice cardiomyocytes (NMCMs) and myocardial infarction (MI) through targeting miR-101a-3p. NMCMs were isolated from neonatal C57BL/6 mice and anoxia was induced in hypoxic chamber. MTT assay and flow cytometry were used to determine proliferation and apoptosis respectively. The target relationship among XIST, miR-101a-3p and FOS was revealed by bioinformatic analysis, luciferase reporter assay, pull-down assay and RNA immunoprecipitation assay. The expression of XIST, miR-101a-3p, FOS and apoptosis-related proteins was determined by qRT-PCR or western blot. MI model was constructed to reveal the role of XIST. We found that XIST was up-regulated in NMCMs under anoxia condition. Moreover, XIST increased FOS expression by sponging miR-101a-3p in anoxia cells. Silencing XIST expression improved cell viability and suppressed apoptosis in vitro and inhibited myocardial infarction by reducing the level of c-FOS and apoptosis-related proteins in vivo. Our findings suggest that XIST is involved in MI, modulation of its level can be used as a new strategy or potential target in the treatment of myocardial infarction.
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MicroRNA-375 exacerbates knee osteoarthritis through repressing chondrocyte autophagy by targeting ATG2B

Hongxing Li, Zhiling Li, Yigang Pi, Yang Chen, Lin Mei, Yong Luo, Jingping Xie, Xinzhan Mao,

https://doi.org/10.18632/aging.103073 pp 7248—7261

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Li H, Li Z, Pi Y, Chen Y, Mei L, Luo Y, Xie J, Mao X, . MicroRNA-375 exacerbates knee osteoarthritis through repressing chondrocyte autophagy by targeting ATG2B. . 12:7248-7261. https://doi.org/10.18632/aging.103073

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                TY  - JOUR
                AU  - Li, Hongxing 
                AU  - Li, Zhiling 
                AU  - Pi, Yigang 
                AU  - Chen, Yang 
                AU  - Mei, Lin 
                AU  - Luo, Yong 
                AU  - Xie, Jingping 
                AU  - Mao, Xinzhan 
                TI  - MicroRNA-375 exacerbates knee osteoarthritis through repressing chondrocyte autophagy by targeting ATG2B
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103073
                DO  - 10.18632/aging.103073
                SP  - 7248
                EP  - 7261
                PY  - 
                AB  - Objective: This study aimed to explore the underlying mechanism of miR-375 in exacerbating osteoarthritis (OA).Results: MiR-375 expression were upregulated in OA cartilage tissues, whereas ATG2B expression was decreased. MiR-375 targeted ATG2B 3&#x2019; UTR and inhibited its expression in the chondrocytes, and then suppressed autophagy and promoted endoplasmic reticulum stress (ERs). The apoptosis rate of chondrocytes was increased after being transfected with miR-375 mimics. In vivo results further verified that inhibition of miR-375 could relieve OA-related symptoms.Conclusion: miR-375 can inhibit the expression of ATG2B in chondrocytes, suppress autophagy and promote the ERs. It suggests that miR-375 could be considered to be a key therapy target for OA.Methods: Differential expression analyses for mRNA and miRNA microarray datasets from ArrayExpress were performed. MiR-375 and ATG2B expressions in cartilage tissues were detected by qRT-PCR. Dual luciferase assay was applied to verify the targeting relationship between ATG2B and miR-375. In vitro, the role of miR-375 on chondrocyte autophagy and ERs was investigated by western blot and immunofluorescence. The apoptotic rate was quantified by flow cytometry. In vivo, OA mice model was established, HE and Safranin O and Fast Green staining, as well as the OARSI and modified Mankin scores, were applied to measure the OA cartilage damage severity.
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Autophagy prevents hippocampal α-synuclein oligomerization and early cognitive dysfunction after anesthesia/surgery in aged rats

Ning Yang, Zhengqian Li, Dengyang Han, Xinning Mi, Miao Tian, Taotao Liu, Yue Li, Jindan He, Chongshen Kuang, Yiyun Cao, Lunxu Li, Cheng Ni, John Q. Wang, Xiangyang Guo,

https://doi.org/10.18632/aging.103074 pp 7262—7281

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Yang N, Li Z, Han D, Mi X, Tian M, Liu T, Li Y, He J, Kuang C, Cao Y, Li L, Ni C, Wang JQ, et al, . Autophagy prevents hippocampal α-synuclein oligomerization and early cognitive dysfunction after anesthesia/surgery in aged rats. . 12:7262-7281. https://doi.org/10.18632/aging.103074

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                TY  - JOUR
                AU  - Yang, Ning 
                AU  - Li, Zhengqian 
                AU  - Han, Dengyang 
                AU  - Mi, Xinning 
                AU  - Tian, Miao 
                AU  - Liu, Taotao 
                AU  - Li, Yue 
                AU  - He, Jindan 
                AU  - Kuang, Chongshen 
                AU  - Cao, Yiyun 
                AU  - Li, Lunxu 
                AU  - Ni, Cheng 
                AU  - Wang, John Q. 
                AU  - Guo, Xiangyang 
                TI  - Autophagy prevents hippocampal α-synuclein oligomerization and early cognitive dysfunction after anesthesia/surgery in aged rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103074
                DO  - 10.18632/aging.103074
                SP  - 7262
                EP  - 7281
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Yang, Ning 
                AU  - Li, Zhengqian 
                AU  - Han, Dengyang 
                AU  - Mi, Xinning 
                AU  - Tian, Miao 
                AU  - Liu, Taotao 
                AU  - Li, Yue 
                AU  - He, Jindan 
                AU  - Kuang, Chongshen 
                AU  - Cao, Yiyun 
                AU  - Li, Lunxu 
                AU  - Ni, Cheng 
                AU  - Wang, John Q. 
                AU  - Guo, Xiangyang 
                TI  - Autophagy prevents hippocampal α-synuclein oligomerization and early cognitive dysfunction after anesthesia/surgery in aged rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103074
                DO  - 10.18632/aging.103074
                SP  - 7262
                EP  - 7281
                PY  - 
                AB  - Stress-induced &#x3B1;-synuclein aggregation, especially the most toxic species (oligomers), may precede synaptic and cognitive dysfunction. Under pathological conditions, &#x3B1;-synuclein is degraded primarily through the autophagic/lysosomal pathway. We assessed the involvement of autophagy in &#x3B1;-synuclein aggregation and cognitive impairment following general anesthesia and surgical stress. Autophagy was found to be suppressed in the aged rat hippocampus after either 4-h propofol anesthesia alone or 2-h propofol anesthesia during a laparotomy surgery. This inhibition of autophagy was accompanied by profound &#x3B1;-synuclein oligomer aggregation and neurotransmitter imbalances in the hippocampus, along with hippocampus-dependent cognitive deficits. These events were not observed 18 weeks after propofol exposure with or without surgical stress. The pharmacological induction of autophagy using rapamycin markedly suppressed &#x3B1;-synuclein oligomerization, restored neurotransmitter equilibrium, and improved cognitive behavior after prolonged anesthesia or anesthesia combined with surgery. Thus, both prolonged propofol anesthesia alone and propofol anesthesia during surgery impaired autophagy, which may have induced abnormal hippocampal &#x3B1;-synuclein aggregation and neurobehavioral deficits in aged rats. These findings suggest that the activation of autophagy and the clearance of pathological &#x3B1;-synuclein oligomers may be novel strategies to ameliorate the common occurrence of postoperative cognitive dysfunction.
                ER  -

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HMGN5 promotes IL-6-induced epithelial-mesenchymal transition of bladder cancer by interacting with Hsp27

Kun Yao, Leye He, Yu Gan, Jianye Liu, Jin Tang, Zhi Long, Jing Tan,

https://doi.org/10.18632/aging.103076 pp 7282—7298

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Yao K, He L, Gan Y, Liu J, Tang J, Long Z, Tan J, . HMGN5 promotes IL-6-induced epithelial-mesenchymal transition of bladder cancer by interacting with Hsp27. . 12:7282-7298. https://doi.org/10.18632/aging.103076

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                TY  - JOUR
                AU  - Yao, Kun 
                AU  - He, Leye 
                AU  - Gan, Yu 
                AU  - Liu, Jianye 
                AU  - Tang, Jin 
                AU  - Long, Zhi 
                AU  - Tan, Jing 
                TI  - HMGN5 promotes IL-6-induced epithelial-mesenchymal transition of bladder cancer by interacting with Hsp27
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103076
                DO  - 10.18632/aging.103076
                SP  - 7282
                EP  - 7298
                PY  - 
                AB  - Bladder cancer (BC) is one of the most common cancers worldwide, with a high rate of recurrence and poor outcomes. High-mobility group nucleosome-binding domain 5 (HMGN5) is overexpressed in many cancers and could cause carcinogenesis in BC. By protein-protein-interaction (PPI) analysis, we found that heat shock protein 27 (Hsp27), also a crucial functional factor in BC carcinogenesis, is significantly related to HMGN5. Hsp27 is required for IL-6-mediated EMT via STAT3/Twist signaling in prostate cancer. Here, we hypothesize that HMGN5 may interact with Hsp27 to affect IL-6-induced EMT and invasion in BC via STAT3 signaling. In the present study, we found that HMGN5 and Hsp27 are highly expressed in BC tissues and positively correlated with each other. HMGN5 interacts with Hsp27 in vitro, to modulate the cell invasion and EMT in BC. Moreover, HMGN5 could modulate IL-6-Hsp27-induced EMT and invasion in BC cells by regulating STAT3 phosphorylation and STAT3 targeting of the Twist promoter. HMGN5 interacts with Hsp27 to promote tumor growth in a human BC xenograft model in nude mice. In summary, HMGN5 interacts with Hsp27 to promote IL-6-induced EMT, therefore promoting invasion in BC and contributing to the progression of BC.
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Melatonin improves mitochondrial biogenesis through the AMPK/PGC1α pathway to attenuate ischemia/reperfusion-induced myocardial damage

Xueyan Qi, Jin Wang,

https://doi.org/10.18632/aging.103078 pp 7299—7312

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Qi X, Wang J, . Melatonin improves mitochondrial biogenesis through the AMPK/PGC1α pathway to attenuate ischemia/reperfusion-induced myocardial damage. . 12:7299-7312. https://doi.org/10.18632/aging.103078

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                TY  - JOUR
                AU  - Qi, Xueyan 
                AU  - Wang, Jin 
                TI  - Melatonin improves mitochondrial biogenesis through the AMPK/PGC1α pathway to attenuate ischemia/reperfusion-induced myocardial damage
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103078
                DO  - 10.18632/aging.103078
                SP  - 7299
                EP  - 7312
                PY  - 
                AB  - Cardiac ischemia/reperfusion injury is associated with reduced mitochondrial turnover and regeneration. There is currently no effective approach to stimulate mitochondrial biogenesis in the reperfused myocardium. In this study, we investigated whether melatonin could increase mitochondrial biogenesis and thus promote mitochondrial homeostasis in cardiomyocytes. Cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) injury with or without melatonin treatment, and various mitochondrial functions were measured. H/R injury repressed mitochondrial biogenesis in cardiomyocytes, whereas melatonin treatment restored mitochondrial biogenesis through the 5&#x2019; adenosine monophosphate-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC1&#x3B1;) pathway. Melatonin enhanced mitochondrial metabolism, inhibited mitochondrial oxidative stress, induced mitochondrial fusion and prevented mitochondrial apoptosis in cardiomyocytes subjected to H/R injury. The melatonin-induced improvement in mitochondrial biogenesis was associated with increased cardiomyocyte survival during H/R injury. On the other hand, silencing of PGC1&#x3B1; attenuated the protective effects of melatonin on cardiomyocyte viability, thereby impairing mitochondrial bioenergetics, disrupting the mitochondrial morphology, and activating mitochondrial apoptosis. Thus, H/R injury suppressed mitochondrial biogenesis, while melatonin activated the AMPK/PGC1&#x3B1; pathway and restored mitochondrial biogenesis, ultimately protecting the reperfused heart.
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Estrogen regulation of germline stem cell differentiation as a mechanism contributing to female reproductive aging

Chonthicha Satirapod, Ning Wang, Julie A. MacDonald, Minghan Sun, Dori C. Woods, Jonathan L. Tilly,

https://doi.org/10.18632/aging.103080 pp 7313—7333

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Satirapod C, Wang N, MacDonald JA, Sun M, Woods DC, Tilly JL, . Estrogen regulation of germline stem cell differentiation as a mechanism contributing to female reproductive aging. . 12:7313-7333. https://doi.org/10.18632/aging.103080

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                TY  - JOUR
                AU  - Satirapod, Chonthicha 
                AU  - Wang, Ning 
                AU  - MacDonald, Julie A. 
                AU  - Sun, Minghan 
                AU  - Woods, Dori C. 
                AU  - Tilly, Jonathan L. 
                TI  - Estrogen regulation of germline stem cell differentiation as a mechanism contributing to female reproductive aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103080
                DO  - 10.18632/aging.103080
                SP  - 7313
                EP  - 7333
                PY  - 
                AB  - Progressive loss of ovarian estrogen (E2) production is a hallmark feature of, if not a driving force behind, reproductive aging and the menopause. Recent genetic studies in mice have shown that female germline or oogonial stem cells (OSCs) contribute to maintenance of adult ovarian function and fertility under physiological conditions through support of de-novo oogenesis. Here we show that mouse OSCs express E2 receptor-&#x3B1; (ER&#x3B1;). In the presence of E2, ER&#x3B1; interacts with the stimulated by retinoic acid gene 8 (Stra8) promoter to drive Stra8 expression followed by oogenesis. Treatment of mice with E2 in vivo increases Stra8 expression and oogenesis, and these effects are nullified by ER&#x3B1; (Esr1), but not ER&#x3B2; (Esr2), gene disruption. Although mice lacking ER&#x3B1; are born with a normal quota of oocytes, ER&#x3B1;-deficient females develop premature ovarian insufficiency in adulthood due to impaired oogenesis. Lastly, mice treated with reversible ER antagonists show a loss of Stra8 expression and oocyte numbers; however, both endpoints rebound to control levels after ceasing drug treatment. These findings establish a key physiological role for E2-ER&#x3B1; signaling in promoting OSC differentiation as a potential mechanism to maintain adequate numbers of ovarian follicles during reproductive life.
                ER  -

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A novel dipeptide from potato protein hydrolysate augments the effects of exercise training against high-fat diet-induced damages in senescence-accelerated mouse-prone 8 by boosting pAMPK / SIRT1/ PGC-1α/ pFOXO3 pathway

Shibu Marthandam Asokan, Ting Wang, Ming-Fu Wang, Wan-Teng Lin,

https://doi.org/10.18632/aging.103081 pp 7334—7349

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Asokan SM, Wang T, Wang M, Lin W, . A novel dipeptide from potato protein hydrolysate augments the effects of exercise training against high-fat diet-induced damages in senescence-accelerated mouse-prone 8 by boosting pAMPK / SIRT1/ PGC-1α/ pFOXO3 pathway. . 12:7334-7349. https://doi.org/10.18632/aging.103081

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                TY  - JOUR
                AU  - Asokan, Shibu Marthandam 
                AU  - Wang, Ting 
                AU  - Wang, Ming-Fu 
                AU  - Lin, Wan-Teng 
                TI  - A novel dipeptide from potato protein hydrolysate augments the effects of exercise training against high-fat diet-induced damages in senescence-accelerated mouse-prone 8 by boosting pAMPK / SIRT1/ PGC-1α/ pFOXO3 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103081
                DO  - 10.18632/aging.103081
                SP  - 7334
                EP  - 7349
                PY  - 
                AB  - The pathological effects of obesity are often severe in aging condition. Although exercise training is found to be advantageous, the intensity of exercise performed is limited in aging condition. Therefore in this study we assessed the effect of a combined treatment regimen with a short-peptide IF isolated from alcalase potato-protein hydrolysates and a moderate exercise training for 15 weeks in a 6 month old HFD induced obese senescence accelerated mouse-prone 8 (SAMP8) mice model. Animals were divided into 6 groups (n=6) (C:Control+BSA); (HF:HFD+BSA); (EX:Control+ BSA+Exercise); (HF+IF:HFD+ IF); (HF+EX:HFD+Exercise); (HF+EX+IF:HFD+Exercise+IF). A moderate incremental swimming exercise training was provided for 6 weeks and after 3 weeks of exercise, IF was orally administered (1 mg/kg body Weight). The results show that combined administration of IF and exercise provides a better protection to aging animals by reducing body weight and regulated tissue damage. IF intake and exercise training provided protection against cardiac hypertrophy and maintains the tissue homeostasis in the heart and liver sections. Interestingly, IF and exercise training showed an effective upregulation in pAMPK/ SIRT1/ PGC-1&#x3B1;/ pFOXO3 mechanism of cellular longevity. Therefore, exercise training with IF intake is a possible strategy for anti-obesity benefits and superior cardiac and hepatic protection in aging condition.
                ER  -

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Inhibition of stearoyl-coenzyme A desaturase 1 ameliorates hepatic steatosis by inducing AMPK-mediated lipophagy

Youping Zhou, Li Zhong, Shengjie Yu, Wei Shen, Can Cai, Huihong Yu,

https://doi.org/10.18632/aging.103082 pp 7350—7362

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Zhou Y, Zhong L, Yu S, Shen W, Cai C, Yu H, . Inhibition of stearoyl-coenzyme A desaturase 1 ameliorates hepatic steatosis by inducing AMPK-mediated lipophagy. . 12:7350-7362. https://doi.org/10.18632/aging.103082

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                TY  - JOUR
                AU  - Zhou, Youping 
                AU  - Zhong, Li 
                AU  - Yu, Shengjie 
                AU  - Shen, Wei 
                AU  - Cai, Can 
                AU  - Yu, Huihong 
                TI  - Inhibition of stearoyl-coenzyme A desaturase 1 ameliorates hepatic steatosis by inducing AMPK-mediated lipophagy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103082
                DO  - 10.18632/aging.103082
                SP  - 7350
                EP  - 7362
                PY  - 
                AB  - SCD1 is a key enzyme controlling lipid metabolism and a link between its activity and NAFLD has been proposed. Lipophagy is a novel regulatory approach to lipid metabolism regulation, which is involved in the development of NAFLD. However, the possible functional connection between SCD1 and lipophagy in NAFLD remains unknown. To investigate the molecular mechanisms through which SCD1 regulates lipophagy in hepatic steatosis, the model of hepatic steatosis was established by inducing mouse primary hepatocytes with sodium palmitate and feeding C57BL/6 mice with HFD. Our results indicated that sodium palmitate-treated hepatocytes exhibited increased SCD1 expression, AMPK inactivation and defective lipophagy. Inhibition of SCD1 expression in hepatocytes resulted in enhanced AMPK activity and lipophagy, and reduced lipid deposition. Although SCD1 overexpression led to decreased AMPK activity and lipophagy, lipid deposition was increased in hepatocytes. SCD1 regulated lipophagy through AMPK to affect lipid metabolism in mouse primary hepatocytes. Additionally, compared to HFD-fed mice, CAY10566(an SCD1-specific inhibitor)-treated mice exhibited significantly decreased hepatic steatosis and hepatic lipid droplet accumulation, as well as enhanced AMPK activity and lipophagy. This study elucidated that SCD1 inhibition ameliorates hepatic steatosis by inducing AMPK-mediated lipophagy, suggesting that the SCD1-AMPK-lipophagy pathway is a potential therapeutic target for NAFLD.
                ER  -

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Nudix hydrolase 1 is a prognostic biomarker in hepatocellular carcinoma

Qifeng Ou, Ning Ma, Zheng Yu, Rongchang Wang, Yucheng Hou, Ziming Wang, Fan Chen, Wen Li, Jiong Bi, Jieyi Ma, Longjuan Zhang, Qiao Su, Xiaohui Huang,

https://doi.org/10.18632/aging.103083 pp 7363—7379

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Ou Q, Ma N, Yu Z, Wang R, Hou Y, Wang Z, Chen F, Li W, Bi J, Ma J, Zhang L, Su Q, Huang X, . Nudix hydrolase 1 is a prognostic biomarker in hepatocellular carcinoma. . 12:7363-7379. https://doi.org/10.18632/aging.103083

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                TY  - JOUR
                AU  - Ou, Qifeng 
                AU  - Ma, Ning 
                AU  - Yu, Zheng 
                AU  - Wang, Rongchang 
                AU  - Hou, Yucheng 
                AU  - Wang, Ziming 
                AU  - Chen, Fan 
                AU  - Li, Wen 
                AU  - Bi, Jiong 
                AU  - Ma, Jieyi 
                AU  - Zhang, Longjuan 
                AU  - Su, Qiao 
                AU  - Huang, Xiaohui 
                TI  - Nudix hydrolase 1 is a prognostic biomarker in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103083
                DO  - 10.18632/aging.103083
                SP  - 7363
                EP  - 7379
                PY  - 
                AB  - We investigated the prognostic significance of Nudix hydrolase 1 (NUDT1) in hepatocellular carcinoma (HCC). NUDT1 mRNA and protein levels were significantly higher in HCC tissues than normal liver tissues. The level of NUDT1 expression correlated with tumor grade, stage, size, differentiation, degree of vascular invasion, overall survival (OS), and disease-free survival (DFS) in HCC patients. Multivariate analysis showed that NUDT1 expression was an independent prognostic factor for OS and DFS in HCC patients. We constructed a prognostic nomogram with NUDT1 expression, AFP levels, vascular invasion, Child&#x2013;Pugh classification, age, sex, AJCC staging, and tumor differentiation as variables. This nomogram was highly accurate in predicting the 5-year OS of HCC patients (c-index= 0.709; AUC= 0.740). NUDT1 silencing in HCC cells significantly reduced their survival, colony formation, migration, and invasiveness. Gene set enrichment analysis showed that biological pathways related to cell cycle, fatty acid metabolism, bile acid and bile salt metabolism, and PLK1 signaling were associated with NUDT1, as were the gene ontology terms &#x201C;DNA binding transcription activator activity,&#x201D; &#x201C;RNA polymerase II,&#x201D; &#x201C;nuclear division,&#x201D; and &#x201C;transmembrane transporter activity.&#x201D; Our study thus demonstrates that NUDT1 is a prognostic biomarker with therapeutic potential in HCC patients.
                ER  -

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Activated CD4⁺ T cells-derived exosomal miR-142-3p boosts post-ischemic ventricular remodeling by activating myofibroblast

Lidong Cai, Gong Chao, Weifeng Li, Jumo Zhu, Fangfang Li, Baozhen Qi, Yong Wei, Songwen Chen, Genqing Zhou, Xiaofeng Lu, Juan Xu, Xiaoyu Wu, Guangjian Fan, Jun Li, Shaowen Liu,

https://doi.org/10.18632/aging.103084 pp 7380—7396

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Cai L, Chao G, Li W, Zhu J, Li F, Qi B, Wei Y, Chen S, Zhou G, Lu X, Xu J, Wu X, Fan G, et al, . Activated CD4⁺ T cells-derived exosomal miR-142-3p boosts post-ischemic ventricular remodeling by activating myofibroblast. . 12:7380-7396. https://doi.org/10.18632/aging.103084

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Provider: 
 TY - JOUR
 AU - Cai, Lidong 
 AU - Chao, Gong 
 AU - Li, Weifeng 
 AU - Zhu, Jumo 
 AU - Li, Fangfang 
 AU - Qi, Baozhen 
 AU - Wei, Yong 
 AU - Chen, Songwen 
 AU - Zhou, Genqing 
 AU - Lu, Xiaofeng 
 AU - Xu, Juan 
 AU - Wu, Xiaoyu 
 AU - Fan, Guangjian 
 AU - Li, Jun 
 AU - Liu, Shaowen 
 TI - Activated CD4+ T cells-derived exosomal miR-142-3p boosts post-ischemic ventricular remodeling by activating myofibroblast
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103084
 DO - 10.18632/aging.103084
 SP - 7380
 EP - 7396
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Cai, Lidong 
 AU - Chao, Gong 
 AU - Li, Weifeng 
 AU - Zhu, Jumo 
 AU - Li, Fangfang 
 AU - Qi, Baozhen 
 AU - Wei, Yong 
 AU - Chen, Songwen 
 AU - Zhou, Genqing 
 AU - Lu, Xiaofeng 
 AU - Xu, Juan 
 AU - Wu, Xiaoyu 
 AU - Fan, Guangjian 
 AU - Li, Jun 
 AU - Liu, Shaowen 
 TI - Activated CD4+ T cells-derived exosomal miR-142-3p boosts post-ischemic ventricular remodeling by activating myofibroblast
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103084
 DO - 10.18632/aging.103084
 SP - 7380
 EP - 7396
 PY - 
 AB - Cardiac fibrosis is a primary phenotype of cardiac remodeling that contributes to cardiac dysfunction and heart failure. The expansion and activation of CD4+ T cells in the heart has been identified to facilitate pathological cardiac remodeling and dysfunction; however, the underlying mechanisms remained not well clarified. Herein, we found that exosomes derived from activated CD4+ T cells (CD4-activated Exos) evoked pro-fibrotic effects of cardiac fibroblasts, and their delivery into the heart aggravated cardiac fibrosis and dysfunction post-infarction. Mechanistically, miR-142-3p that was enriched in CD4-activated Exos recapitulated the pro-fibrotic effects of CD4-activated Exos in cardiac fibroblasts, and vice versa. Furthermore, miR-142-3p directly targeted and inhibited the expression of Adenomatous Polyposis Coli (APC), a negative WNT signaling pathway regulator, contributing to the activation of WNT signaling pathway and cardiac fibroblast activation. Thus, CD4-activated Exos promote post-ischemic cardiac fibrosis through exosomal miR-142-3p-WNT signaling cascade-mediated activation of myofibroblasts. Targeting miR-142-3p in CD4-activated Exos may hold promise for treating cardiac remodeling post-MI.
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c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis

Liang Li, Chenju Yi, WenJie Xia, Bihui Huang, Shichao Chen, Junyan Zhong, Xiaoyi Fang, Liuming Yang, Hongwu Xin, Shiying Silvia Zheng, Beng H Chong, Yingyun Fu, Chun Chen, Mo Yang,

https://doi.org/10.18632/aging.103086 pp 7397—7410

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Li L, Yi C, Xia W, Huang B, Chen S, Zhong J, Fang X, Yang L, Xin H, Zheng SS, Chong BH, Fu Y, Chen C, et al, . c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis. . 12:7397-7410. https://doi.org/10.18632/aging.103086

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                TY  - JOUR
                AU  - Li, Liang 
                AU  - Yi, Chenju 
                AU  - Xia, WenJie 
                AU  - Huang, Bihui 
                AU  - Chen, Shichao 
                AU  - Zhong, Junyan 
                AU  - Fang, Xiaoyi 
                AU  - Yang, Liuming 
                AU  - Xin, Hongwu 
                AU  - Zheng, Shiying Silvia 
                AU  - Chong, Beng H 
                AU  - Fu, Yingyun 
                AU  - Chen, Chun 
                AU  - Yang, Mo 
                TI  - c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103086
                DO  - 10.18632/aging.103086
                SP  - 7397
                EP  - 7410
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, Liang 
                AU  - Yi, Chenju 
                AU  - Xia, WenJie 
                AU  - Huang, Bihui 
                AU  - Chen, Shichao 
                AU  - Zhong, Junyan 
                AU  - Fang, Xiaoyi 
                AU  - Yang, Liuming 
                AU  - Xin, Hongwu 
                AU  - Zheng, Shiying Silvia 
                AU  - Chong, Beng H 
                AU  - Fu, Yingyun 
                AU  - Chen, Chun 
                AU  - Yang, Mo 
                TI  - c-Mpl and TPO expression in the human central nervous system neurons inhibits neuronal apoptosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103086
                DO  - 10.18632/aging.103086
                SP  - 7397
                EP  - 7410
                PY  - 
                AB  - Thrombopoietin (TPO) is a growth factor for the megakaryocytic/platelet lineage. In this study, we investigated the expression of TPO and its receptor, c-Mpl, in the human central nervous system (CNS) and their roles after a neural insult. Our results demonstrate that both TPO and c-Mpl are expressed in the neurons of the human CNS. TPO was also detected in human cerebrospinal fluid. TPO was found to be neuroprotective in hypoxic-ischemic neonatal rat brain models. In these rat models, treatment with TPO reduced brain damage and improved sensorimotor functions. In addition, TPO promoted C17.2 cell proliferation through activation of the PI3K/Akt signaling pathway. Via the Bcl-2/BAX signaling pathway, TPO exerted an antiapoptotic effect by suppressing mitochondrial membrane potentials. Taken together, our results indicate that TPO is neuroprotective in the CNS.
                ER  -

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PGC-1α activator ZLN005 promotes maturation of cardiomyocytes derived from human embryonic stem cells

Yanping Liu, Huajun Bai, Fengfeng Guo, Phung N. Thai, Xiaoling Luo, Peng Zhang, Chunli Yang, Xueqin Feng, Dan Zhu, Jun Guo, Ping Liang, Zhice Xu, Huangtian Yang, Xiyuan Lu,

https://doi.org/10.18632/aging.103088 pp 7411—7430

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Liu Y, Bai H, Guo F, Thai PN, Luo X, Zhang P, Yang C, Feng X, Zhu D, Guo J, Liang P, Xu Z, Yang H, et al, . PGC-1α activator ZLN005 promotes maturation of cardiomyocytes derived from human embryonic stem cells. . 12:7411-7430. https://doi.org/10.18632/aging.103088

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                TY  - JOUR
                AU  - Liu, Yanping 
                AU  - Bai, Huajun 
                AU  - Guo, Fengfeng 
                AU  - Thai, Phung N. 
                AU  - Luo, Xiaoling 
                AU  - Zhang, Peng 
                AU  - Yang, Chunli 
                AU  - Feng, Xueqin 
                AU  - Zhu, Dan 
                AU  - Guo, Jun 
                AU  - Liang, Ping 
                AU  - Xu, Zhice 
                AU  - Yang, Huangtian 
                AU  - Lu, Xiyuan 
                TI  - PGC-1α activator ZLN005 promotes maturation of cardiomyocytes derived from human embryonic stem cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103088
                DO  - 10.18632/aging.103088
                SP  - 7411
                EP  - 7430
                PY  - 
                AB  - Human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) have great potential in biomedical applications. However, the immature state of cardiomyocytes obtained using existing protocols limits the application of hPSC-CMs. Unlike adult cardiac myocytes, hPSC-CMs generate ATP through an immature metabolic pathway&#x2014;aerobic glycolysis, instead of mitochondrial oxidative phosphorylation (OXPHOS). Hence, metabolic switching is critical for functional maturation in hPSC-CMs. Peroxisome proliferator-activated receptor gamma coactivator 1&#x3B1; (PGC-1&#x3B1;) is a key regulator of mitochondrial biogenesis and metabolism, which may help promote cardiac maturation during development. In this study, we investigated the effects of PGC-1&#x3B1; and its activator ZLN005 on the maturation of human embryonic stem cell-derived cardiomyocyte (hESC-CM). hESC-CMs were generated using a chemically defined differentiation protocol and supplemented with either ZLN005 or DMSO (control) on differentiating days 10 to 12. Biological assays were then performed around day 30. ZLN005 treatment upregulated the expressions of PGC-1&#x3B1; and mitochondrial function-related genes in hESC-CMs and induced more mature energy metabolism compared with the control group. In addition, ZLN005 treatment increased cell sarcomere length, improved cell calcium handling, and enhanced intercellular connectivity. These findings support an effective approach to promote hESC-CM maturation, which is critical for the application of hESC-CM in disease modeling, drug screening, and engineering cardiac tissue.
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Sirt1 is regulated by miR-135a and involved in DNA damage repair during mouse cellular reprogramming

Andy Chun Hang Chen, Qian Peng, Sze Wan Fong, William Shu Biu Yeung, Yin Lau Lee,

https://doi.org/10.18632/aging.103090 pp 7431—7447

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Chen ACH, Peng Q, Fong SW, Yeung WSB, Lee YL, . Sirt1 is regulated by miR-135a and involved in DNA damage repair during mouse cellular reprogramming. . 12:7431-7447. https://doi.org/10.18632/aging.103090

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Provider: 
 TY - JOUR
 AU - Chen, Andy Chun Hang 
 AU - Peng, Qian 
 AU - Fong, Sze Wan 
 AU - Yeung, William Shu Biu 
 AU - Lee, Yin Lau 
 TI - Sirt1 is regulated by miR-135a and involved in DNA damage repair during mouse cellular reprogramming
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103090
 DO - 10.18632/aging.103090
 SP - 7431
 EP - 7447
 PY - 
 AB - Sirt1 facilitates the reprogramming of mouse somatic cells into induced pluripotent stem cells (iPSCs). It is regulated by micro-RNA and reported to be a target of miR-135a. However, their relationship and roles on cellular reprogramming remain unknown. In this study, we found negative correlations between miR-135a and Sirt1 during mouse embryonic stem cells differentiation and mouse embryonic fibroblasts reprogramming. We further found that the reprogramming efficiency was reduced by the overexpression of miR-135a precursor but induced by the miR-135a inhibitor. Co-immunoprecipitation followed by mass spectrometry identified 21 SIRT1 interacting proteins including KU70 and WRN, which were highly enriched for DNA damage repair. In accordance, Sirt1 activator resveratrol reduced DNA damage during the reprogramming process. Wrn was regulated by miR-135a and resveratrol partly rescued the impaired reprogramming efficiency induced by Wrn knockdown. This study showed Sirt1, being partly regulated by miR-135a, bound proteins involved in DNA damage repair and enhanced the iPSCs production.
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Overexpression of LINC00160 predicts poor outcome and promotes progression of clear cell renal cell carcinoma

Gong Cheng, Yi Yu, Longwang Wang, Qiufeng Pan,

https://doi.org/10.18632/aging.103091 pp 7448—7464

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Cheng G, Yu Y, Wang L, Pan Q, . Overexpression of LINC00160 predicts poor outcome and promotes progression of clear cell renal cell carcinoma. . 12:7448-7464. https://doi.org/10.18632/aging.103091

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                TY  - JOUR
                AU  - Cheng, Gong 
                AU  - Yu, Yi 
                AU  - Wang, Longwang 
                AU  - Pan, Qiufeng 
                TI  - Overexpression of LINC00160 predicts poor outcome and promotes progression of clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103091
                DO  - 10.18632/aging.103091
                SP  - 7448
                EP  - 7464
                PY  - 
                AB  - Clear cell renal cell carcinoma (ccRCC) is the most common subtype of renal carcinoma and exhibits a high risk of invasion and metastasis. It is urgent to uncover a novel biomarker and clarify the underlying mechanism for ccRCC progression and metastasis. Although accumulating research has demonstrated that long non-coding RNAs (lncRNAs) play crucial roles in tumor progression, numerous lncRNAs in ccRCC are largely unknown. Therefore, we screened the differentially expressed lncRNAs among several GEO datasets and chose LNC00160 for further investigation. LNC00160 was significantly upregulated in ccRCC and high expression predicted poor prognosis; higher expression of LNC00160 was associated with advanced clinic pathological parameters in TCGA_KIRC Cohort. Knockdown of LNC00160 suppressed malignancy of ccRCC in vitro and in vivo. Correlation analysis and gene set enrichment analysis (GSEA) revealed that LNC00160 might be associated with Wnt signaling pathway, mTOR signaling pathway, fatty acid metabolism and cell cycle. In conclusion, our results demonstrated that LNC00160 acted as an oncogenic gene and a specific prognostic indicator for patients with ccRCC, and that LNC00160 might be a targeted intervention for ccRCC patients in the future.
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ATM gene polymorphisms are associated with poor prognosis of non-small cell lung cancer receiving radiation therapy

Junjun Mou, Tao Hu, Zhiwu Wang, Wei Chen, Yang Wang, Wei Zhang,

https://doi.org/10.18632/aging.103094 pp 7465—7479

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Mou J, Hu T, Wang Z, Chen W, Wang Y, Zhang W, . ATM gene polymorphisms are associated with poor prognosis of non-small cell lung cancer receiving radiation therapy. . 12:7465-7479. https://doi.org/10.18632/aging.103094

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 TY - JOUR
 AU - Mou, Junjun 
 AU - Hu, Tao 
 AU - Wang, Zhiwu 
 AU - Chen, Wei 
 AU - Wang, Yang 
 AU - Zhang, Wei 
 TI - ATM gene polymorphisms are associated with poor prognosis of non-small cell lung cancer receiving radiation therapy
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103094
 DO - 10.18632/aging.103094
 SP - 7465
 EP - 7479
 PY - 
 AB - We investigated the prognostic significance of ataxia telangiectasia mutated (ATM) single nucleotide polymorphisms (SNPs) in 720 Han Chinese non-small cell lung cancer (NSCLC) patients who underwent radiation or chemoradiation therapy. Kaplan-Meier survival curves showed that overall survival (OS) and disease-free survival (DFS) rates were significantly associated with two ATM SNPs, rs664143 and rs189037. Patients with the rs664143 GA or AA genotype had poorer DFS (hazard ratio (HR) = 1.40, 95% confidence interval (CI) = 1.05&#x2013;1.86, P = 0.021) and OS (HR = 1.28, 95%CI = 1.12&#x2013;1.78, P = 0.040) than those with the rs664143 GG phenotype. Patients with the rs189037 AG/GG genotypes had poorer prognoses than those with the rs189037 AA genotype (AG/GG vs. AA: DFS, HR = 1.44, 95%CI = 1.06&#x2013;1.95, P=0.019; OS, HR = 1.16, 95%CI = 1.16&#x2013;1.17&#x2013;2.21, P=0.004). These results were confirmed by subgroup analysis based on clinical factors such as smoking, histology, tumor stage, treatment, and radiation dose, all of which were significantly associated with DFS and OS rates in NSCLC patients. These findings show that ATM rs664143 and rs189037 variants determine prognosis in NSCLC patients that have undergone radiation or chemoradiation therapies.
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High miR-31-5p expression promotes colon adenocarcinoma progression by targeting TNS1

Bobin Mi, Qiushi Li, Tong Li, Guohui Liu, Jiayang Sai,

https://doi.org/10.18632/aging.103096 pp 7480—7490

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Mi B, Li Q, Li T, Liu G, Sai J, . High miR-31-5p expression promotes colon adenocarcinoma progression by targeting TNS1. . 12:7480-7490. https://doi.org/10.18632/aging.103096

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                TY  - JOUR
                AU  - Mi, Bobin 
                AU  - Li, Qiushi 
                AU  - Li, Tong 
                AU  - Liu, Guohui 
                AU  - Sai, Jiayang 
                TI  - High miR-31-5p expression promotes colon adenocarcinoma progression by targeting TNS1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103096
                DO  - 10.18632/aging.103096
                SP  - 7480
                EP  - 7490
                PY  - 
                AB  - Overexpression of the miR-31-5p contributes to tumorigenesis and metastasis in diverse neoplasms. In this study, we evaluated expression of miR-31-5p in patients with colon adenocarcinoma (COAD). We found that miR-31-5p was overexpressed in four cohorts (GSE30454, GSE41655, GSE18392, GSE108153) of COAD patients. Importantly, a LinkedOmics analysis revealed that high miR-31-5p expression was associated with poor overall survival of COAD patients. At total of 133 putative target genes of miR-31-5p were identified from TargetScan, miRDB, and TargetMiner. After integrating the target genes with 1,556 deregulated genes in COAD, 8 were acquired that may be targeted by miR-31-5p and contribute to COAD progression. Among these, tensin 1 (TNS1) showed the greatest prognostic ability in COAD and was strongly correlated with M2 macrophages, regulatory T cells, and other immune cells. These findings indicate that, in COAD, miR-31-5p is a potential prognostic factor that affects immune infiltration by targeting TNS1.
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RNA-seq analysis of potential lncRNAs for age-related hearing loss in a mouse model

Tong Zhao, Xiuzhen Liu, Zehua Sun, Jinjin Zhang, Xiaolin Zhang, Chaoyun Wang, Ruishuang Geng, Tihua Zheng, Bo Li, Qing Yin Zheng,

https://doi.org/10.18632/aging.103103 pp 7491—7510

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Zhao T, Liu X, Sun Z, Zhang J, Zhang X, Wang C, Geng R, Zheng T, Li B, Zheng QY, . RNA-seq analysis of potential lncRNAs for age-related hearing loss in a mouse model. . 12:7491-7510. https://doi.org/10.18632/aging.103103

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                TY  - JOUR
                AU  - Zhao, Tong 
                AU  - Liu, Xiuzhen 
                AU  - Sun, Zehua 
                AU  - Zhang, Jinjin 
                AU  - Zhang, Xiaolin 
                AU  - Wang, Chaoyun 
                AU  - Geng, Ruishuang 
                AU  - Zheng, Tihua 
                AU  - Li, Bo 
                AU  - Zheng, Qing Yin 
                TI  - RNA-seq analysis of potential lncRNAs for age-related hearing loss in a mouse model
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103103
                DO  - 10.18632/aging.103103
                SP  - 7491
                EP  - 7510
                PY  - 
                AB  - Age-related hearing loss (AHL) is an important health problem in the elderly population. Its molecular mechanisms have not been fully elucidated. In this study, we analyzed the differential expression of lncRNAs and mRNAs in the cochleae of six-week-old and one-year-old C57BL/6J mice through RNA-seq analysis. We found 738 and 2033 differentially expressed lncRNAs and mRNAs, respectively, in these two groups (corrected P &lt; 0.05). We focused on the intersection of known genes associated with hearing loss and differentially expressed mRNAs in RNA-seq. There are 34 mRNAs in this intersection, which include all 29 mRNAs enriched in the sensory perception of sound (GO: 0007605). We selected 11 lncRNAs that are predicted to regulate the 34 mRNAs to validate their expression levels in animal and cellular models of AHL by qRT-PCR. Among these lncRNAs, four were significantly different in both animal and cellular models of AHL, and the lncRNA NONMMUT010961.2 was the most markedly different. Knocking down lncRNA NONMMUT010961.2, we found the expression of oxidative stress and apoptosis-related gene Ar and hearing loss-related gene Hgf is significantly reduced in HEI-OC1 cells. Our results suggest that lncRNAs NONMMUT010961.2 may be associated with AHL and may thus lead to a new treatment for AHL.
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Expression of Nik-related kinase in smooth muscle cells attenuates vascular inflammation and intimal hyperplasia

Yi-Jhu Lu, Yee-Jee Jan, Bor-Sheng Ko, Shu-Man Liang, Lujen Chen, Chih-Cheng Wu, Chih-Hui Chin, Cheng-Chin Kuo, Shaw-Fang Yet, Jun-Yang Liou,

https://doi.org/10.18632/aging.103104 pp 7511—7533

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Lu Y, Jan Y, Ko B, Liang S, Chen L, Wu C, Chin C, Kuo C, Yet S, Liou J, . Expression of Nik-related kinase in smooth muscle cells attenuates vascular inflammation and intimal hyperplasia. . 12:7511-7533. https://doi.org/10.18632/aging.103104

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                TY  - JOUR
                AU  - Lu, Yi-Jhu 
                AU  - Jan, Yee-Jee 
                AU  - Ko, Bor-Sheng 
                AU  - Liang, Shu-Man 
                AU  - Chen, Lujen 
                AU  - Wu, Chih-Cheng 
                AU  - Chin, Chih-Hui 
                AU  - Kuo, Cheng-Chin 
                AU  - Yet, Shaw-Fang 
                AU  - Liou, Jun-Yang 
                TI  - Expression of Nik-related kinase in smooth muscle cells attenuates vascular inflammation and intimal hyperplasia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103104
                DO  - 10.18632/aging.103104
                SP  - 7511
                EP  - 7533
                PY  - 
                AB  - Inflammation of the vascular microenvironment modulates distinct types of vascular cells, and plays important roles in promoting atherosclerosis, stenosis/restenosis, and vascular-related diseases. Nik-related kinase (Nrk), a member of the Ste20-type kinase family, has been reported to be selectively expressed in embryonic skeletal muscle. However, whether Nrk is expressed in adult vascular smooth muscle, and if it influences intimal hyperplasia is unclear. Here, we found that Nrk is abundantly expressed in cultured vascular smooth muscle cells (VSMC) and mouse arterial intima. Treatment of mouse VSMCs with lipopolysaccharide (LPS) or platelet-derived growth factor significantly reduced Nrk expression. In addition, expression of Nrk was significantly reduced in regions of neointimal formation caused by guide-wire carotid artery injuries in mice, as well as in human atherosclerotic tissues, when compared to normal vessels. We identified that expression of matrix metalloproteinases (MMP3, MMP8 and MMP12) and inflammatory cytokines/chemokines (CCL6, CCL8, CCL11, CXCL1, CXCL3, CXCL5 and CXCL9) are synergistically induced by Nrk siRNA in LPS-treated mouse VSMCs. Moreover, we found that resveratrol significantly impaired LPS- and Nrk siRNA-induced expression of MMP3, CCL8, CCL11, CXCL3 and CXCL5. These results suggested that Nrk may play important roles in regulating pathological progression of atherosclerosis or neointimal- hyperplasia-related vascular diseases.
                ER  -

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Protective effects of autophagy and NFE2L2 on reactive oxygen species-induced pyroptosis of human nucleus pulposus cells

Zhibiao Bai, Wei Liu, Danshuang He, Yiyang Wang, Weiwei Yi, Changqi Luo, Jieliang Shen, Zhenming Hu,

https://doi.org/10.18632/aging.103109 pp 7534—7548

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Bai Z, Liu W, He D, Wang Y, Yi W, Luo C, Shen J, Hu Z, . Protective effects of autophagy and NFE2L2 on reactive oxygen species-induced pyroptosis of human nucleus pulposus cells. . 12:7534-7548. https://doi.org/10.18632/aging.103109

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                TY  - JOUR
                AU  - Bai, Zhibiao 
                AU  - Liu, Wei 
                AU  - He, Danshuang 
                AU  - Wang, Yiyang 
                AU  - Yi, Weiwei 
                AU  - Luo, Changqi 
                AU  - Shen, Jieliang 
                AU  - Hu, Zhenming 
                TI  - Protective effects of autophagy and NFE2L2 on reactive oxygen species-induced pyroptosis of human nucleus pulposus cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103109
                DO  - 10.18632/aging.103109
                SP  - 7534
                EP  - 7548
                PY  - 
                AB  - Intervertebral disc degeneration (IDD) is characterized by the decrease of nucleus pulposus cells (NPCs). With the increase of the degree of degeneration, the reactive oxygen species (ROS) in nucleus pulposus tissue increases. Pyroptosis is a newly discovered form of cell death and its relationship with oxidative stress in NPCs remains unclear. This study was performed to investigate the mechanisms of pyroptosis of NPCs under oxidative stress. NPCs were isolated from IDD patients by surgical treatment. Pyroptosis related proteins like NLR family pyrin domain containing 3(NLRP3) and PYD and CARD domain containing (PYCARD) were detected by western blot, and membrane pore formation was observed by hochest33342/PI double staining or scanning electron microscope. The results showed that ROS induced the pyroptosis of NPCs and it depended on the expression of NLRP3 and PYCARD. The increased ROS level also increased transcription factor nuclear factor, erythroid 2 like 2 (NFE2L2, Nrf2) and the autophagy of NPCs, both of which attenuated the pyroptosis. In summary, ROS induces the pyroptosis of NPCs through the NLRP3/ PYCARD pathway, and establishes negative regulation by increasing autophagy and NFE2L2. These findings may provide a better understanding of the mechanism of IDD and potential therapeutic approaches for IDD treatment.
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Validation of the 8^th edition of the American Joint Committee on Cancer Pathological Prognostic Staging for young breast cancer patients

Juan Zhou, Jian Lei, Jun Wang, Chen-Lu Lian, Li Hua, Li-Chao Yang, San-Gang Wu,

https://doi.org/10.18632/aging.103111 pp 7549—7560

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Zhou J, Lei J, Wang J, Lian C, Hua L, Yang L, Wu S, . Validation of the 8^th edition of the American Joint Committee on Cancer Pathological Prognostic Staging for young breast cancer patients. . 12:7549-7560. https://doi.org/10.18632/aging.103111

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Provider: 
 TY - JOUR
 AU - Zhou, Juan 
 AU - Lei, Jian 
 AU - Wang, Jun 
 AU - Lian, Chen-Lu 
 AU - Hua, Li 
 AU - Yang, Li-Chao 
 AU - Wu, San-Gang 
 TI - Validation of the 8th edition of the American Joint Committee on Cancer Pathological Prognostic Staging for young breast cancer patients
 JO - 
 JA - 
 VL - 12
 IS - 8
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103111
 DO - 10.18632/aging.103111
 SP - 7549
 EP - 7560
 PY - 
 AB - Purpose: This study aimed to validate the newly proposed American Joint Committee on Cancer (AJCC) pathological prognostic staging system for young breast cancer patients (aged &#x2264;40 years).Results: We included 12811 women in this study. Overall, 52.8% of patients in the 7th AJCC stages were restaged to the 8th AJCC pathological staging system, including 10.7% upstaged and 42.1% downstaged. The receiver operating characteristics analysis showed that the new staging system had a better role in predicting breast cancer-specific survival (BCSS) compared with 7th edition staging (P&lt;0.001). The results of the multivariate prognostic analysis showed that the hazard ratio of BCSS increased with the 8th AJCC stages, while the 7th anatomic stages had no significant difference in BCSS.Conclusions: The novel pathological staging system could provide more accurate prognostic stratification for young women with breast cancer because of the high proportion of stage migration.Patients and Methods: Data for young breast cancer patients diagnosed between 2010 and 2014 were included from the Surveillance, Epidemiology, and End Results program. Chi-squared test, Kaplan&#x2013;Meier method, receiver operating characteristics curve, and Cox proportional hazard analysis were applied to statistical analysis.
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Using a genetic algorithm to derive a highly predictive and context-specific frailty index

Alberto Zucchelli, Alessandra Marengoni, Debora Rizzuto, Amaia Calderón-Larrañaga, Maurizio Zucchelli, Roberto Bernabei, Graziano Onder, Laura Fratiglioni, Davide Liborio Vetrano,

https://doi.org/10.18632/aging.103118 pp 7561—7575

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Zucchelli A, Marengoni A, Rizzuto D, Calderón-Larrañaga A, Zucchelli M, Bernabei R, Onder G, Fratiglioni L, Vetrano DL, . Using a genetic algorithm to derive a highly predictive and context-specific frailty index. . 12:7561-7575. https://doi.org/10.18632/aging.103118

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                TY  - JOUR
                AU  - Zucchelli, Alberto 
                AU  - Marengoni, Alessandra 
                AU  - Rizzuto, Debora 
                AU  - Calderón-Larrañaga, Amaia 
                AU  - Zucchelli, Maurizio 
                AU  - Bernabei, Roberto 
                AU  - Onder, Graziano 
                AU  - Fratiglioni, Laura 
                AU  - Vetrano, Davide Liborio 
                TI  - Using a genetic algorithm to derive a highly predictive and context-specific frailty index
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103118
                DO  - 10.18632/aging.103118
                SP  - 7561
                EP  - 7575
                PY  - 
                AB  - The frailty index (FI) is one of the most widespread tools used to predict poor, health-related outcomes in older persons. The selection of clinical and functional deficits to include in a FI is mostly based on the users&#x2019; clinical experience. However, this approach may not be sufficiently accurate to predict health outcomes in particular subgroups of individuals. In this study, we implemented an optimization algorithm, the genetic algorithm, to create a highly performant (FI) based on our prediction goals, rather than on a predetermined clinical selection of deficits, using data from the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) and 109 potential deficits identified in the dataset. The algorithm was personalized to obtain a FI with high discrimination ability in the prediction of mortality. The resulting FI included 40 deficits and showed areas under the curve consistently higher than 0.80 (range 0.81-0.90) in the prediction of 3-year and 6-year mortality in the whole sample and in sex and age subgroups. This methodology represents a promising opportunity to optimize the exploitation of medical and administrative databases in the construction of clinically relevant frailty indices.
                ER  -

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The effect of rapamycin on bovine oocyte maturation success and metaphase telomere length maintenance

Pawel Kordowitzki, Meriem Hamdi, Aksinya Derevyanko, Dimitrios Rizos, Maria Blasco,

https://doi.org/10.18632/aging.103126 pp 7576—7584

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Kordowitzki P, Hamdi M, Derevyanko A, Rizos D, Blasco M, . The effect of rapamycin on bovine oocyte maturation success and metaphase telomere length maintenance. . 12:7576-7584. https://doi.org/10.18632/aging.103126

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                TY  - JOUR
                AU  - Kordowitzki, Pawel 
                AU  - Hamdi, Meriem 
                AU  - Derevyanko, Aksinya 
                AU  - Rizos, Dimitrios 
                AU  - Blasco, Maria 
                TI  - The effect of rapamycin on bovine oocyte maturation success and metaphase telomere length maintenance
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103126
                DO  - 10.18632/aging.103126
                SP  - 7576
                EP  - 7584
                PY  - 
                AB  - Maternal aging-associated reduction of oocyte viability is a common feature in mammals, but more research is needed to counteract this process. In women, the first aging phenotype appears with a decline in reproductive function, and the follicle number gradually decreases from menarche to menopause. Cows can be used as a model of early human embryonic development and reproductive aging because both species share a very high degree of similarity during follicle selection, cleavage, and blastocyst formation. Recently, it has been proposed that the main driver of aging is the mammalian target of rapamycin (mTOR) signaling rather than reactive oxygen species. Based on these observations, the study aimed to investigate for the first time the possible role of rapamycin on oocyte maturation, embryonic development, and telomere length in the bovine species, as a target for future strategies for female infertility caused by advanced maternal age. The 1nm rapamycin in vitro treatment showed the best results for maturation rates (95.21&#xB1;4.18%) of oocytes and was considered for further experiments. In conclusion, rapamycin influenced maturation rates of oocytes in a concentration-dependent manner. Our results also suggest a possible link between mTOR, telomere maintenance, and bovine blastocyst formation.
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PTX3 modulates the immunoflogosis in tumor microenvironment and is a prognostic factor for patients with clear cell renal cell carcinoma

Giuseppe Stefano Netti, Giuseppe Lucarelli, Federica Spadaccino, Giuseppe Castellano, Margherita Gigante, Chiara Divella, Maria Teresa Rocchetti, Federica Rascio, Vito Mancini, Giovanni Stallone, Giuseppe Carrieri, Loreto Gesualdo, Michele Battaglia, Elena Ranieri,

https://doi.org/10.18632/aging.103169 pp 7585—7602

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Netti GS, Lucarelli G, Spadaccino F, Castellano G, Gigante M, Divella C, Rocchetti MT, Rascio F, Mancini V, Stallone G, Carrieri G, Gesualdo L, Battaglia M, et al, . PTX3 modulates the immunoflogosis in tumor microenvironment and is a prognostic factor for patients with clear cell renal cell carcinoma. . 12:7585-7602. https://doi.org/10.18632/aging.103169

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                TY  - JOUR
                AU  - Netti, Giuseppe Stefano 
                AU  - Lucarelli, Giuseppe 
                AU  - Spadaccino, Federica 
                AU  - Castellano, Giuseppe 
                AU  - Gigante, Margherita 
                AU  - Divella, Chiara 
                AU  - Rocchetti, Maria Teresa 
                AU  - Rascio, Federica 
                AU  - Mancini, Vito 
                AU  - Stallone, Giovanni 
                AU  - Carrieri, Giuseppe 
                AU  - Gesualdo, Loreto 
                AU  - Battaglia, Michele 
                AU  - Ranieri, Elena 
                TI  - PTX3 modulates the immunoflogosis in tumor microenvironment and is a prognostic factor for patients with clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103169
                DO  - 10.18632/aging.103169
                SP  - 7585
                EP  - 7602
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Netti, Giuseppe Stefano 
                AU  - Lucarelli, Giuseppe 
                AU  - Spadaccino, Federica 
                AU  - Castellano, Giuseppe 
                AU  - Gigante, Margherita 
                AU  - Divella, Chiara 
                AU  - Rocchetti, Maria Teresa 
                AU  - Rascio, Federica 
                AU  - Mancini, Vito 
                AU  - Stallone, Giovanni 
                AU  - Carrieri, Giuseppe 
                AU  - Gesualdo, Loreto 
                AU  - Battaglia, Michele 
                AU  - Ranieri, Elena 
                TI  - PTX3 modulates the immunoflogosis in tumor microenvironment and is a prognostic factor for patients with clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103169
                DO  - 10.18632/aging.103169
                SP  - 7585
                EP  - 7602
                PY  - 
                AB  - Pentraxin-3 (PTX3) belongs to the pentraxine family, innate immune regulators involved in angiogenesis, proliferation and immune escape in cancer. Here, we evaluated PTX3 tissue expression and serum levels as biomarkers of clear cell renal cell carcinoma (ccRCC) and analyzed the possible role of complement system activation on tumor site. A 10-year retrospective cohort study including patients undergoing nephrectomy for ccRCC was also performed. PTX3 expression was elevated in both neoplastic renal cell lines and tissues, while it was absent in both normal renal proximal tubular cells (HK2) and normal renal tissues. Analysis of complement system activation on tumor tissues showed the co-expression of PTX3 with C1q, C3aR, C5R1 and CD59, but not with C5b-9 terminal complex. RCC patients showed higher serum PTX3 levels as compared to non-neoplastic patients (p&lt;0.0001). Higher PTX3 serum levels were observed in patients with higher Fuhrman grade (p&lt;0.01), lymph node (p&lt;0.0001), and visceral metastases (p&lt;0.001). Patients with higher PTX3 levels also showed significantly lower survival rates (p=0.002). Our results suggest that expression of PTX3 can affect the immunoflogosis in the ccRCC microenvironment, by activating the classical pathway of CS (C1q) and releasing pro-angiogenic factors (C3a, C5a). The up-regulation of CD59 also inhibits the complement-mediated cellular lysis.
                ER  -

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LUCS: a high-resolution nucleic acid sequencing tool for accurate long-read analysis of individual DNA molecules

Sofia Annis, Zoë Fleischmann, Robert Logan, Zachary Mullin-Bernstein, Melissa Franco, Josefin Saürich, Jonathan L. Tilly, Dori C. Woods, Konstantin Khrapko,

https://doi.org/10.18632/aging.103171 pp 7603—7613

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Annis S, Fleischmann Z, Logan R, Mullin-Bernstein Z, Franco M, Saürich J, Tilly JL, Woods DC, Khrapko K, . LUCS: a high-resolution nucleic acid sequencing tool for accurate long-read analysis of individual DNA molecules. . 12:7603-7613. https://doi.org/10.18632/aging.103171

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                TY  - JOUR
                AU  - Annis, Sofia 
                AU  - Fleischmann, Zoë 
                AU  - Logan, Robert 
                AU  - Mullin-Bernstein, Zachary 
                AU  - Franco, Melissa 
                AU  - Saürich, Josefin 
                AU  - Tilly, Jonathan L. 
                AU  - Woods, Dori C. 
                AU  - Khrapko, Konstantin 
                TI  - LUCS: a high-resolution nucleic acid sequencing tool for accurate long-read analysis of individual DNA molecules
                JO  - 
                JA  - 
                VL  - 12
                IS  - 8
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103171
                DO  - 10.18632/aging.103171
                SP  - 7603
                EP  - 7613
                PY  - 
                AB  - Nucleic acid sequence analyses are fundamental to all aspects of biological research, spanning aging, mitochondrial DNA (mtDNA) and cancer, as well as microbial and viral evolution. Over the past several years, significant improvements in DNA sequencing, including consensus sequence analysis, have proven invaluable for high-throughput studies. However, all current DNA sequencing platforms have limited utility for studies of complex mixtures or of individual long molecules, the latter of which is crucial to understanding evolution and consequences of single nucleotide variants and their combinations. Here we report a new technology termed LUCS (Long-molecule UMI-driven Consensus Sequencing), in which reads from third-generation sequencing are aggregated by unique molecular identifiers (UMIs) specific for each individual DNA molecule. This enables in-silico reconstruction of highly accurate consensus reads of each DNA molecule independent of other molecules in the sample. Additionally, use of two UMIs enables detection of artificial recombinants (chimeras). As proof of concept, we show that application of LUCS to assessment of mitochondrial genomes in complex mixtures from single cells was associated with an error rate of 1X10-4 errors/nucleotide. Thus, LUCS represents a major step forward in DNA sequencing that offers high-throughput capacity and high-accuracy reads in studies of long DNA templates and nucleotide variants in heterogenous samples.
                ER  -

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Volume 12, Issue 8

About the Cover

Editorial

COVID-19 Biomarkers of biological age as predictors of COVID-19 disease severity

Gordan Lauc, David Sinclair,

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Research Perspectives

COVID-19 Geroprotective and senoremediative strategies to reduce the comorbidity, infection rates, severity, and lethality in gerophilic and gerolavic infections

Alex Zhavoronkov,

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COVID-19 COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?

Camillo Sargiacomo, Federica Sotgia, Michael P. Lisanti,

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Research Papers

COVID-19 ACE2 correlated with immune infiltration serves as a prognostic biomarker in endometrial carcinoma and renal papillary cell carcinoma: implication for COVID-19

Jing Yang, Hongxia Li, Shengda Hu, Yafeng Zhou,

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COVID-19 Anti-SARS-CoV-2 virus antibody levels in convalescent plasma of six donors who have recovered from COVID-19

Libo Zhang, Rongrong Pang, Xiang Xue, Jingjing Bao, Sheng Ye, Yudong Dai, Yishan Zheng, Qiang Fu, Zhiliang Hu, Yongxiang Yi,

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Shanshan Du, Jingzhi Shao, Ying Qi, Xuhui Liu, Jingjing Liu, Fengyan Zhang,

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Yang Hou, Guodong Shi, Yongfei Guo, Jiangang Shi,

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Meng-Ying Yao, Wei-Hong Zhang, Wen-Tao Ma, Qiu-Hong Liu, Li-Hua Xing, Gao-Feng Zhao,

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Puchun Er, Dong Qian, Wencheng Zhang, Baozhong Zhang, Hui Wei, Tian Zhang, Xi Chen, Yuwen Wang, Jingjing Zhao, Qi Wang, Qingsong Pang, Ping Wang,

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Yuhua Chi, Haiyan Wang, Fengsong Wang, Mingcui Ding,

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Zhaoyuan Zhang, Weili Wang, Dan Ma, Jie Xiong, Xingyi Kuang, Siyu Zhang, Qin Fang, Jishi Wang,

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Yen-Shuo Chiu, Jia-Lin Wu, Chi-Tai Yeh, Vijesh Kumar Yadav, Hsu-Shan Huang, Liang-Shun Wang,

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Kewei Zhu, Yang Yuan, Jie Wen, Ding Chen, Weihong Zhu, Zhengxiao Ouyang, Wanchun Wang,

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Yang Zhang, Jingyu Sun, He Yao, Yajun Lin, Jie Wei, Gang Hu, Jun Guo, Jian Li,

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Bo Wang, Yangyang Zhang, Haitian Zhang, Faquan Lin, Qixin Tan, Qinghong Qin, Wei Bao, Yi Liu, Jiaying Xie, Qiyan Zeng,

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Yun Yeong Lee, Yeon Seung Choi, Do Wan Kim, Jae Youn Cheong, Kye Yong Song, Min Sook Ryu, In Kyoung Lim,

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Yongtao Wang, Tao Yu, Yanying Zhou, Shike Wang, Xunian Zhou, Limin Wang, Tianmiao Ou, Yixin Chen, Yawen Zhou, Huizhen Zhang, Ying Wang, Xiaomei Fan, Pan Chen, Frank J. Gonzalez, Aiming Yu, Peng Huang, Min Huang, Huichang Bi,

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Jun Cui, Haiyan Wang, Xiaohe Zhang, Xiaodong Sun, Jin Zhang, Jinji Ma,

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COVID-19
Biomarkers of biological age as predictors of COVID-19 disease severity

COVID-19
Geroprotective and senoremediative strategies to reduce the comorbidity, infection rates, severity, and lethality in gerophilic and gerolavic infections

COVID-19
COVID-19 and chronological aging: senolytics and other anti-aging drugs for the treatment or prevention of corona virus infection?

COVID-19
ACE2 correlated with immune infiltration serves as a prognostic biomarker in endometrial carcinoma and renal papillary cell carcinoma: implication for COVID-19

COVID-19
Anti-SARS-CoV-2 virus antibody levels in convalescent plasma of six donors who have recovered from COVID-19