Volume 12, Issue 16

Varela-Eirín M, Carpintero-Fernández P, Sánchez-Temprano A, Varela-Vázquez A, Paíno CL, Casado-Díaz A, Continente AC, Mato V, Fonseca E, Kandouz M, Blanco A, Caeiro JR, Mayán MD, . Senolytic activity of small molecular polyphenols from olive restores chondrocyte redifferentiation and promotes a pro-regenerative environment in osteoarthritis. . 12:15882-15905. https://doi.org/10.18632/aging.103801

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                TY  - JOUR
                AU  - Varela-Eirín, Marta 
                AU  - Carpintero-Fernández, Paula 
                AU  - Sánchez-Temprano, Agustín 
                AU  - Varela-Vázquez, Adrián 
                AU  - Paíno, Carlos Luis 
                AU  - Casado-Díaz, Antonio 
                AU  - Continente, Alfonso Calañas 
                AU  - Mato, Virginia 
                AU  - Fonseca, Eduardo 
                AU  - Kandouz, Mustapha 
                AU  - Blanco, Alfonso 
                AU  - Caeiro, José Ramón 
                AU  - Mayán, María D. 
                TI  - Senolytic activity of small molecular polyphenols from olive restores chondrocyte redifferentiation and promotes a pro-regenerative environment in osteoarthritis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103801
                DO  - 10.18632/aging.103801
                SP  - 15882
                EP  - 15905
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Varela-Eirín, Marta 
                AU  - Carpintero-Fernández, Paula 
                AU  - Sánchez-Temprano, Agustín 
                AU  - Varela-Vázquez, Adrián 
                AU  - Paíno, Carlos Luis 
                AU  - Casado-Díaz, Antonio 
                AU  - Continente, Alfonso Calañas 
                AU  - Mato, Virginia 
                AU  - Fonseca, Eduardo 
                AU  - Kandouz, Mustapha 
                AU  - Blanco, Alfonso 
                AU  - Caeiro, José Ramón 
                AU  - Mayán, María D. 
                TI  - Senolytic activity of small molecular polyphenols from olive restores chondrocyte redifferentiation and promotes a pro-regenerative environment in osteoarthritis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103801
                DO  - 10.18632/aging.103801
                SP  - 15882
                EP  - 15905
                PY  - 
                AB  - Articular cartilage and synovial tissue from patients with osteoarthritis (OA) show an overactivity of connexin43 (Cx43) and accumulation of senescent cells associated with disrupted tissue regeneration and disease progression. The aim of this study was to determine the effect of oleuropein on Cx43 and cellular senescence for tissue engineering and regenerative medicine strategies for OA treatment. Oleuropein regulates Cx43 promoter activity and enhances the propensity of hMSCs to differentiate into chondrocytes and bone cells, reducing adipogenesis. This small molecule reduce Cx43 levels and decrease Twist-1 activity in osteoarthritic chondrocytes (OACs), leading to redifferentiation, restoring the synthesis of cartilage ECM components (Col2A1 and proteoglycans), and reducing the inflammatory and catabolic factors mediated by NF-kB (IL-1&#xDF;, IL-6, COX-2 and MMP-3), in addition to lowering cellular senescence in OACs, synovial and bone cells. Our in vitro results demonstrate the use of olive-derived polyphenols, such as oleuropein, as potentially effective therapeutic agents to improve chondrogenesis of hMSCs, to induce chondrocyte re-differentiation in OACs and clearing out senescent cells in joint tissues in order to prevent or stop the progression of the disease.
                ER  -

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Dynamics of telomeric repeat-containing RNA expression in early embryonic cleavage stages with regards to maternal age

Paweł Kordowitzki, Isabel López de Silanes, Ana Guío-Carrión, Maria A. Blasco,

https://doi.org/10.18632/aging.103922 pp 15906—15917

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Kordowitzki P, López de Silanes I, Guío-Carrión A, Blasco MA, . Dynamics of telomeric repeat-containing RNA expression in early embryonic cleavage stages with regards to maternal age. . 12:15906-15917. https://doi.org/10.18632/aging.103922

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                TY  - JOUR
                AU  - Kordowitzki, Paweł 
                AU  - López de Silanes, Isabel 
                AU  - Guío-Carrión, Ana 
                AU  - Blasco, Maria A. 
                TI  - Dynamics of telomeric repeat-containing RNA expression in early embryonic cleavage stages with regards to maternal age
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103922
                DO  - 10.18632/aging.103922
                SP  - 15906
                EP  - 15917
                PY  - 
                AB  - Telomeres are transcribed into long non-coding RNAs known as Telomeric Repeat-Containing RNA (TERRA). They have been shown to be essential regulators of telomeres and to act as epigenomic modulators at extra-telomeric sites. However the role of TERRA during early embryonic development has never been investigated. Here, we show that TERRA is expressed in murine and bovine early development following a wave pattern. It starts at 4-cell stage, reaching a maximum at the 16-cell followed by a decline at the morula and blastocyst stages. Moreover, TERRA expression is not affected by increasing oocyte donor age whereas telomere length does. This indicates that TERRA expression is independent of the telomere length in early development. Our findings anticipate an essential role of TERRA in early stages of development and this might be useful in the future for a better understanding of age related female infertility.
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COVID-19
Early coagulation tests predict risk stratification and prognosis of COVID-19

Lili Luo, Min Xu, Mengyi Du, Haiming Kou, Danying Liao, Zhipeng Cheng, Heng Mei, Yu Hu,

https://doi.org/10.18632/aging.103581 pp 15918—15937

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Luo L, Xu M, Du M, Kou H, Liao D, Cheng Z, Mei H, Hu Y, . Early coagulation tests predict risk stratification and prognosis of COVID-19. . 12:15918-15937. https://doi.org/10.18632/aging.103581

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                TY  - JOUR
                AU  - Luo, Lili 
                AU  - Xu, Min 
                AU  - Du, Mengyi 
                AU  - Kou, Haiming 
                AU  - Liao, Danying 
                AU  - Cheng, Zhipeng 
                AU  - Mei, Heng 
                AU  - Hu, Yu 
                TI  - Early coagulation tests predict risk stratification and prognosis of COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103581
                DO  - 10.18632/aging.103581
                SP  - 15918
                EP  - 15937
                PY  - 
                AB  - The ongoing outbreak of Coronavirus Disease 2019 (COVID-19) is hitting the world hard, but the relationship between coagulation disorders and COVID-19 is still not clear. This study aimed to explore whether early coagulation tests can predict risk stratification and prognosis. PubMed, Web of Science, Cochrane Library, and Scopus were searched electronically for relevant research studies published up to March 24, 2020, producing 24 articles for the final inclusion. The pooled standard mean difference (SMD) of coagulation parameters at admission were calculated to determine severe and composite endpoint conditions (ICU or death) in COVID-19 patients. Meta-analyses revealed that platelet count was not statistically related to disease severity and composite endpoint; elevated D-dimer correlated positively with disease severity (SMD 0.787 (0.277-1.298), P= 0.003, I2= 96.7%) but had no significant statistical relationship with composite endpoints. Similarly, patients with prolonged prothrombin time (PT) had an increased risk of ICU and increased risk of death (SMD 1.338 (0.551-2.125), P = 0.001, I2 = 92.7%). Besides, increased fibrin degradation products (FDP) and decreased antithrombin might also mean the disease is worsening. Therefore, early coagulation tests followed by dynamic monitoring is useful for recognizing coagulation disorders accompanied by COVID-19 and guiding timely therapy to improve prognosis.
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COVID-19
Clinical characteristics of chronic liver disease with coronavirus disease 2019 (COVID-19): a cohort study in Wuhan, China

Chaowei Li, Qingshi Chen, Jianwen Wang, Huasong Lin, Yalan Lin, Jinhuang Lin, Fangzhan Peng, Jiangmu Chen, Zhirong Yang,

https://doi.org/10.18632/aging.103632 pp 15938—15945

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Li C, Chen Q, Wang J, Lin H, Lin Y, Lin J, Peng F, Chen J, Yang Z, . Clinical characteristics of chronic liver disease with coronavirus disease 2019 (COVID-19): a cohort study in Wuhan, China. . 12:15938-15945. https://doi.org/10.18632/aging.103632

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                TY  - JOUR
                AU  - Li, Chaowei 
                AU  - Chen, Qingshi 
                AU  - Wang, Jianwen 
                AU  - Lin, Huasong 
                AU  - Lin, Yalan 
                AU  - Lin, Jinhuang 
                AU  - Peng, Fangzhan 
                AU  - Chen, Jiangmu 
                AU  - Yang, Zhirong 
                TI  - Clinical characteristics of chronic liver disease with coronavirus disease 2019 (COVID-19): a cohort study in Wuhan, China
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103632
                DO  - 10.18632/aging.103632
                SP  - 15938
                EP  - 15945
                PY  - 
                AB  - Background: Previous work has described acute liver injury (ALI) in coronavirus disease 2019 (COVID-19) pneumonia patients, However, there is limited analyses available investigating chronic liver disease (CLD) in COVID-19 patients. This study aimed to investigate clinical characteristics and outcomes of CLD confirmed in COVID-19 patients.
                Results: A total of 104 cases (each group containing 52 patients) were analyzed in this study. The CLD group showed an average of 14 (10.0~21.2) length of stay (LOS) days, compared to the group without CLD that only showed an average of 12.5 (10~16) LOS days (Relative Risk [RR] = 1.34, 95% CI (1.22~1.48), P&lt;0.001; Adjusted Relative Risk was 1.24 (95% CI: 1.12~1.39)). The CLD group contained a higher mortality rate and slight liver injury. Furthermore, COX regression model analyses suggested that the neutrophil-to-lymphocyte ratio (NLR) was an independent predictor of mortality risk (P &lt; 0.001) in the CLD group. Additionally, a high NLR significantly correlated with a shorter overall survival (P &lt;0.001).
                Conclusions: COVID-19 patients also diagnosed with CLD suffered longer LOS, slight liver injuries and a higher mortality when compared to COVID-19 patients without CLD. The NLR was an independent risk factor for in-hospital deaths. Increased expression of NLR was an indicator of poor prognosis in COVID-19 patients with CLD. Thus, COVID-19 patients diagnosed with CLD and who show a higher NLR need additional care.
                Methods: A retrospective cohort study was performed at the Wuhan Jin Yin-tan Hospital from February 2, 2020 to April 2, 2020. COVID-19 patients diagnosed with CLD or not diagnosed with CLD were enrolled in this study. The clinical characteristics and outcomes of these patients were compared.
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COVID-19
Clinical course and characteristics of patients with coronavirus disease 2019 in Wuhan, China: a single-centered, retrospective, observational study

Yanfang Liu, Lina Liu, Ye Wang, Xinyang Du, Hong Ma, Jing Yao,

https://doi.org/10.18632/aging.103745 pp 15946—15953

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Liu Y, Liu L, Wang Y, Du X, Ma H, Yao J, . Clinical course and characteristics of patients with coronavirus disease 2019 in Wuhan, China: a single-centered, retrospective, observational study. . 12:15946-15953. https://doi.org/10.18632/aging.103745

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                TY  - JOUR
                AU  - Liu, Yanfang 
                AU  - Liu, Lina 
                AU  - Wang, Ye 
                AU  - Du, Xinyang 
                AU  - Ma, Hong 
                AU  - Yao, Jing 
                TI  - Clinical course and characteristics of patients with coronavirus disease 2019 in Wuhan, China: a single-centered, retrospective, observational study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103745
                DO  - 10.18632/aging.103745
                SP  - 15946
                EP  - 15953
                PY  - 
                AB  - Background: Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) is the virus responsible for the coronavirus disease 2019(COVID-19) pandemic. Despite the extensive studies aiming to understand the pathology of COVID-19, the clinicopathological characteristics and risk factors associated with COVID-19 remain mostly unclear. In this study, we assessed the clinical course and features of COVID-19 patients.
Findings: There were 59 patients (54.1%) that had no fever. One-hundred(91.7%) patients required oxygen therapy, which improved percutaneous oxygen saturation (SpO2). Seventy-two (66.1%) patients aged over 60; these patients were more likely to develop respiratory symptoms. Only 13(11.9%) patients were positive for anti-SARS-CoV-2 antibodies, SARS-CoV-2 nucleic acid, and computed tomography (CT) findings. We found significant differences in age, respiratory symptoms, and heart rates between patients with and without underlying conditions.
Conclusions: Our findings suggest that oxygen plays an important role in the treatment of COVID-19 patients and that age and underlying diseases are significant risk factors for COVID-19. Most COVID-19 patients have no fever, and CT provides higher detection rates than antibody- and nucleic acid-based detection methods.
Methods: We analyzed data from 109 confirmed COVID-19 cases. We compared the clinicopathological characteristic of patients stratified according to age and underlying diseases, as well as assessed the detection rates of different diagnostic methods.
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COVID-19
COVID-19: a probable role of the anticoagulant Protein S in managing COVID-19-associated coagulopathy

Sabyasachi Chatterjee, Tanusree Sengupta, Samarpan Majumder, Rinku Majumder,

https://doi.org/10.18632/aging.103869 pp 15954—15961

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Chatterjee S, Sengupta T, Majumder S, Majumder R, . COVID-19: a probable role of the anticoagulant Protein S in managing COVID-19-associated coagulopathy. . 12:15954-15961. https://doi.org/10.18632/aging.103869

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                TY  - JOUR
                AU  - Chatterjee, Sabyasachi 
                AU  - Sengupta, Tanusree 
                AU  - Majumder, Samarpan 
                AU  - Majumder, Rinku 
                TI  - COVID-19: a probable role of the anticoagulant Protein S in managing COVID-19-associated coagulopathy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103869
                DO  - 10.18632/aging.103869
                SP  - 15954
                EP  - 15961
                PY  - 
                AB  - The COVID-19 pandemic has caused monumental mortality, and there are still no adequate therapies. Most severely ill COVID-19 patients manifest a hyperactivated immune response, instigated by interleukin 6 (IL6) that triggers a so called &#x201C;cytokine storm&#x201D; and coagulopathy. Hypoxia is also associated with COVID-19. So far overlooked is the fact that both IL6 and hypoxia depress the abundance of a key anticoagulant, Protein S. We speculate that the IL6-driven cytokine explosion plus hypoxemia causes a severe drop in Protein S level that exacerbates the thrombotic risk in COVID-19 patients. Here we highlight a mechanism by which the IL6-hypoxia curse causes a deadly hypercoagulable state in COVID-19 patients, and we suggest a path to therapy.
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Genetic variation between long-lived versus short-lived bats illuminates the molecular signatures of longevity

Zixia Huang, Conor V. Whelan, Dina Dechmann, Emma C. Teeling,

https://doi.org/10.18632/aging.103725 pp 15962—15977

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Huang Z, Whelan CV, Dechmann D, Teeling EC, . Genetic variation between long-lived versus short-lived bats illuminates the molecular signatures of longevity. . 12:15962-15977. https://doi.org/10.18632/aging.103725

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                TY  - JOUR
                AU  - Huang, Zixia 
                AU  - Whelan, Conor V. 
                AU  - Dechmann, Dina 
                AU  - Teeling, Emma C. 
                TI  - Genetic variation between long-lived versus short-lived bats illuminates the molecular signatures of longevity
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103725
                DO  - 10.18632/aging.103725
                SP  - 15962
                EP  - 15977
                PY  - 
                AB  - Bats are the longest-lived mammals given their body size with majority of species exhibiting exceptional longevity. However, there are some short-lived species that do not exhibit extended lifespans. Here we conducted a comparative genomic and transcriptomic study on long-lived Myotis myotis (maximum lifespan = 37.1 years) and short-lived Molossus molossus (maximum lifespan = 5.6 years) to ascertain the genetic difference underlying their divergent longevities. Genome-wide selection tests on 12,467 single-copy genes between M. myotis and M. molossus revealed only three genes (CCDC175, FATE1 and MLKL) that exhibited significant positive selection. Although 97.96% of 12,467 genes underwent purifying selection, we observed a significant heterogeneity in their expression patterns. Using a linear mixed model, we obtained expression of 2,086 genes that may truly represent the genetic difference between M. myotis and M. molossus. Expression analysis indicated that long-lived M. myotis exhibited a transcriptomic profile of enhanced DNA repair and autophagy pathways, compared to M. molossus. Further investigation of the longevity-associated genes suggested that long-lived M. myotis have naturally evolved a diminished anti-longevity transcriptomic profile. Together with observations from other long-lived species, our results suggest that heightened DNA repair and autophagy activity may represent a universal mechanism to achieve longevity in long-lived mammals.
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A human MMTV-like betaretrovirus linked to breast cancer has been present in humans at least since the copper age

Francesca Lessi, Nicole Grandi, Chiara Maria Mazzanti, Prospero Civita, Cristian Scatena, Paolo Aretini, Pasquale Bandiera, Antonio Fornaciari, Valentina Giuffra, Gino Fornaciari, Antonio Giuseppe Naccarato, Enzo Tramontano, Generoso Bevilacqua,

https://doi.org/10.18632/aging.103780 pp 15978—15994

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Lessi F, Grandi N, Mazzanti CM, Civita P, Scatena C, Aretini P, Bandiera P, Fornaciari A, Giuffra V, Fornaciari G, Naccarato AG, Tramontano E, Bevilacqua G, . A human MMTV-like betaretrovirus linked to breast cancer has been present in humans at least since the copper age. . 12:15978-15994. https://doi.org/10.18632/aging.103780

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                TY  - JOUR
                AU  - Lessi, Francesca 
                AU  - Grandi, Nicole 
                AU  - Mazzanti, Chiara Maria 
                AU  - Civita, Prospero 
                AU  - Scatena, Cristian 
                AU  - Aretini, Paolo 
                AU  - Bandiera, Pasquale 
                AU  - Fornaciari, Antonio 
                AU  - Giuffra, Valentina 
                AU  - Fornaciari, Gino 
                AU  - Naccarato, Antonio Giuseppe 
                AU  - Tramontano, Enzo 
                AU  - Bevilacqua, Generoso 
                TI  - A human MMTV-like betaretrovirus linked to breast cancer has been present in humans at least since the copper age
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103780
                DO  - 10.18632/aging.103780
                SP  - 15978
                EP  - 15994
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Lessi, Francesca 
                AU  - Grandi, Nicole 
                AU  - Mazzanti, Chiara Maria 
                AU  - Civita, Prospero 
                AU  - Scatena, Cristian 
                AU  - Aretini, Paolo 
                AU  - Bandiera, Pasquale 
                AU  - Fornaciari, Antonio 
                AU  - Giuffra, Valentina 
                AU  - Fornaciari, Gino 
                AU  - Naccarato, Antonio Giuseppe 
                AU  - Tramontano, Enzo 
                AU  - Bevilacqua, Generoso 
                TI  - A human MMTV-like betaretrovirus linked to breast cancer has been present in humans at least since the copper age
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103780
                DO  - 10.18632/aging.103780
                SP  - 15978
                EP  - 15994
                PY  - 
                AB  - The betaretrovirus Mouse Mammary Tumor Virus (MMTV) is the well characterized etiological agent of mammary tumors in mice. In contrast, the etiology of sporadic human breast cancer (BC) is unknown, but accumulating data indicate a possible viral origin also for these malignancies. The presence of MMTVenv-like sequences (MMTVels) in the human salivary glands and saliva supports the latter as possible route of inter-human dissemination. In the absence of the demonstration of a mouse-man transmission of MMTV, we considered the possibility that a cross-species transmission could have occurred in ancient times. Therefore, we investigated MMTVels in the ancient dental calculus, which originates from saliva and is an excellent material for paleovirology. The calculus was collected from 36 ancient human skulls, excluding any possible mouse contamination. MMTV-like sequences were identified in the calculus of 6 individuals dated from the Copper Age to the 17th century. The MMTV-like sequences were compared with known human endogenous betaretroviruses and with animal exogenous betaretroviruses, confirming their exogenous origin and relation to MMTV. These data reveal that a human exogenous betaretrovirus similar to MMTV has existed at least since 4,500 years ago and indirectly support the hypothesis that it could play a role in human breast cancer.
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Neuroprotective effects of p62(SQSTM1)-engineered lactic acid bacteria in Alzheimer’s disease: a pre-clinical study

Valentina Cecarini, Laura Bonfili, Olee Gogoi, Solomon Lawrence, Franco M. Venanzi, Vasco Azevedo, Pamela Mancha-Agresti, Mariana Martins Drumond, Giacomo Rossi, Sara Berardi, Livio Galosi, Massimiliano Cuccioloni, Mauro Angeletti, Jan S. Suchodolski, Rachel Pilla, Jonathan A. Lidbury, Anna Maria Eleuteri,

https://doi.org/10.18632/aging.103900 pp 15995—16020

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Cecarini V, Bonfili L, Gogoi O, Lawrence S, Venanzi FM, Azevedo V, Mancha-Agresti P, Drumond MM, Rossi G, Berardi S, Galosi L, Cuccioloni M, Angeletti M, et al, . Neuroprotective effects of p62(SQSTM1)-engineered lactic acid bacteria in Alzheimer’s disease: a pre-clinical study. . 12:15995-16020. https://doi.org/10.18632/aging.103900

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                TY  - JOUR
                AU  - Cecarini, Valentina 
                AU  - Bonfili, Laura 
                AU  - Gogoi, Olee 
                AU  - Lawrence, Solomon 
                AU  - Venanzi, Franco M. 
                AU  - Azevedo, Vasco 
                AU  - Mancha-Agresti, Pamela 
                AU  - Drumond, Mariana Martins 
                AU  - Rossi, Giacomo 
                AU  - Berardi, Sara 
                AU  - Galosi, Livio 
                AU  - Cuccioloni, Massimiliano 
                AU  - Angeletti, Mauro 
                AU  - Suchodolski, Jan S. 
                AU  - Pilla, Rachel 
                AU  - Lidbury, Jonathan A. 
                AU  - Eleuteri, Anna Maria 
                TI  - Neuroprotective effects of p62(SQSTM1)-engineered lactic acid bacteria in Alzheimer’s disease: a pre-clinical study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103900
                DO  - 10.18632/aging.103900
                SP  - 15995
                EP  - 16020
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Cecarini, Valentina 
                AU  - Bonfili, Laura 
                AU  - Gogoi, Olee 
                AU  - Lawrence, Solomon 
                AU  - Venanzi, Franco M. 
                AU  - Azevedo, Vasco 
                AU  - Mancha-Agresti, Pamela 
                AU  - Drumond, Mariana Martins 
                AU  - Rossi, Giacomo 
                AU  - Berardi, Sara 
                AU  - Galosi, Livio 
                AU  - Cuccioloni, Massimiliano 
                AU  - Angeletti, Mauro 
                AU  - Suchodolski, Jan S. 
                AU  - Pilla, Rachel 
                AU  - Lidbury, Jonathan A. 
                AU  - Eleuteri, Anna Maria 
                TI  - Neuroprotective effects of p62(SQSTM1)-engineered lactic acid bacteria in Alzheimer’s disease: a pre-clinical study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103900
                DO  - 10.18632/aging.103900
                SP  - 15995
                EP  - 16020
                PY  - 
                AB  - Alzheimer&#x2019;s disease (AD) is a progressive neurodegeneration characterized by neuron death ending in memory and cognitive decline. A major concern in AD research is the identification of new therapeutics that could prevent or delay the onset of the disorder, with current treatments being effective only in reducing symptoms. In this perspective, the use of engineered probiotics as therapeutic tools for the delivery of molecules to eukaryotic cells is finding application in several disorders. This work introduces a new strategy for AD treatment based on the use of a Lactobacillus lactis strain carrying one plasmid (pExu) that contains a eukaryotic expression cassette encoding the human p62 protein. 3xTg-AD mice orally administered with these bacteria for two months showed an increased expression of endogenous p62 in the brain, with a protein delivery mechanism involving both lymphatic vessels and neural terminations, and positive effects on the major AD hallmarks. Mice showed ameliorated memory, modulation of the ubiquitin-proteasome system and autophagy, reduced levels of amyloid peptides, and diminished neuronal oxidative and inflammatory processes. Globally, we demonstrate that these extremely safe, non-pathogenic and non-invasive bacteria used as delivery vehicles for the p62 protein represent an innovative and realistic therapeutic approach in AD.
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Long non-coding RNA DLX6-AS1 facilitates bladder cancer progression through modulating miR-195-5p/VEGFA signaling pathway

Hengbing Wang, Xiaobing Niu, Hesong Jiang, Fei Mao, Bing Zhong, Xi Jiang, Guangbo Fu,

https://doi.org/10.18632/aging.103374 pp 16021—16034

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Wang H, Niu X, Jiang H, Mao F, Zhong B, Jiang X, Fu G, . Long non-coding RNA DLX6-AS1 facilitates bladder cancer progression through modulating miR-195-5p/VEGFA signaling pathway. . 12:16021-16034. https://doi.org/10.18632/aging.103374

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                TY  - JOUR
                AU  - Wang, Hengbing 
                AU  - Niu, Xiaobing 
                AU  - Jiang, Hesong 
                AU  - Mao, Fei 
                AU  - Zhong, Bing 
                AU  - Jiang, Xi 
                AU  - Fu, Guangbo 
                TI  - Long non-coding RNA DLX6-AS1 facilitates bladder cancer progression through modulating miR-195-5p/VEGFA signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103374
                DO  - 10.18632/aging.103374
                SP  - 16021
                EP  - 16034
                PY  - 
                AB  - In this study, we aim at investigating the expression and regulation role of long non-coding RNA (lncRNA) DLX6-AS1 in bladder cancer (BC). DLX6-AS1 was highly expressed in BC tissues and significant negative correlation with the 5-year survival in the BC patients. The results showed that the proliferation, migration and invasion activities of BC cells were promoted by DLX6-AS1 overexpression, while cell apoptosis was repressed. However, knockdown DLX6-AS1 presented an pposite regulatory effect, and DLX6-AS1 knockdown delayed tumor in vivo. The potential target of DLX6-AS1 in BC was predicted and verified by RIP, RNA pull-down, and dual-luciferase reporter assays as miR-195-5p. The results showed that miR-195-5p was down-regulated in BC tissues, the expression of which was significantly negative correlated with DLX6-AS1 expression. In addition, the results also showed that miR-195-5p targeted and down-regulated the VEGFA. Knockdown of DLX6-AS1 up-regulated miR-195-5p expression and down-regulated VEGFA expression. Moreover, down-regulation of VEGFA expression caused by DLX6-AS1 inhibited phosphorylation of Raf-1, MEK1/2, and ERK1/2, while miR-195-5p inhibitors abolished the effect of silencing DLX6-AS1 expression. Our study demonstrated that DLX6-AS1 played an oncogenic role in BC through miR-195-5p-mediated VEGFA/Ras/Raf/MEK/ERK pathway.
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Systems biology approach to exploring the effect of cyclic stretching on cardiac cell physiology

Chien-Cheng Chen, Tzyy-Yue Wong, Tzu-Yun Chin, Wen-Hsien Lee, Chan-Yen Kuo, Yi-Chiung Hsu,

https://doi.org/10.18632/aging.103465 pp 16035—16045

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Chen C, Wong T, Chin T, Lee W, Kuo C, Hsu Y, . Systems biology approach to exploring the effect of cyclic stretching on cardiac cell physiology. . 12:16035-16045. https://doi.org/10.18632/aging.103465

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                TY  - JOUR
                AU  - Chen, Chien-Cheng 
                AU  - Wong, Tzyy-Yue 
                AU  - Chin, Tzu-Yun 
                AU  - Lee, Wen-Hsien 
                AU  - Kuo, Chan-Yen 
                AU  - Hsu, Yi-Chiung 
                TI  - Systems biology approach to exploring the effect of cyclic stretching on cardiac cell physiology
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103465
                DO  - 10.18632/aging.103465
                SP  - 16035
                EP  - 16045
                PY  - 
                AB  - Although mechanical forces are involved in pressure-overloaded cardiomyopathy, their effects on gene transcription profiles are not fully understood. Here, we used next-generation sequencing (NGS) to investigate changes in genomic profiles after cyclic mechanical stretching of human cardiomyocytes. We found that 85, 87, 32, 29, and 28 genes were differentially expressed after 1, 4, 12, 24, and 48 hours of stretching. Furthermore, 10 of the 29 genes that were up-regulated and 11 of the 28 that were down-regulated after 24 h showed the same changes after 48 h. We then examined expression of the genes that encode serpin family E member 1 (SERPINE1), DNA-binding protein inhibitor 1 (ID1), DNA-binding protein inhibitor 3 (ID3), and CCL2, a cytokine that acts as chemotactic factor in monocytes, in an RT-PCR experiment. The same changes were observed for all four genes after all cyclic stretching durations, confirming the NGS results. Taken together, these findings suggest that cyclical stretching can alter cardiac cell physiology by activating cardiac cell metabolism and impacting cholesterol biosynthesis signaling.
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Pan-metastatic cancer analysis of prognostic factors and a prognosis-based metastatic cancer classification system

Chao Zhang, Guijun Xu, Yao Xu, Haixiao Wu, Xu Guo, Min Mao, Vladimir P. Baklaushev, Vladimir P. Chekhonin, Karl Peltzer, Ye Bai, Guowen Wang, Wenjuan Ma, Xin Wang,

https://doi.org/10.18632/aging.103467 pp 16046—16061

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Zhang C, Xu G, Xu Y, Wu H, Guo X, Mao M, Baklaushev VP, Chekhonin VP, Peltzer K, Bai Y, Wang G, Ma W, Wang X, . Pan-metastatic cancer analysis of prognostic factors and a prognosis-based metastatic cancer classification system. . 12:16046-16061. https://doi.org/10.18632/aging.103467

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                TY  - JOUR
                AU  - Zhang, Chao 
                AU  - Xu, Guijun 
                AU  - Xu, Yao 
                AU  - Wu, Haixiao 
                AU  - Guo, Xu 
                AU  - Mao, Min 
                AU  - Baklaushev, Vladimir P. 
                AU  - Chekhonin, Vladimir P. 
                AU  - Peltzer, Karl 
                AU  - Bai, Ye 
                AU  - Wang, Guowen 
                AU  - Ma, Wenjuan 
                AU  - Wang, Xin 
                TI  - Pan-metastatic cancer analysis of prognostic factors and a prognosis-based metastatic cancer classification system
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103467
                DO  - 10.18632/aging.103467
                SP  - 16046
                EP  - 16061
                PY  - 
                AB  - We aimed to perform a pan-metastatic cancer analysis on survival and prognostic factors and to create a prognosis-based classification system. We selected distant metastasis patients from the Surveillance, Epidemiology, and End Results (SEER) database. The associations between the characteristics of the patients at admission and overall survival were determined. A prognosis-based metastatic cancer classification was established based on the identified prognostic factors. The differences in prognosis among these categories were tested. The survival rate and prognostic factors were not consistent across cancers. Three metastatic cancer categories were generated, each with different prognoses. The prognostic differences among the categories were satisfactorily validated. Different metastatic cancer types had homogeneous and heterogeneous survival rates and prognostic factors. A prognosis-based classification system for synchronous distant metastasis cancer patients at admission was created. This classification system reflects the grade of malignancy in metastatic cancers and may guide the prediction of survival and individualized treatment. Moreover, it may have important implications for the management of synchronous metastatic cancers and aid clinicians in properly allocating medical resources to metastatic patients.
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Synergistic effect of electric stimulation and mesenchymal stem cells against Parkinson's disease

Chunhui Yang, Yiqing Qiu, Yuan Qing, Jinyu Xu, Wei Dai, Xiaowu Hu, Xi Wu,

https://doi.org/10.18632/aging.103477 pp 16062—16071

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Yang C, Qiu Y, Qing Y, Xu J, Dai W, Hu X, Wu X, . Synergistic effect of electric stimulation and mesenchymal stem cells against Parkinson's disease. . 12:16062-16071. https://doi.org/10.18632/aging.103477

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                TY  - JOUR
                AU  - Yang, Chunhui 
                AU  - Qiu, Yiqing 
                AU  - Qing, Yuan 
                AU  - Xu, Jinyu 
                AU  - Dai, Wei 
                AU  - Hu, Xiaowu 
                AU  - Wu, Xi 
                TI  - Synergistic effect of electric stimulation and mesenchymal stem cells against Parkinson's disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103477
                DO  - 10.18632/aging.103477
                SP  - 16062
                EP  - 16071
                PY  - 
                AB  - Electroconvulsive therapy (ECT) has known beneficial effects on the core motor symptoms of Parkinson&apos;s disease (PD), likely through induction of dopamine release and sensitivity of dopamine receptors. Mesenchymal stem cells (MSCs) can salvage loss of dopamine in PD through their differentiation into dopaminergic neurons. However, it is not known if combined ECT and MSC transplantation may have a synergistic effect against PD. Here, we showed that ECT significantly increased the differentiation of the transplanted MSCs into dopaminergic neurons in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. On the other hand, transplantation of MSCs significantly increased dopamine levels after ECT. Co-application of ECT and MSC transplantation generated a synergistic effect through increases in dopamine and decreases in pro-inflammatory cytokines, resulting in significantly attenuated defect in stepping test and rotational behavior in MPTP-mice. Together, our data suggest that combined ECT and MSC transplantation can be a valuable treatment of PD.
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Controlled attenuation parameter value-based diagnostic algorithm improves the accuracy of liver stiffness measurement in chronic hepatitis B patients

Yaoxin Fan, Lin Wang, Yang Ding, Qiuju Sheng, Chong Zhang, Yanwei Li, Chao Han, Xiaoguang Dou,

https://doi.org/10.18632/aging.103522 pp 16072—16082

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Fan Y, Wang L, Ding Y, Sheng Q, Zhang C, Li Y, Han C, Dou X, . Controlled attenuation parameter value-based diagnostic algorithm improves the accuracy of liver stiffness measurement in chronic hepatitis B patients. . 12:16072-16082. https://doi.org/10.18632/aging.103522

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                TY  - JOUR
                AU  - Fan, Yaoxin 
                AU  - Wang, Lin 
                AU  - Ding, Yang 
                AU  - Sheng, Qiuju 
                AU  - Zhang, Chong 
                AU  - Li, Yanwei 
                AU  - Han, Chao 
                AU  - Dou, Xiaoguang 
                TI  - Controlled attenuation parameter value-based diagnostic algorithm improves the accuracy of liver stiffness measurement in chronic hepatitis B patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103522
                DO  - 10.18632/aging.103522
                SP  - 16072
                EP  - 16082
                PY  - 
                AB  - Liver stiffness measurement (LSM) frequently overestimates the severity of liver fibrosis because of steatosis. However, the impact of the controlled attenuation parameter (CAP) on liver stiffness cutoff values remains unknown; CAP was used to quantify and diagnose the severity of hepatic steatosis. The study was conducted to determine the effect of CAP on liver stiffness cutoff values in chronic hepatitis B (CHB) patients. A retrospective cross-sectional study was performed in liver biopsy-proven CHB patients. The median LSM (kPa) in the elevated CAP group was higher than that in the normal CAP group at the same fibrosis stage. For S2-4, the area under the receiver operating characteristic (AUROC) curve of LSM was 0.78 and 0.72 in the normal and elevated CAP groups, respectively. When a cutoff value of 8.9 kPa was used, the diagnostic accuracy was 77.82% and 63.41% in the normal and elevated CAP groups, respectively. Compared with the alanine transaminase (ALT)-based LSM algorithm, the CAP-based LSM algorithm had a similar correct diagnosis rate (33.64% vs. 33.94%, respectively) but a lower misdiagnosis rate (16.97% vs. 20.30%, respectively). The new CAP-based LSM diagnostic algorithm will improve the diagnostic accuracy of liver fibrosis in CHB patients.
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Chidamide, a histone deacetylase inhibitor, inhibits autophagy and exhibits therapeutic implication in chronic lymphocytic leukemia

Yi-Lin Kong, Bi-Hui Pan, Jin-Hua Liang, Hua-Yuan Zhu, Li Wang, Yi Xia, Jia-Zhu Wu, Lei Fan, Jian-Yong Li, Wei Xu,

https://doi.org/10.18632/aging.103536 pp 16083—16098

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Kong Y, Pan B, Liang J, Zhu H, Wang L, Xia Y, Wu J, Fan L, Li J, Xu W, . Chidamide, a histone deacetylase inhibitor, inhibits autophagy and exhibits therapeutic implication in chronic lymphocytic leukemia. . 12:16083-16098. https://doi.org/10.18632/aging.103536

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                TY  - JOUR
                AU  - Kong, Yi-Lin 
                AU  - Pan, Bi-Hui 
                AU  - Liang, Jin-Hua 
                AU  - Zhu, Hua-Yuan 
                AU  - Wang, Li 
                AU  - Xia, Yi 
                AU  - Wu, Jia-Zhu 
                AU  - Fan, Lei 
                AU  - Li, Jian-Yong 
                AU  - Xu, Wei 
                TI  - Chidamide, a histone deacetylase inhibitor, inhibits autophagy and exhibits therapeutic implication in chronic lymphocytic leukemia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103536
                DO  - 10.18632/aging.103536
                SP  - 16083
                EP  - 16098
                PY  - 
                AB  - Novel agents have made the management of chronic lymphocytic leukemia (CLL) more promising and personalized. However, long-term treatment is still warranted which may result in toxicity and resistance. Thus, new combination therapy may help achieve deeper remission and limited-duration therapy. Histone deacetylase inhibitors (HDACi) can affect many tumors by modulating key biological functions including autophagy. Studies have shown that some novel targeted agents including ibrutinib induce autophagy. This study aimed to explore the effect of oral HDAC inhibitor, chidamide, on CLL cells as well as the role of autophagy in this process. Here, we showed that autophagy flux in CLL cells was inhibited by chidamide via post-transcriptional modulation and chidamide had cytostatic and cytotoxic effects on CLL cells. Besides, the pro-survival role of autophagy in CLL cells was validated by using autophagy inhibitor and knocking down critical autophagy gene. Notably, a combination of chidamide and ibrutinib showed significant synergism and downregulated ibrutinib-induced autophagy. This work highlights the therapeutic potential of chidamide via its effect on autophagy, especially in combination with ibrutinib.
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IL-21 mediates microRNA-423-5p /claudin-5 signal pathway and intestinal barrier function in inflammatory bowel disease

Mu Wang, Jian Guo, Yi-Qing Zhao, Jun-Ping Wang,

https://doi.org/10.18632/aging.103566 pp 16099—16110

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Wang M, Guo J, Zhao Y, Wang J, . IL-21 mediates microRNA-423-5p /claudin-5 signal pathway and intestinal barrier function in inflammatory bowel disease. . 12:16099-16110. https://doi.org/10.18632/aging.103566

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                TY  - JOUR
                AU  - Wang, Mu 
                AU  - Guo, Jian 
                AU  - Zhao, Yi-Qing 
                AU  - Wang, Jun-Ping 
                TI  - IL-21 mediates microRNA-423-5p /claudin-5 signal pathway and intestinal barrier function in inflammatory bowel disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103566
                DO  - 10.18632/aging.103566
                SP  - 16099
                EP  - 16110
                PY  - 
                AB  - Inflammatory bowel disease (IBD) is a group of chronic and recurrent nonspecific inflammatory disorders, including Crohn&apos;s disease (CD) and ulcerative colitis (UC). Due to the persistent inflammation of intestinal mucosa caused by immune disorders, barrier dysfunction may be an essential cause of the pathogenesis of IBD. Therefore, exploring the mechanism is very important to clarify the pathogenesis of IBD. In our research, we provided evidence of IL-21 function in IBD. The junction complex protein claudin-5 may be a downstream gene of the IL-21. Anti-IL-21 administrated prevented DSS-simulative colitis via recovering claudin-5 expression in the human colonic epithelial cells. Meanwhile, we described that miR-423-5p could be involved in IL-21/ claudin-5 pathway by regulating NF-&#x3BA;B/MAPKs/JNK signaling pathway, which may provide a new therapeutic target for IBD.
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Testosterone ameliorates vascular aging via the Gas6/Axl signaling pathway

Yan-Qing Chen, Hui-Min Zhou, Fang-Fang Chen, Ya-Peng Liu, Lu Han, Ming Song, Zhi-Hao Wang, Wei Zhang, Yuan-Yuan Shang, Ming Zhong,

https://doi.org/10.18632/aging.103584 pp 16111—16125

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Chen Y, Zhou H, Chen F, Liu Y, Han L, Song M, Wang Z, Zhang W, Shang Y, Zhong M, . Testosterone ameliorates vascular aging via the Gas6/Axl signaling pathway. . 12:16111-16125. https://doi.org/10.18632/aging.103584

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                TY  - JOUR
                AU  - Chen, Yan-Qing 
                AU  - Zhou, Hui-Min 
                AU  - Chen, Fang-Fang 
                AU  - Liu, Ya-Peng 
                AU  - Han, Lu 
                AU  - Song, Ming 
                AU  - Wang, Zhi-Hao 
                AU  - Zhang, Wei 
                AU  - Shang, Yuan-Yuan 
                AU  - Zhong, Ming 
                TI  - Testosterone ameliorates vascular aging via the Gas6/Axl signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103584
                DO  - 10.18632/aging.103584
                SP  - 16111
                EP  - 16125
                PY  - 
                AB  - Low serum testosterone level is associated with aging-related vascular stiffness, but the underlying mechanism is unclear. The Growth arrest-specific protein 6 (Gas6) /Axl pathway has been proved to play important roles in cell senescence. In this study, we intend to explore whether Gas6/Axl is involved in the effect of testosterone on vascular aging amelioration. Vascular aging models of wild type and Axl-/- mice were established by natural aging. Mice of these two gene types were randomized into young group, aging group and testosterone undecanoate (TU) treatment group. Mice were treated with TU (37.9 mg/kg) in the TU group, which treated with solvent reagent served as control. The aging mice exhibited decreases in serum testosterone, Gas6 and Axl levels and an increase in cell senescence, manifested age-related vascular remodeling. Testosterone treatment induced testosterone and Gas6 levels in serum, and ameliorated cell senescence and vascular remodeling in aging mice. Furthermore, we uncover the underlying molecular mechanism and show that testosterone treatment restored the phosphorylation of Akt and FoxO1a. Axl knockout accelerated cell senescence and vascular remodeling, and resisted the anti-aging effect of testosterone. Testosterone might exert a protective effect on vascular aging by improving cell senescence and vascular remodeling through the Gas6/Axl pathway.
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SIRT1 alleviates high-magnitude compression-induced senescence in nucleus pulposus cells via PINK1-dependent mitophagy

Yiyang Wang, Haoming Wang, Yunyun Zhuo, Yanzhu Hu, Zetong Zhang, Jixing Ye, Liehua Liu, Lei Luo, Chen Zhao, Qiang Zhou, Pei Li,

https://doi.org/10.18632/aging.103587 pp 16126—16141

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Wang Y, Wang H, Zhuo Y, Hu Y, Zhang Z, Ye J, Liu L, Luo L, Zhao C, Zhou Q, Li P, . SIRT1 alleviates high-magnitude compression-induced senescence in nucleus pulposus cells via PINK1-dependent mitophagy. . 12:16126-16141. https://doi.org/10.18632/aging.103587

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                TY  - JOUR
                AU  - Wang, Yiyang 
                AU  - Wang, Haoming 
                AU  - Zhuo, Yunyun 
                AU  - Hu, Yanzhu 
                AU  - Zhang, Zetong 
                AU  - Ye, Jixing 
                AU  - Liu, Liehua 
                AU  - Luo, Lei 
                AU  - Zhao, Chen 
                AU  - Zhou, Qiang 
                AU  - Li, Pei 
                TI  - SIRT1 alleviates high-magnitude compression-induced senescence in nucleus pulposus cells via PINK1-dependent mitophagy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103587
                DO  - 10.18632/aging.103587
                SP  - 16126
                EP  - 16141
                PY  - 
                AB  - Mechanical overloading-induced nucleus pulposus (NP) cells senescence plays an important role in the pathogenesis of intervertebral disc degeneration (IVDD). The silent mating type information regulator 2 homolog-1 (SIRT1)-mediated pathway preserves the normal NP cell phenotype and mitochondrial homeostasis under multiple stresses. We aimed to investigate the role of SIRT1 in IVDD by assessing the effects of SIRT1 overexpression on high-magnitude compression-induced senescence in NP cells. High-magnitude compression induced cellular senescence and mitochondrial dysfunction in human NP cells. Moreover, SIRT1 overexpression tended to alleviate NP cell senescence and mitochondrial dysfunction under compressive stress. Given the mitophagy-inducing property of SIRT1, activity of mitophagy was evaluated in NP cells to further demonstrate the underlying mechanism. The results showed that SIRT1-overexpression attenuated senescence and mitochondrial injury in NP cells subjected to high-magnitude compression. However, depletion of PINK1, a key mitophagic regulator, impaired mitophagy and blocked the protective role of SIRT1 against compression induced senescence in NP cells. In summary, these results suggest that SIRT1 plays a protective role in alleviating NP cell senescence and mitochondrial dysfunction under high-magnitude compression, the mechanism of which is associated with the regulation of PINK1-dependent mitophagy. Our findings may provide a potential therapeutic approach for IVDD treatment.
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LAIR-1 suppresses cell growth of ovarian cancer cell via the PI3K-AKT-mTOR pathway

Yan Liu, Li Ma, Fugen Shangguan, Xuena Zhao, Wenjie Wang, Zhiyue Gao, Huimin Zhou, Guiwu Qu, Yumei Huang, Jing An, Jiangnan Xue, Shude Yang, Qizhi Cao,

https://doi.org/10.18632/aging.103589 pp 16142—16154

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Liu Y, Ma L, Shangguan F, Zhao X, Wang W, Gao Z, Zhou H, Qu G, Huang Y, An J, Xue J, Yang S, Cao Q, . LAIR-1 suppresses cell growth of ovarian cancer cell via the PI3K-AKT-mTOR pathway. . 12:16142-16154. https://doi.org/10.18632/aging.103589

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                TY  - JOUR
                AU  - Liu, Yan 
                AU  - Ma, Li 
                AU  - Shangguan, Fugen 
                AU  - Zhao, Xuena 
                AU  - Wang, Wenjie 
                AU  - Gao, Zhiyue 
                AU  - Zhou, Huimin 
                AU  - Qu, Guiwu 
                AU  - Huang, Yumei 
                AU  - An, Jing 
                AU  - Xue, Jiangnan 
                AU  - Yang, Shude 
                AU  - Cao, Qizhi 
                TI  - LAIR-1 suppresses cell growth of ovarian cancer cell via the PI3K-AKT-mTOR pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103589
                DO  - 10.18632/aging.103589
                SP  - 16142
                EP  - 16154
                PY  - 
                AB  - Recently, over-expression of LAIR-1 has been found in some solid cancers, including ovarian cancer. The role of LAIR-1 in cancer progression needs further investigation. In this study, we identified the LAIR-1 cDNA sequence of the ovarian cancer cells HO8910. Using SKOV3 cells, we confirmed the finding from our previous study that LAIR-1 could suppress in vitro cell proliferation and cell migration. We also found LAIR-1 overexpression can induce apoptosis of SKOV3 cells. We revealed LAIR-1 suppressed cell growth by inhibiting the PI3K-AKT-mTOR axis. Moreover, the LAIR-1 antitumor activity and its mechanism were also identified in vivo. We used Co-IP assay and mass spectrometry to identify potential LAIR-1-binding proteins in LAIR-1 overexpressing SKOV3 cells. MS analysis identified 167 potentially interacting proteins. GO analyses indicated a possible involvement of LAIR-1 in mRNA processing through its interaction with some eukaryotic translation initiation factors (eIF4E1B, eIF2S3, eIF3D, eIF4G2, eIF5B) and eukaryotic translation elongation factors (eEF1A2 and eEF1B2). Our findings suggest that LAIR-1 may suppress the growth of ovarian cancer cells by serving as a modulator that suppresses PI3K-AKT-mTOR directly or regulating protein synthesis at the translational level. Our results indicate that a LAIR-1-based strategy may prevent or suppress the progression of ovarian cancer.
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RPP30, a transcriptional regulator, is a potential pathogenic factor in glioblastoma

Guanzhang Li, You Zhai, Hanjie Liu, Zhiliang Wang, Ruoyu Huang, Haoyu Jiang, Yuemei Feng, Yuanhao Chang, Fan Wu, Fan Zeng, Tao Jiang, Wei Zhang,

https://doi.org/10.18632/aging.103596 pp 16155—16171

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Li G, Zhai Y, Liu H, Wang Z, Huang R, Jiang H, Feng Y, Chang Y, Wu F, Zeng F, Jiang T, Zhang W, . RPP30, a transcriptional regulator, is a potential pathogenic factor in glioblastoma. . 12:16155-16171. https://doi.org/10.18632/aging.103596

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                TY  - JOUR
                AU  - Li, Guanzhang 
                AU  - Zhai, You 
                AU  - Liu, Hanjie 
                AU  - Wang, Zhiliang 
                AU  - Huang, Ruoyu 
                AU  - Jiang, Haoyu 
                AU  - Feng, Yuemei 
                AU  - Chang, Yuanhao 
                AU  - Wu, Fan 
                AU  - Zeng, Fan 
                AU  - Jiang, Tao 
                AU  - Zhang, Wei 
                TI  - RPP30, a transcriptional regulator, is a potential pathogenic factor in glioblastoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103596
                DO  - 10.18632/aging.103596
                SP  - 16155
                EP  - 16171
                PY  - 
                AB  - Background: Old age has been demonstrated to be a risk factor for GBM, but the underlying biological mechanism is still unclear. We designed this study intending to determine a mechanistic explanation for the link between age and pathogenesis in GBM.Results: The expression of RPP30, an independent prognostic factor in GBM, was negatively correlated with age in both tumor and non-tumor brain samples. However, the post-transcriptional modifications carried out by RPP30 were different in primary GBM and non-tumor brain samples. RPP30 affected protein expression of cancer pathways by performing RNA modifications. Further, we found that RPP30 was related to drug metabolism pathways important in GBM. The decreased expression of RPP30 in older patients might be a pathogenic factor for GBM.Conclusion: This study revealed the role of RPP30 in gliomagenesis and provided the theoretical foundation for targeted therapy.Methods: In total, 616 primary GBM samples and 41 non-tumor brain samples were enrolled in this study. Transcriptome data and clinical information were obtained from the CGGA, TCGA, and GSE53890 databases. Gene Set Variation Analysis and Gene Ontology analyses were the primary analytical methods used in this study. All statistical analyses were performed using R.
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Leptin promotes bone metastasis of breast cancer by activating the SDF-1/CXCR4 axis

Lixia Duan, Yongkui Lu, Weimin Xie, Li Nong, Yuxian Jia, Aihua Tan, Yan Liu,

https://doi.org/10.18632/aging.103599 pp 16172—16182

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Duan L, Lu Y, Xie W, Nong L, Jia Y, Tan A, Liu Y, . Leptin promotes bone metastasis of breast cancer by activating the SDF-1/CXCR4 axis. . 12:16172-16182. https://doi.org/10.18632/aging.103599

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                TY  - JOUR
                AU  - Duan, Lixia 
                AU  - Lu, Yongkui 
                AU  - Xie, Weimin 
                AU  - Nong, Li 
                AU  - Jia, Yuxian 
                AU  - Tan, Aihua 
                AU  - Liu, Yan 
                TI  - Leptin promotes bone metastasis of breast cancer by activating the SDF-1/CXCR4 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103599
                DO  - 10.18632/aging.103599
                SP  - 16172
                EP  - 16182
                PY  - 
                AB  - Obesity is associated with an increased risk of tumorigenesis, and increased leptin levels can promote tumor metastasis. However, the effects of leptin on bone metastasis in breast cancer are not fully understood. Here, we examined leptin receptor expression and bone metastasis in tissue samples from 96 breast cancer patients. In addition, we investigated the effects of leptin on the metastatic capacity of breast cancer cells in vitro using a transwell assays. The results indicated that higher leptin receptor levels in breast cancer cells are associated with increased incidence of bone metastasis in breast cancer patients. Additionally, leptin promoted migration and invasion of breast cancer cells. The SDF-1/CXCR4 axis activated by leptin also promoted bone metastasis of breast cancer. Finally, increased CXCR4 expression was accompanied by high leptin receptor expression in bone metastatic tissues from breast cancer patients. These results indicate that leptin induces bone metastasis of breast cancer by activating the SDF-1/CXCR4 axis.
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Differential functional dysconnectivity of caudate nucleus subdivisions in Parkinson’s disease

Xiuqin Jia, Zhenyu Pan, Huimin Chen, Zhijiang Wang, Kun Li, Xuemei Wang, Zhan Wang, Huizi Ma, Tao Feng, Qi Yang,

https://doi.org/10.18632/aging.103628 pp 16183—16194

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Jia X, Pan Z, Chen H, Wang Z, Li K, Wang X, Wang Z, Ma H, Feng T, Yang Q, . Differential functional dysconnectivity of caudate nucleus subdivisions in Parkinson’s disease. . 12:16183-16194. https://doi.org/10.18632/aging.103628

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                TY  - JOUR
                AU  - Jia, Xiuqin 
                AU  - Pan, Zhenyu 
                AU  - Chen, Huimin 
                AU  - Wang, Zhijiang 
                AU  - Li, Kun 
                AU  - Wang, Xuemei 
                AU  - Wang, Zhan 
                AU  - Ma, Huizi 
                AU  - Feng, Tao 
                AU  - Yang, Qi 
                TI  - Differential functional dysconnectivity of caudate nucleus subdivisions in Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103628
                DO  - 10.18632/aging.103628
                SP  - 16183
                EP  - 16194
                PY  - 
                AB  - Caudate dopaminergic dysfunction is implied in the pathophysiology of patients with Parkinson&#x2019;s disease (PD). Still, connectivity specificities of the caudate nucleus (CN) subdivisions and the effect of dopamine are poorly understood. We collected MRI and neuropsychological data from 34 PD patients and 26 age- and sex-matched healthy elderly individuals (HEs) in this study. Resting-state functional connectivity analysis revealed that compared to the other CN subdivisions, the CN head was more strongly connected to the default mode network (DMN), the CN body to the frontoparietal network (FPN), and the CN tail to the visual network in HEs. PD patients off medication showed reduced connectivity within all these subdivision networks. In PD patients on medication, functional connectivity in the CN head network was significantly improved in the medial prefrontal cortex and in the body network it was improved in the dorsolateral prefrontal cortex. These improvements contributed to ameliorated motivation and cognitive function in PD patients. Our results highlighted the specific alterations and dopamine modulation in these CN subdivision networks in PD, which may provide insight into the pathophysiology and therapeutics of this disease.
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Cortical aging – new insights with multiparametric quantitative MRI

Alexander Seiler, Sophie Schöngrundner, Benjamin Stock, Ulrike Nöth, Elke Hattingen, Helmuth Steinmetz, Johannes C. Klein, Simon Baudrexel, Marlies Wagner, Ralf Deichmann, René-Maxime Gracien,

https://doi.org/10.18632/aging.103629 pp 16195—16210

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Seiler A, Schöngrundner S, Stock B, Nöth U, Hattingen E, Steinmetz H, Klein JC, Baudrexel S, Wagner M, Deichmann R, Gracien R, . Cortical aging – new insights with multiparametric quantitative MRI. . 12:16195-16210. https://doi.org/10.18632/aging.103629

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                TY  - JOUR
                AU  - Seiler, Alexander 
                AU  - Schöngrundner, Sophie 
                AU  - Stock, Benjamin 
                AU  - Nöth, Ulrike 
                AU  - Hattingen, Elke 
                AU  - Steinmetz, Helmuth 
                AU  - Klein, Johannes C. 
                AU  - Baudrexel, Simon 
                AU  - Wagner, Marlies 
                AU  - Deichmann, Ralf 
                AU  - Gracien, René-Maxime 
                TI  - Cortical aging – new insights with multiparametric quantitative MRI
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103629
                DO  - 10.18632/aging.103629
                SP  - 16195
                EP  - 16210
                PY  - 
                AB  - Understanding the microstructural changes related to physiological aging of the cerebral cortex is pivotal to differentiate healthy aging from neurodegenerative processes. The aim of this study was to investigate the age-related global changes of cortical microstructure and regional patterns using multiparametric quantitative MRI (qMRI) in healthy subjects with a wide age range. 40 healthy participants (age range: 2nd to 8th decade) underwent high-resolution qMRI including T1, PD as well as T2, T2* and T2&#x2032; mapping at 3 Tesla. Cortical reconstruction was performed with the FreeSurfer toolbox, followed by tests for correlations between qMRI parameters and age. Cortical T1 values were negatively correlated with age (p=0.007) and there was a widespread age-related decrease of cortical T1 involving the frontal and the parietotemporal cortex, while T2 was correlated positively with age, both in frontoparietal areas and globally (p=0.004). Cortical T2&#x2032; values showed the most widespread associations across the cortex and strongest correlation with age (r= -0.724, p=0.0001). PD and T2* did not correlate with age. Multiparametric qMRI allows to characterize cortical aging, unveiling parameter-specific patterns. Quantitative T2&#x2032; mapping seems to be a promising imaging biomarker of cortical age-related changes, suggesting that global cortical iron deposition is a prominent process in healthy aging.
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Mst1 promotes mitochondrial dysfunction and apoptosis in oxidative stress-induced rheumatoid arthritis synoviocytes

Yingjie Wang, Qi Yang, Songpo Shen, Linjie Zhang, Yongbo Xiang, Xisheng Weng,

https://doi.org/10.18632/aging.103643 pp 16211—16223

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Wang Y, Yang Q, Shen S, Zhang L, Xiang Y, Weng X, . Mst1 promotes mitochondrial dysfunction and apoptosis in oxidative stress-induced rheumatoid arthritis synoviocytes. . 12:16211-16223. https://doi.org/10.18632/aging.103643

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                TY  - JOUR
                AU  - Wang, Yingjie 
                AU  - Yang, Qi 
                AU  - Shen, Songpo 
                AU  - Zhang, Linjie 
                AU  - Xiang, Yongbo 
                AU  - Weng, Xisheng 
                TI  - Mst1 promotes mitochondrial dysfunction and apoptosis in oxidative stress-induced rheumatoid arthritis synoviocytes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103643
                DO  - 10.18632/aging.103643
                SP  - 16211
                EP  - 16223
                PY  - 
                AB  - In this study, we investigated the role of macrophage stimulating 1 (Mst1) and the AMPK-Sirt1 signaling pathway in the oxidative stress-induced mitochondrial dysfunction and apoptosis seen in rheumatoid arthritis-related fibroblast-like synoviocytes (RA-FLSs). Mst1 mRNA and protein expression was significantly higher in hydrogen peroxide (H2O2)-treated RA-FLSs than untreated controls. H2O2 treatment induced the mitochondrial apoptotic pathway by activating caspase3/9 and Bax in the RA-FLSs. Moreover, H2O2 treatment significantly reduced mitochondrial membrane potential and mitochondrial state-3 and state-4 respiration, but increased reactive oxygen species (ROS). Mst1 silencing significantly reduced oxidative stress-induced mitochondrial dysfunction and apoptosis in RA-FLSs. Sirt1 expression was significantly reduced in the H2O2-treated RA-FLSs, but was higher in the H2O2-treated Mst1-silenced RA-FLSs. Pretreatment with selisistat (Sirt1-specific inhibitor) or compound C (AMPK antagonist) significantly reduced the viability and mitochondrial function in H2O2-treated Mst1-silenced RA-FLSs by inhibiting Sirt1 function or Sirt1 expression, respectively. These findings demonstrate that oxidative stress-related upregulation and activation of Mst1 promotes mitochondrial dysfunction and apoptosis in RA-FLSs by inhibiting the AMPK-Sirt1 signaling pathway. This suggests the Mst1-AMPK-Sirt1 axis is a potential target for RA therapy.
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SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury

Ting Xin, Chengzhi Lu,

https://doi.org/10.18632/aging.103644 pp 16224—16237

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Xin T, Lu C, . SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury. . 12:16224-16237. https://doi.org/10.18632/aging.103644

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                TY  - JOUR
                AU  - Xin, Ting 
                AU  - Lu, Chengzhi 
                TI  - SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103644
                DO  - 10.18632/aging.103644
                SP  - 16224
                EP  - 16237
                PY  - 
                AB  - Sirtuin-3 (SirT3) and AMPK stimulate mitochondrial biogenesis, which increases mitochondrial turnover and cardiomyocyte regeneration. We studied the effects of SirT3, AMPK, and mitochondrial biogenesis on sepsis-induced myocardial injury. Our data showed that after treating cardiomyocytes with lipopolysaccharide, SirT3 and AMPK levels decreased, and this was followed by mitochondrial dysfunction and cardiomyocyte death. Overexpression of SirT3 activated the AMPK pathway and improved mitochondrial biogenesis, which is required to sustain mitochondrial redox balance, maintain mitochondrial respiration, and suppress mitochondrial apoptosis. Inhibition of mitochondrial biogenesis abolished SirT3/AMPK-induced cardioprotection by causing mitochondrial damage. These findings indicate that SirT3 reduces sepsis-induced myocardial injury by activating AMPK-related mitochondrial biogenesis.
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Prognostic values of GPNMB identified by mining TCGA database and STAD microenvironment

Kunhou Yao, Lunshou Wei, Junjie Zhang, Chenyu Wang, Chaoyang Wang, Changjiang Qin, Song Li,

https://doi.org/10.18632/aging.103646 pp 16238—16254

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Yao K, Wei L, Zhang J, Wang C, Wang C, Qin C, Li S, . Prognostic values of GPNMB identified by mining TCGA database and STAD microenvironment. . 12:16238-16254. https://doi.org/10.18632/aging.103646

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                TY  - JOUR
                AU  - Yao, Kunhou 
                AU  - Wei, Lunshou 
                AU  - Zhang, Junjie 
                AU  - Wang, Chenyu 
                AU  - Wang, Chaoyang 
                AU  - Qin, Changjiang 
                AU  - Li, Song 
                TI  - Prognostic values of GPNMB identified by mining TCGA database and STAD microenvironment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103646
                DO  - 10.18632/aging.103646
                SP  - 16238
                EP  - 16254
                PY  - 
                AB  - The survival rate of stomach adenocarcinoma patients with immune and stromal scores and different clinicopathological features obtained from the TCGA datasets was systematically compared. A list of genes that are correlated with stomach adenocarcinoma microenvironment were extracted using the TCGA database to predict the prognosis and survival. In addition, the differentially expressed genes were extracted by comparing the immune and stromal scores of the groups. The protein-protein interaction network, and functional and pathway enrichment analyses of differentially expressed genes were performed. A total of 8 hub genes were selected from the differentially expressed genes to predict the overall survival and disease-free survival rates. GPNMB was selected from the hub genes based on the survival and prognosis analyses. A nomogram was built by including the potential risk factors based on multivariate Cox analysis. Cell function experiments and xenograft tumors were conducted in vivo to further verify the role of GPNMB in tumor progression. The predicted microRNA, miR-30b-3p, might act as upstream negative regulator and binding to 3&#x2019; UTR of GPNMB, confirming by fluorescent enzyme reporter gene experiment. In summary, immune-related scores are crucial factors in the malignant progression of stomach adenocarcinoma and GPNMB acts as a potentially useful prognostic factor for stratification and in developing the treatment strategy
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Glucose and cholesterol induce abnormal cell divisions via DAF-12 and MPK-1 in C. elegans

Zhi Qu, Shaoping Ji, Shanqing Zheng,

https://doi.org/10.18632/aging.103647 pp 16255—16269

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Qu Z, Ji S, Zheng S, . Glucose and cholesterol induce abnormal cell divisions via DAF-12 and MPK-1 in C. elegans. . 12:16255-16269. https://doi.org/10.18632/aging.103647

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Provider: 
 TY - JOUR
 AU - Qu, Zhi 
 AU - Ji, Shaoping 
 AU - Zheng, Shanqing 
 TI - Glucose and cholesterol induce abnormal cell divisions via DAF-12 and MPK-1 in C. elegans
 JO - 
 JA - 
 VL - 12
 IS - 16
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103647
 DO - 10.18632/aging.103647
 SP - 16255
 EP - 16269
 PY - 
 AB - People exposed to starvation have a high risk of developing cancer later in life, and prior studies have shown these individuals have high insulin and cholesterol levels and are sensitive to glucose. Using C. elegans as a model, we found that glucose and cholesterol can promote survival and cause starved L1 diapause worms to undergo abnormal neuronal cell divisions. Starvation has also been shown to promote long-term survival; however, we found that the functions of glucose and cholesterol in relation to these cell divisions are distinct from their effects on survival. We demonstrate that glucose functions in a DAF-16/FOXO-independent IIS pathway to activate the MAPK ontogenetic signaling to induce neuronal Q-cell divisions, and cholesterol works through DAF-12/steroidogenic pathways to promote these cell divisions. daf-12 and mpk-1/MAPK mutants suppress the function of glucose and cholesterol in these divisions, and a fully functioning dpMPK-1 requires the steroid hormone receptor DAF-12 for these divisions to occur. These afflictions also can be passed on to the immediate progeny. This work indicates a possible link between glucose and cholesterol in starved animals and an increased risk of cancer.
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CTCF promotes colorectal cancer cell proliferation and chemotherapy resistance to 5-FU via the P53-Hedgehog axis

Qiuhua Lai, Qingyuan Li, Chengcheng He, Yuxin Fang, Simin Lin, Jianqun Cai, Jian Ding, Qian Zhong, Yue Zhang, Changjie Wu, Xinke Wang, Juan He, Yongfeng Liu, Qun Yan, Aimin Li, Side Liu,

https://doi.org/10.18632/aging.103648 pp 16270—16293

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Lai Q, Li Q, He C, Fang Y, Lin S, Cai J, Ding J, Zhong Q, Zhang Y, Wu C, Wang X, He J, Liu Y, et al, . CTCF promotes colorectal cancer cell proliferation and chemotherapy resistance to 5-FU via the P53-Hedgehog axis. . 12:16270-16293. https://doi.org/10.18632/aging.103648

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                TY  - JOUR
                AU  - Lai, Qiuhua 
                AU  - Li, Qingyuan 
                AU  - He, Chengcheng 
                AU  - Fang, Yuxin 
                AU  - Lin, Simin 
                AU  - Cai, Jianqun 
                AU  - Ding, Jian 
                AU  - Zhong, Qian 
                AU  - Zhang, Yue 
                AU  - Wu, Changjie 
                AU  - Wang, Xinke 
                AU  - He, Juan 
                AU  - Liu, Yongfeng 
                AU  - Yan, Qun 
                AU  - Li, Aimin 
                AU  - Liu, Side 
                TI  - CTCF promotes colorectal cancer cell proliferation and chemotherapy resistance to 5-FU via the P53-Hedgehog axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103648
                DO  - 10.18632/aging.103648
                SP  - 16270
                EP  - 16293
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Lai, Qiuhua 
                AU  - Li, Qingyuan 
                AU  - He, Chengcheng 
                AU  - Fang, Yuxin 
                AU  - Lin, Simin 
                AU  - Cai, Jianqun 
                AU  - Ding, Jian 
                AU  - Zhong, Qian 
                AU  - Zhang, Yue 
                AU  - Wu, Changjie 
                AU  - Wang, Xinke 
                AU  - He, Juan 
                AU  - Liu, Yongfeng 
                AU  - Yan, Qun 
                AU  - Li, Aimin 
                AU  - Liu, Side 
                TI  - CTCF promotes colorectal cancer cell proliferation and chemotherapy resistance to 5-FU via the P53-Hedgehog axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103648
                DO  - 10.18632/aging.103648
                SP  - 16270
                EP  - 16293
                PY  - 
                AB  - CTCF is overexpressed in several cancers and plays crucial roles in regulating aggressiveness, but little is known about whether CTCF drives colorectal cancer progression. Here, we identified a tumor-promoting role for CTCF in colorectal cancer. Our study demonstrated that CTCF was upregulated in colorectal cancer specimens compared with adjacent noncancerous colorectal tissues. The overexpression of CTCF promoted colorectal cancer cell proliferation and tumor growth, while the opposite effects were observed in CTCF knockdown cells. Increased GLI1, Shh, PTCH1, and PTCH2 levels were observed in CTCF-overexpressing cells using western blot analyses. CCK-8 and apoptosis assays revealed that 5-fluorouracil chemosensitivity was negatively associated with CTCF expression. Furthermore, we identified that P53 is a direct transcriptional target gene of CTCF in colorectal cancer. Western blot and nuclear&#x2002;extract assays showed that inhibition of P53 can counteract Hedgehog signaling pathway repression induced by CTCF knockdown. In conclusion, we uncovered a crucial role for CTCF regulation that possibly involves the P53-Hedgehog axis and highlighted the clinical utility of colorectal cancer-specific potential therapeutic target as disease progression or clinical response biomarkers.
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Circulating exosomal miR-144-3p inhibits the mobilization of endothelial progenitor cells post myocardial infarction via regulating the MMP9 pathway

Yihai Liu, Jiamin Xu, Rong Gu, Zhu Li, Kun Wang, Yu Qi, Xuan Sun, Jun Xie, Lian Wang, Biao Xu, Lina Kang,

https://doi.org/10.18632/aging.103651 pp 16294—16303

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Liu Y, Xu J, Gu R, Li Z, Wang K, Qi Y, Sun X, Xie J, Wang L, Xu B, Kang L, . Circulating exosomal miR-144-3p inhibits the mobilization of endothelial progenitor cells post myocardial infarction via regulating the MMP9 pathway. . 12:16294-16303. https://doi.org/10.18632/aging.103651

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                TY  - JOUR
                AU  - Liu, Yihai 
                AU  - Xu, Jiamin 
                AU  - Gu, Rong 
                AU  - Li, Zhu 
                AU  - Wang, Kun 
                AU  - Qi, Yu 
                AU  - Sun, Xuan 
                AU  - Xie, Jun 
                AU  - Wang, Lian 
                AU  - Xu, Biao 
                AU  - Kang, Lina 
                TI  - Circulating exosomal miR-144-3p inhibits the mobilization of endothelial progenitor cells post myocardial infarction via regulating the MMP9 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103651
                DO  - 10.18632/aging.103651
                SP  - 16294
                EP  - 16303
                PY  - 
                AB  - Background: The angiogenesis post myocardial infarction (MI) is compromised in diabetes. MiR-144-3p is reported to be highly expressed in circulating exosomes of diabetic patients, implying its role in diabetic complications. However, whether circulating exosomes and enriched miR-144-3p are involved in the impaired neovascularization in diabetes and the underlying mechanism is unclear.
                Results: DMexo and miR-144-3p mimic-treated MSCs had elevated miR-144-3p levels and decreased MMP9, Ets1 and PLG expression. The percentage of EPCs were relatively lower in DMexo-treated or agomir-treated MI mice compared with MI mice. Finally, the luciferase assay confirmed the direct binding between miR-144-3p and Ets1.
                Conclusion: Exosomal miR-144-3p could impair the mobilization ability of EPCs, which was associated with impaired ischemia-induced neovascularization.
                Methods: Circulating exosomes were isolated from Streptozotocin (STZ)-induced mice. In vitro, mesenchymal stem cells (MSCs) were incubated with exosomes from diabetic mice (DMexo), and miR-144-3p mimic or inhibitor. miR-144-3p, and MMP9 pathway were measured using qPCR and immunoblotting. In vivo, MI mice induced by left anterior descending ligation were treated with DMexo, as well as miR-144-3p agomir. Flow cytometry was used to profile endothelial progenitor cells (EPCs) in peripheral blood and bone marrow post 24 hours respectively.
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SP1-induced HOXD-AS1 promotes malignant progression of cholangiocarcinoma by regulating miR-520c-3p/MYCN

Jinglin Li, Xingming Jiang, Zhenglong Li, Lining Huang, Daolin Ji, Liang Yu, Yongxu Zhou, Yunfu Cui,

https://doi.org/10.18632/aging.103660 pp 16304—16325

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Li J, Jiang X, Li Z, Huang L, Ji D, Yu L, Zhou Y, Cui Y, . SP1-induced HOXD-AS1 promotes malignant progression of cholangiocarcinoma by regulating miR-520c-3p/MYCN. . 12:16304-16325. https://doi.org/10.18632/aging.103660

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                TY  - JOUR
                AU  - Li, Jinglin 
                AU  - Jiang, Xingming 
                AU  - Li, Zhenglong 
                AU  - Huang, Lining 
                AU  - Ji, Daolin 
                AU  - Yu, Liang 
                AU  - Zhou, Yongxu 
                AU  - Cui, Yunfu 
                TI  - SP1-induced HOXD-AS1 promotes malignant progression of cholangiocarcinoma by regulating miR-520c-3p/MYCN
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103660
                DO  - 10.18632/aging.103660
                SP  - 16304
                EP  - 16325
                PY  - 
                AB  - The purpose of this article is to explore the function and mechanism of HOXD-AS1 in cholangiocarcinoma. TCGA, StarBase and JASPAR were applied to predict the differential expression and molecular mechanism. The qRT-PCR was conducted to detect molecular expression. The effect of HOXD-AS1 on tumor proliferation, metastasis and stemness was measured through corresponding experiments. ChIP, luciferase reporter and RIP assays were implemented to explore the regulatory mechanism of HOXD-AS1 in CCA. In this study, HOXD-AS1 expression was significantly upregulated in CCA tissues and cells compared with control groups, respectively. Increased HOXD-AS1 was markedly correlated with lymph node invasion, advanced TNM stage and poor survival of CCA patients. Moreover, HOXD-AS1 was confirmed to be an unfavorable independent prognostic factor for CCA patients. Functionally, gain- and loss-of-function experiments demonstrated that HOXD-AS1 facilitated tumor proliferation, migration, invasion, EMT, stemness and drug resistance in vitro and in vivo. For the mechanism, transcription factor SP1-induced HOXD-AS1 upregulated oncogene MYCN through competitively binding to miR-520c-3p. Furthermore, HOXD-AS1-induced malignant phenotypes were rescued by interfering miR-520c-3p and MYCN, respectively. SP1/HOXD-AS1/miR-520c-3p/MYCN plays a vital role in initiation and progression of CCA, and HOXD-AS1 is expected to be an efficient biomarker and therapeutic target.
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PTEN participates in airway remodeling of asthma by regulating CD38/Ca²⁺/CREB signaling

Yuanyuan Wu, Yiyi Lu, Fan Zou, Xinping Fan, Xudong Li, Hongni Zhang, Haijuan Chen, Xiuzhen Sun, Yun Liu,

https://doi.org/10.18632/aging.103664 pp 16326—16340

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Wu Y, Lu Y, Zou F, Fan X, Li X, Zhang H, Chen H, Sun X, Liu Y, . PTEN participates in airway remodeling of asthma by regulating CD38/Ca²⁺/CREB signaling. . 12:16326-16340. https://doi.org/10.18632/aging.103664

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Provider: 
 TY - JOUR
 AU - Wu, Yuanyuan 
 AU - Lu, Yiyi 
 AU - Zou, Fan 
 AU - Fan, Xinping 
 AU - Li, Xudong 
 AU - Zhang, Hongni 
 AU - Chen, Haijuan 
 AU - Sun, Xiuzhen 
 AU - Liu, Yun 
 TI - PTEN participates in airway remodeling of asthma by regulating CD38/Ca2+/CREB signaling
 JO - 
 JA - 
 VL - 12
 IS - 16
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103664
 DO - 10.18632/aging.103664
 SP - 16326
 EP - 16340
 PY - 
 AB - Both phosphatase and tensin homologue deleted on chromosome ten (PTEN) and cluster of differentiation 38 (CD38) have been suggested to be key regulators of the pathogenesis of asthma. However, the precise role and molecular mechanisms by which PTEN and CD38 are involved in airway remodeling throughout asthma pathogenesis remains poorly understood. This study aimed to elucidate the role of PTEN and CD38 in airway remodeling of asthma. Exposure to tumor necrosis factor-&#x3B1; (TNF-&#x3B1;) in airway smooth muscle (ASM) cells markedly decreased PTEN expression, and increased expression of CD38. Overexpression of PTEN suppressed the expression of CD38 and downregulated proliferation and migration induced by TNF-&#x3B1; stimulation, which was partially reversed by CD38 overexpression. PTEN/CD38 axis regulated Ca2+ levels and cyclic AMP response-element binding protein (CREB) phosphorylation in TNF-&#x3B1;-stimulated ASM cells. The in vitro knockdown of CD38 or overexpression of PTEN remarkably restricted airway remodeling and decreased Ca2+ concentrations and CREB phosphorylation in asthmatic mice. CD38 overexpression abolished the inhibitory effects of PTEN overexpression on airway remodeling. These findings demonstrate that PTEN inhibits airway remodeling of asthma through the downregulation of CD38-mediated Ca2+/CREB signaling, highlighting a key role of PTEN/CD38/Ca2+/CREB signaling in the molecular pathogenesis of asthma.
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Abnormal static and dynamic functional connectivity of resting-state fMRI in multiple system atrophy

Weimin Zheng, Yunxiang Ge, Shan Ren, Weizheng Ran, Xinning Zhang, Wenyang Tian, Zhigang Chen, Weibei Dou, Zhiqun Wang,

https://doi.org/10.18632/aging.103676 pp 16341—16356

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Zheng W, Ge Y, Ren S, Ran W, Zhang X, Tian W, Chen Z, Dou W, Wang Z, . Abnormal static and dynamic functional connectivity of resting-state fMRI in multiple system atrophy. . 12:16341-16356. https://doi.org/10.18632/aging.103676

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                TY  - JOUR
                AU  - Zheng, Weimin 
                AU  - Ge, Yunxiang 
                AU  - Ren, Shan 
                AU  - Ran, Weizheng 
                AU  - Zhang, Xinning 
                AU  - Tian, Wenyang 
                AU  - Chen, Zhigang 
                AU  - Dou, Weibei 
                AU  - Wang, Zhiqun 
                TI  - Abnormal static and dynamic functional connectivity of resting-state fMRI in multiple system atrophy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103676
                DO  - 10.18632/aging.103676
                SP  - 16341
                EP  - 16356
                PY  - 
                AB  - In order to explore the topological alterations in functional brain networks between multiple system atrophy (MSA) patients and healthy controls (HC), a new joint analysis method of static and dynamic functional connectivity (FC) is proposed in this paper. Twenty-four MSA patients and twenty HCs were enrolled in this study. We constructed static and dynamic brain networks from resting-state fMRI data and calculated four graph theory attributes. Statistical comparisons and correlation analysis were carried out for static and dynamic FC separately before combining both cases. We found decreased local efficiency (LE) and weighted degree (WD) in cerebellum from both static and dynamic graph attributes. For static FC alone, we identified increased betweenness centrality (BC) at left dorsolateral prefrontal cortex, left Cerebellum_Crus9 and decreased WD at Vermis_6. For dynamic FC alone, decreased BC, clustering coefficients and LE at several cortical regions and cerebellum were identified. All the features had significant correlation with total UMSARS scores. Receiver operating characteristic analysis showed that dynamic features had the highest area under the curve value. Our work not only added new evidence for the underlying neurobiology and disrupted dynamic disconnection syndrome of MSA, but also proved the possibility of disease diagnosis and progression tracking using rs-fMRI.
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Association between Nrf2 and CDKN2A expression in patients with end-stage renal disease: a pilot study

Keiichi Sumida, Zhongji Han, Ankur A. Dashputre, Praveen K. Potukuchi, Csaba P. Kovesdy,

https://doi.org/10.18632/aging.103685 pp 16357—16367

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Sumida K, Han Z, Dashputre AA, Potukuchi PK, Kovesdy CP, . Association between Nrf2 and CDKN2A expression in patients with end-stage renal disease: a pilot study. . 12:16357-16367. https://doi.org/10.18632/aging.103685

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                TY  - JOUR
                AU  - Sumida, Keiichi 
                AU  - Han, Zhongji 
                AU  - Dashputre, Ankur A. 
                AU  - Potukuchi, Praveen K. 
                AU  - Kovesdy, Csaba P. 
                TI  - Association between Nrf2 and CDKN2A expression in patients with end-stage renal disease: a pilot study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103685
                DO  - 10.18632/aging.103685
                SP  - 16357
                EP  - 16367
                PY  - 
                AB  - Patients with end-stage renal disease (ESRD) display phenotypic features of premature biological aging, characterized by disproportionately high morbidity and mortality at a younger age. Nuclear factor erythroid 2-related factor 2 (Nrf2) activity, a master regulator of antioxidative responses, declines with age and is implicated in the pathogenesis of age-related disorders; however, little is known about the association between Nrf2 and premature biological aging in ESRD patients. In a cross-sectional pilot cohort of 34 ESRD patients receiving maintenance hemodialysis, we measured the expression of Nrf2 and cyclin-dependent kinase inhibitor 2A (CDKN2A, or p16INK4a, a biomarker of biological aging) genes in whole blood and examined the association of Nrf2 with CDKN2A expression, using Spearman&#x2019;s rank correlation and multivariable linear regression models with adjustment for potential confounders. There was a significant negative correlation between Nrf2 and CDKN2A expression (rho=-0.51, P=0.002); while no significant correlation was found between Nrf2 expression and chronological age (rho=-0.02, P=0.91). After multivariable adjustment, Nrf2 expression remained significantly and negatively associated with CDKN2A expression (&#x3B2; coefficient=-1.51, P=0.01), independent of chronological age, gender, race, and diabetes status. These findings suggest a potential contribution of Nrf2 dysfunction to the development of premature biological aging and its related morbidities in ESRD patients.
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Flavonoids from Rosa roxburghii Tratt prevent reactive oxygen species-mediated DNA damage in thymus cells both combined with and without PARP-1 expression after exposure to radiation in vivo

Sai-Juan Xu, Xia Wang, Tao-Yang Wang, Zheng-Zhan Lin, Yong-Jian Hu, Zhong-Lin Huang, Xian-Jun Yang, Ping Xu,

https://doi.org/10.18632/aging.103688 pp 16368—16389

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Xu S, Wang X, Wang T, Lin Z, Hu Y, Huang Z, Yang X, Xu P, . Flavonoids from Rosa roxburghii Tratt prevent reactive oxygen species-mediated DNA damage in thymus cells both combined with and without PARP-1 expression after exposure to radiation in vivo. . 12:16368-16389. https://doi.org/10.18632/aging.103688

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Provider: 
 TY - JOUR
 AU - Xu, Sai-Juan 
 AU - Wang, Xia 
 AU - Wang, Tao-Yang 
 AU - Lin, Zheng-Zhan 
 AU - Hu, Yong-Jian 
 AU - Huang, Zhong-Lin 
 AU - Yang, Xian-Jun 
 AU - Xu, Ping 
 TI - Flavonoids from Rosa roxburghii Tratt prevent reactive oxygen species-mediated DNA damage in thymus cells both combined with and without PARP-1 expression after exposure to radiation in vivo
 JO - 
 JA - 
 VL - 12
 IS - 16
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103688
 DO - 10.18632/aging.103688
 SP - 16368
 EP - 16389
 PY - 
 AB - This study aimed to evaluate the role of FRT in ROS/DNA regulation with or without PARP-1 in radiation-injured thymus cells. The administration of FRT to PARP-1-/- (KO) mice demonstrated that FRT significantly increased the viability of thymus cells and decreased their rate of apoptosis through PARP-1. Radiation increased the levels of ROS, &#x3B3;-H2AX and 53BP1, and induced DNA double strand breaks. Compared with wild type (WT) mice, levels of ROS, &#x3B3;-H2AX and 53BP1 in KO mice were much less elevated. The FRT treatment groups also showed little reduction in these indicators in KO mice compared with WT mice. The results of the KO mice study indicated that FRT reduced ROS activation through inhibition of PARP-1. Furthermore, FRT reduced the concentrations of &#x3B3;-H2AX by decreasing ROS activation. However, we found that FRT did not regulate 53BP1, a marker of DNA damage, because of its elimination of ROS. Levels of apoptosis-inducing factor (AIF), exhibited no significant difference after irradiation in KO mice. To summarize, ROS suppression by PARP-1 knockout in KO mice highlights potential therapeutic target either by PARP-1 inhibition combined with radiation or by treatment with a drug therapy alone. AIF-induced apoptosis could not be activated in KO mice.
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PRDX2 removal inhibits the cell cycle and autophagy in colorectal cancer cells

Xiangru Zheng, Jinlai Wei, Wenjun Li, Xiaoli Li, Wuyi Wang, Jinbao Guo, Zhongxue Fu,

https://doi.org/10.18632/aging.103690 pp 16390—16409

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Zheng X, Wei J, Li W, Li X, Wang W, Guo J, Fu Z, . PRDX2 removal inhibits the cell cycle and autophagy in colorectal cancer cells. . 12:16390-16409. https://doi.org/10.18632/aging.103690

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                TY  - JOUR
                AU  - Zheng, Xiangru 
                AU  - Wei, Jinlai 
                AU  - Li, Wenjun 
                AU  - Li, Xiaoli 
                AU  - Wang, Wuyi 
                AU  - Guo, Jinbao 
                AU  - Fu, Zhongxue 
                TI  - PRDX2 removal inhibits the cell cycle and autophagy in colorectal cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103690
                DO  - 10.18632/aging.103690
                SP  - 16390
                EP  - 16409
                PY  - 
                AB  - Colorectal cancer (CRC) is a prevalent worldwide disease in which the antioxidant enzyme peroxiredoxin 2 (PRDX2) plays an important role. To investigate the molecular mechanism of PRDX2 in CRC, we performed bioinformatics analysis of The Cancer Genome Atlas (TCGA) datasets and Gene Expression Omnibus (GEO) DataSets (accession no. GSE81429). Our results suggest that PRDX2 is associated with cell-cycle progression and autophagy activated by the P38 MAPK/FOXO signaling pathway. Using a short-hairpin RNA vector, we verified that PRDX2 is essential for CRC cell proliferation and S-phase progression. Immunostaining, electron microscopy and western blotting assays verified the effect of PRDX2 knockdown on autophagy flux and p38 activation. The P38 activator dehydrocorydaline chloride partially rescued the effects of sh-PRDX2 on the expression of proteins related to cell-cycle progression and autophagy. We verified the correlation between PRDX2 expression and the expression of an array of cell-cycle and autophagy-related genes using data from an independent set of 222 CRC patient samples. A mouse xenoplast model was consistent with in vitro results. Our results suggest that PRDX2 promotes CRC cell-cycle progression via activation of the p38 MAPK pathway.
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The association of serum vitamin K2 levels with Parkinson's disease: from basic case-control study to big data mining analysis

Yan-Xia Yu, Xiao-Dan Yu, Qin-zhang Cheng, Lian Tang, Ming-Qiang Shen,

https://doi.org/10.18632/aging.103691 pp 16410—16419

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Yu Y, Yu X, Cheng Q, Tang L, Shen M, . The association of serum vitamin K2 levels with Parkinson's disease: from basic case-control study to big data mining analysis. . 12:16410-16419. https://doi.org/10.18632/aging.103691

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                TY  - JOUR
                AU  - Yu, Yan-Xia 
                AU  - Yu, Xiao-Dan 
                AU  - Cheng, Qin-zhang 
                AU  - Tang, Lian 
                AU  - Shen, Ming-Qiang 
                TI  - The association of serum vitamin K2 levels with Parkinson's disease: from basic case-control study to big data mining analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103691
                DO  - 10.18632/aging.103691
                SP  - 16410
                EP  - 16419
                PY  - 
                AB  - Although it is known that inflammation is involved in Parkinson&#x2019;s disease (PD) pathogenesis and vitamin K2 (VK2) has anti-inflammatory effects, to date few studies have been reported on the relationship between VK2 and PD development. Herein we presented a case-control study involving 93 PD patients and 95 healthy controls. Overall, the serum VK2 level of PD patients (3.49 &#xB1; 1.68 ng/ml) was significantly lower than that of healthy controls (5.77 &#xB1; 2.71 ng/ml). When the PD patients were stratified by disease progression, we observed that the serum VK2 level of late stage patients was further decreased to 3.15 &#xB1; 1.18 ng/ml while the serum VK2 level of early stage patients was 3.92 &#xB1; 2.09 ng/ml. Furthermore, the curve analysis showed that the serum VK2 level decreased gradually with the increment of PD Hoehn-Yahr (H-Y) stage. We also confirmed the dysregulated inflammatory responses and coagulation cascades in PD patients by public dataset, which are associated to the decreased VK2 level. In summary, we found the serum VK2 level in PD patients is lower than that in healthy controls. The decrease of VK2 level may be related to the occurrence and progression of PD by loosening the regulation of inflammatory responses and coagulation cascades signal.
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Prognostic value and underlying mechanism of KIAA0101 in hepatocellular carcinoma: database mining and co-expression analysis

Weiyu Xu, Xuezhu Wang, Xiaoqian Wu, Si Yu, Jianping Xiong, Xinting Sang, Yongchang Zheng, Zhongtao Zhang,

https://doi.org/10.18632/aging.103704 pp 16420—16436

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Xu W, Wang X, Wu X, Yu S, Xiong J, Sang X, Zheng Y, Zhang Z, . Prognostic value and underlying mechanism of KIAA0101 in hepatocellular carcinoma: database mining and co-expression analysis. . 12:16420-16436. https://doi.org/10.18632/aging.103704

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                TY  - JOUR
                AU  - Xu, Weiyu 
                AU  - Wang, Xuezhu 
                AU  - Wu, Xiaoqian 
                AU  - Yu, Si 
                AU  - Xiong, Jianping 
                AU  - Sang, Xinting 
                AU  - Zheng, Yongchang 
                AU  - Zhang, Zhongtao 
                TI  - Prognostic value and underlying mechanism of KIAA0101 in hepatocellular carcinoma: database mining and co-expression analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103704
                DO  - 10.18632/aging.103704
                SP  - 16420
                EP  - 16436
                PY  - 
                AB  - Although KIAA0101 is involved in many diseases, its expression and prognostic value in HCC remain undefined. According to CCLE, KIAA0101 is highly expressed in HCC, with a weak positive correlation between copy number and gene expression. Four studies involving 760 samples in ONCOMINE report elevated KIAA0101 expression in HCC (p=3.11E-22). The KM plotter revealed high KIAA0101 expression to be associated with worse overall survival in HCC (HR=2.09, p=4.1e-05); this prognostic power was stronger for male than female, early-stage than advanced-stage, and Asian than Caucasian patients. RNA sequencing data for 8 pairs of HCC and adjacent tissue samples validated the significantly high KIAA0101 level (p=0.00497). Moreover, functional annotations of 31 KIAA0101-coexpressed genes show enrichment of terms associated with mitosis, cytoskeleton construction, and chromosome segregation. Among 9 genes having STRING-validated protein-protein interactions with KIAA0101, two are involved in virus-related pathways. Alternative splicing analysis indicated higher expression of variant 1 and variant 2 in HCC and no significant differences in exon usage of KIAA0101 between cancer and normal tissues. These findings support that KIAA0101 is a potential prognostic biomarker for HCC and highlight the association between virus infection and the mechanism underlying the process by which KIAA0101 contributes to poor prognosis of patients.
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KCNN4 is a diagnostic and prognostic biomarker that promotes papillary thyroid cancer progression

Jialiang Wen, Bangyi Lin, Lizhi Lin, Yizuo Chen, Ouchen Wang,

https://doi.org/10.18632/aging.103710 pp 16437—16456

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Wen J, Lin B, Lin L, Chen Y, Wang O, . KCNN4 is a diagnostic and prognostic biomarker that promotes papillary thyroid cancer progression. . 12:16437-16456. https://doi.org/10.18632/aging.103710

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Provider: 
 TY - JOUR
 AU - Wen, Jialiang 
 AU - Lin, Bangyi 
 AU - Lin, Lizhi 
 AU - Chen, Yizuo 
 AU - Wang, Ouchen 
 TI - KCNN4 is a diagnostic and prognostic biomarker that promotes papillary thyroid cancer progression
 JO - 
 JA - 
 VL - 12
 IS - 16
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103710
 DO - 10.18632/aging.103710
 SP - 16437
 EP - 16456
 PY - 
 AB - The incidence of thyroid cancer remains high worldwide, and papillary thyroid cancer (PTC) is the most common type. Potassium Calcium-Activated Channel Subfamily N Member 4 (KCNN4) has been reported as an oncogene in various cancers. We examined expression of KCNN4 in public databases and discovered that it is upregulated in PTC. We verified this finding using our own validated cohort and RNA sequencing data. We also found that KCNN4 is a diagnostic and prognostic biomarker that is associated with disease-free survival, immune infiltration, and several other clinicopathological features of PTC. Gene Set Enrichment Analysis indicated that apoptotic and epithelial-mesenchymal transition gene sets are both upregulated in PTC patients with higher KCNN4 levels. In PTC cell lines, silencing KCNN4 inhibited cell proliferation, migration and invasion. Moreover, quantitative real-time PCR and Western blotting indicated that silencing KCNN4 increased expression of apoptotic genes in PTC cells and reduced the expression of genes involved in their epithelial-mesenchymal transition. These results suggest that KCNN4 promotes PTC progression by inducing epithelial-mesenchymal transition and suppressing apoptosis, which suggests KCNN4 may be a useful diagnostic and prognostic biomarker of PTC.
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Risk stratification of cutaneous melanoma reveals carcinogen metabolism enrichment and immune inhibition in high-risk patients

Xia Li, Yunpeng Cai,

https://doi.org/10.18632/aging.103734 pp 16457—16475

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Li X, Cai Y, . Risk stratification of cutaneous melanoma reveals carcinogen metabolism enrichment and immune inhibition in high-risk patients. . 12:16457-16475. https://doi.org/10.18632/aging.103734

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                TY  - JOUR
                AU  - Li, Xia 
                AU  - Cai, Yunpeng 
                TI  - Risk stratification of cutaneous melanoma reveals carcinogen metabolism enrichment and immune inhibition in high-risk patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103734
                DO  - 10.18632/aging.103734
                SP  - 16457
                EP  - 16475
                PY  - 
                AB  - Cutaneous melanoma (CM) is the most lethal form of skin cancer. Risk assessment should facilitate stratified surveillance and guide treatment selection. Here, based on the mRNA-seq data from 419 CM patients in the Cancer Genome Atlas (TCGA), we developed a prognostic 21-gene signature to distinguish the outcomes of high- and low-risk patients, which was further validated in two external cohorts. The signature achieved a higher C-index as compared with other known biomarkers and clinical characteristics in both the TCGA and validation cohorts. Notably, in high-risk patients the expression levels of three driver genes, BRAF, NRAS, and NF1 in the MAPK pathway, were lower but exhibited a stronger positive correlation as compared with low-risk patients. Moreover, the genes involved in nicotinamide adenine dinucleotide metabolism were negatively correlated with the expression of BRAF in the high-risk group. Function analysis revealed that the upregulated genes in the high-risk group were enriched in the cytochrome P450-mediated metabolism of chemical carcinogens. Furthermore, the low-risk group had high levels of gamma delta T cells infiltration, while regulatory T cells were accumulated in the high-risk group. The present study offers a promising new prognostic signature for CM, and provides insight into the mechanisms of melanoma progression.
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Relationship closeness buffers the effects of perceived stress on transcriptomic indicators of cellular stress and biological aging marker p16^INK4a

Kelly E. Rentscher, Judith E. Carroll, Steve W. Cole, Rena L. Repetti, Theodore F. Robles,

https://doi.org/10.18632/aging.103739 pp 16476—16490

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Rentscher KE, Carroll JE, Cole SW, Repetti RL, Robles TF, . Relationship closeness buffers the effects of perceived stress on transcriptomic indicators of cellular stress and biological aging marker p16^INK4a. . 12:16476-16490. https://doi.org/10.18632/aging.103739

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Provider: 
 TY - JOUR
 AU - Rentscher, Kelly E. 
 AU - Carroll, Judith E. 
 AU - Cole, Steve W. 
 AU - Repetti, Rena L. 
 AU - Robles, Theodore F. 
 TI - Relationship closeness buffers the effects of perceived stress on transcriptomic indicators of cellular stress and biological aging marker p16INK4a
 JO - 
 JA - 
 VL - 12
 IS - 16
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103739
 DO - 10.18632/aging.103739
 SP - 16476
 EP - 16490
 PY - 
 AB - Chronic stress can accelerate biological aging, offering one mechanism through which stress may increase age-related disease risk. Chronic activation of the sympathoadrenal system increases cellular energy production, resulting in cell stress that can initiate cellular senescence, a permanent state of cell growth arrest. Our previous research linked psychosocial stress with increased expression of senescence marker p16INK4a; however, less is known about the role of protective psychosocial factors in biological aging. We examined relationship closeness (perceived interconnectedness with one&#x2019;s spouse) as a protective buffer of the effects of stress on expression of the p16INK4a-encoding gene (CDKN2A) and transcription control pathways activated under cell stress. Seventy parents (Mage=43.2) completed interview-based and questionnaire measures of psychosocial stress and relationship closeness. Blood samples assessed CDKN2A expression and inferred activity of a priori-selected transcription factors Nrf2 and heat shock factors (HSFs) via genome-wide transcriptome profiling. Random intercept models adjusting for age, sex, and ethnicity/race revealed that perceived stress was associated with elevated CDKN2A expression for parents with low but not high closeness. Secondary bioinformatics analyses linked the interaction of perceived stress and relationship closeness to Nrf2 and HSF-1 activity. Findings identify relationship closeness as a protective factor that may buffer the impact of stress on cellular stress and senescence pathways.
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Eight immune-related genes predict survival outcomes and immune characteristics in breast cancer

Han Xu, Gangjian Wang, Lili Zhu, Hong Liu, Bingjie Li,

https://doi.org/10.18632/aging.103753 pp 16491—16513

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Xu H, Wang G, Zhu L, Liu H, Li B, . Eight immune-related genes predict survival outcomes and immune characteristics in breast cancer. . 12:16491-16513. https://doi.org/10.18632/aging.103753

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                TY  - JOUR
                AU  - Xu, Han 
                AU  - Wang, Gangjian 
                AU  - Zhu, Lili 
                AU  - Liu, Hong 
                AU  - Li, Bingjie 
                TI  - Eight immune-related genes predict survival outcomes and immune characteristics in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103753
                DO  - 10.18632/aging.103753
                SP  - 16491
                EP  - 16513
                PY  - 
                AB  - Advancements in immunotherapy have improved our understanding of the immune characteristics of breast cancer. Here, we analyzed gene expression profiles and clinical data obtained from The Cancer Genome Atlas database to identify genes that were differentially expressed between breast tumor tissues and normal breast tissues. Comparisons with the Immunology Database and Analysis Portal (ImmPort) indicated that many of the identified differentially expressed genes were immune-related. Risk scores calculated based on an eight-gene signature constructed from these immune-related genes predicted both overall survival and relapse-free survival outcomes in breast cancer patients. The predictive value of the eight-gene signature was validated in different breast cancer subtypes using external datasets. Associations between risk score and breast cancer immune characteristics were also identified; in vitro experiments using breast cancer cell lines confirmed those associations. Thus, the novel eight-gene signature described here accurately predicts breast cancer survival outcomes as well as immune checkpoint expression and immune cell infiltration processes.
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Coupled immune stratification and identification of therapeutic candidates in patients with lung adenocarcinoma

Weilei Hu, Guosheng Wang, Yundi Chen, Lonny B. Yarmus, Biao Liu, Yuan Wan,

https://doi.org/10.18632/aging.103775 pp 16514—16538

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Hu W, Wang G, Chen Y, Yarmus LB, Liu B, Wan Y, . Coupled immune stratification and identification of therapeutic candidates in patients with lung adenocarcinoma. . 12:16514-16538. https://doi.org/10.18632/aging.103775

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                TY  - JOUR
                AU  - Hu, Weilei 
                AU  - Wang, Guosheng 
                AU  - Chen, Yundi 
                AU  - Yarmus, Lonny B. 
                AU  - Liu, Biao 
                AU  - Wan, Yuan 
                TI  - Coupled immune stratification and identification of therapeutic candidates in patients with lung adenocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103775
                DO  - 10.18632/aging.103775
                SP  - 16514
                EP  - 16538
                PY  - 
                AB  - In recent years, personalized cancer immunotherapy, especially stratification-driven precision treatments have gained significant traction. However, due to the heterogeneity in clinical cohorts, the uncombined analysis of stratification/therapeutics may lead to confusion in determining ideal therapeutic options. We report that the coupled immune stratification and drug repurposing could facilitate identification of therapeutic candidates in patients with lung adenocarcinoma (LUAD). First, we categorized the patients into four groups based on immune gene profiling, associated with distinct molecular characteristics and clinical outcomes. Then, the weighted gene co-expression network analysis (WGCNA) algorithm was used to identify co-expression modules of each groups. We focused on C3 group which is characterized by low immune infiltration (cold tumor) and wild-type EGFR, posing a significant challenge for treatment of LUAD. Five drug candidates against the C3 status were identified which have potential dual functions to correct aberrant immune microenvironment and also halt tumorigenesis. Furthermore, their steady binding affinity against the targets was verified through molecular docking analysis. In sum, our findings suggest that such coupled analysis could be a promising methodology for identification and exploration of therapeutic candidates in the practice of personalized immunotherapy.
                ER  -

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Accelerated epigenetic aging as a risk factor for chronic obstructive pulmonary disease and decreased lung function in two prospective cohort studies

Miyuki Breen, Jamaji C. Nwanaji-Enwerem, Stefan Karrasch, Claudia Flexeder, Holger Schulz, Melanie Waldenberger, Sonja Kunze, Markus Ollert, Stefan Weidinger, Elena Colicino, Xu Gao, Cuicui Wang, Jincheng Shen, Allan C. Just, Pantel Vokonas, David Sparrow, Lifang Hou, Joel D. Schwartz, Andrea A. Baccarelli, Annette Peters, Cavin K. Ward-Caviness,

https://doi.org/10.18632/aging.103784 pp 16539—16554

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Breen M, Nwanaji-Enwerem JC, Karrasch S, Flexeder C, Schulz H, Waldenberger M, Kunze S, Ollert M, Weidinger S, Colicino E, Gao X, Wang C, Shen J, et al, . Accelerated epigenetic aging as a risk factor for chronic obstructive pulmonary disease and decreased lung function in two prospective cohort studies. . 12:16539-16554. https://doi.org/10.18632/aging.103784

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Provider: 
                TY  - JOUR
                AU  - Breen, Miyuki 
                AU  - Nwanaji-Enwerem, Jamaji C. 
                AU  - Karrasch, Stefan 
                AU  - Flexeder, Claudia 
                AU  - Schulz, Holger 
                AU  - Waldenberger, Melanie 
                AU  - Kunze, Sonja 
                AU  - Ollert, Markus 
                AU  - Weidinger, Stefan 
                AU  - Colicino, Elena 
                AU  - Gao, Xu 
                AU  - Wang, Cuicui 
                AU  - Shen, Jincheng 
                AU  - Just, Allan C. 
                AU  - Vokonas, Pantel 
                AU  - Sparrow, David 
                AU  - Hou, Lifang 
                AU  - Schwartz, Joel D. 
                AU  - Baccarelli, Andrea A. 
                AU  - Peters, Annette 
                AU  - Ward-Caviness, Cavin K. 
                TI  - Accelerated epigenetic aging as a risk factor for chronic obstructive pulmonary disease and decreased lung function in two prospective cohort studies
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103784
                DO  - 10.18632/aging.103784
                SP  - 16539
                EP  - 16554
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Breen, Miyuki 
                AU  - Nwanaji-Enwerem, Jamaji C. 
                AU  - Karrasch, Stefan 
                AU  - Flexeder, Claudia 
                AU  - Schulz, Holger 
                AU  - Waldenberger, Melanie 
                AU  - Kunze, Sonja 
                AU  - Ollert, Markus 
                AU  - Weidinger, Stefan 
                AU  - Colicino, Elena 
                AU  - Gao, Xu 
                AU  - Wang, Cuicui 
                AU  - Shen, Jincheng 
                AU  - Just, Allan C. 
                AU  - Vokonas, Pantel 
                AU  - Sparrow, David 
                AU  - Hou, Lifang 
                AU  - Schwartz, Joel D. 
                AU  - Baccarelli, Andrea A. 
                AU  - Peters, Annette 
                AU  - Ward-Caviness, Cavin K. 
                TI  - Accelerated epigenetic aging as a risk factor for chronic obstructive pulmonary disease and decreased lung function in two prospective cohort studies
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103784
                DO  - 10.18632/aging.103784
                SP  - 16539
                EP  - 16554
                PY  - 
                AB  - Chronic obstructive pulmonary disease (COPD) is a frequent diagnosis in older individuals and contributor to global morbidity and mortality. Given the link between lung disease and aging, we need to understand how molecular indicators of aging relate to lung function and disease. Using data from the population-based KORA (Cooperative Health Research in the Region of Augsburg) surveys, we associated baseline epigenetic (DNA methylation) age acceleration with incident COPD and lung function. Models were adjusted for age, sex, smoking, height, weight, and baseline lung disease as appropriate. Associations were replicated in the Normative Aging Study. Of 770 KORA participants, 131 developed incident COPD over 7 years. Baseline accelerated epigenetic aging was significantly associated with incident COPD. The change in age acceleration (follow-up &#x2013; baseline) was more strongly associated with COPD than baseline aging alone. The association between the change in age acceleration between baseline and follow-up and incident COPD replicated in the Normative Aging Study. Associations with spirometric lung function parameters were weaker than those with COPD, but a meta-analysis of both cohorts provide suggestive evidence of associations. Accelerated epigenetic aging, both baseline measures and changes over time, may be a risk factor for COPD and reduced lung function.
                ER  -

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Prognostic model of patients with liver cancer based on tumor stem cell content and immune process

Weikaixin Kong, Miaomiao Gao, Yuchen Jin, Weiran Huang, Zhuo Huang, Zhengwei Xie,

https://doi.org/10.18632/aging.103832 pp 16555—16578

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Kong W, Gao M, Jin Y, Huang W, Huang Z, Xie Z, . Prognostic model of patients with liver cancer based on tumor stem cell content and immune process. . 12:16555-16578. https://doi.org/10.18632/aging.103832

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                TY  - JOUR
                AU  - Kong, Weikaixin 
                AU  - Gao, Miaomiao 
                AU  - Jin, Yuchen 
                AU  - Huang, Weiran 
                AU  - Huang, Zhuo 
                AU  - Xie, Zhengwei 
                TI  - Prognostic model of patients with liver cancer based on tumor stem cell content and immune process
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103832
                DO  - 10.18632/aging.103832
                SP  - 16555
                EP  - 16578
                PY  - 
                AB  - Globally, liver hepatocellular carcinoma (LIHC) has a high mortality and recurrence rate, leading to poor prognosis. The recurrence of LIHC is closely related to two aspects: degree of immune infiltration and content of tumor stem cells. Hence, this study aimed to used RNA-seq and clinical data of LIHC from The Cancer Genome Atlas, Estimation of Stromal and Immune cells in Malignant Tumours, mRNA stemness index score, and weighted gene correlation network analysis methods to find genes significantly linked to the aforementioned two aspects. Key genes and clinical factors were used as input. Lasso regression and multivariate Cox regression were conducted to build an effective prognostic model for patients with liver cancer. Finally, four key genes (KLHL30, PLN, LYVE1, and TIMD4) and four clinical factors (Asian, age, grade, and bilirubin) were included in the prognostic model, namely Immunity and Cancer-stem-cell Related Prognosis (ICRP) score. The ICRP score achieved a great performance in test set. The area under the curve value of the ICRP score in test set for 1, 3, and 5 years was 0.708, 0.723, and 0.765, respectively, which was better than that of other prognostic prediction methods for LIHC. The C-index evaluation method also reached the same conclusion.
                ER  -

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Suppressing endoplasmic reticulum stress-related autophagy attenuates retinal light injury

Jing-Yao Song, Bin Fan, Lin Che, Yi-Ran Pan, Si-Ming Zhang, Ying Wang, Victoria Bunik, Guang-Yu Li,

https://doi.org/10.18632/aging.103846 pp 16579—16596

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Song J, Fan B, Che L, Pan Y, Zhang S, Wang Y, Bunik V, Li G, . Suppressing endoplasmic reticulum stress-related autophagy attenuates retinal light injury. . 12:16579-16596. https://doi.org/10.18632/aging.103846

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                TY  - JOUR
                AU  - Song, Jing-Yao 
                AU  - Fan, Bin 
                AU  - Che, Lin 
                AU  - Pan, Yi-Ran 
                AU  - Zhang, Si-Ming 
                AU  - Wang, Ying 
                AU  - Bunik, Victoria 
                AU  - Li, Guang-Yu 
                TI  - Suppressing endoplasmic reticulum stress-related autophagy attenuates retinal light injury
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103846
                DO  - 10.18632/aging.103846
                SP  - 16579
                EP  - 16596
                PY  - 
                AB  - Excessive light exposure is a principal environmental factor, which can cause damage to photoreceptors and retinal pigment epithelium (RPE) cells and may accelerate the progression of age-related macular degeneration (AMD). In this study, oxidative stress, endoplasmic reticulum (ER) stress and autophagy caused by light exposure were evaluated in vitro and in vivo. Light exposure caused severe photo-oxidative stress and ER stress in photoreceptors (661W cells) and RPE cells (ARPE-19 cells). Suppressing either oxidative stress or ER stress was protective against light damage in 661W and ARPE-19 cells and N-acetyl-L-cysteine treatment markedly inhibited the activation of ER stress caused by light exposure. Moreover, suppressing autophagy with 3-methyladenine significantly attenuated light-induced cell death. Additionally, inhibiting ER stress either by knocking down PERK signals or with GSK2606414 treatment remarkably suppressed prolonged autophagy and protected the cells against light injury. In vivo experiments verified neuroprotection via inhibiting ER stress-related autophagy in light-damaged retinas of mice. In conclusion, the above results suggest that light-induced photo-oxidative stress may trigger subsequent activation of ER stress and prolonged autophagy in photoreceptors and RPE cells. Suppressing ER stress may abrogate over-activated autophagy and protect the retina against light injury.
                ER  -

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Balloon aortic valvuloplasty as a palliative treatment in patients with severe aortic stenosis and limited life expectancy: a single center experience

Francesca Mantovani, Marie-Annick Clavel, Antonella Potenza, Chiara Leuzzi, Teresa Grimaldi, Luigi Vignali, Alessandro Navazio, Vincenzo Guiducci,

https://doi.org/10.18632/aging.103862 pp 16597—16608

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Mantovani F, Clavel M, Potenza A, Leuzzi C, Grimaldi T, Vignali L, Navazio A, Guiducci V, . Balloon aortic valvuloplasty as a palliative treatment in patients with severe aortic stenosis and limited life expectancy: a single center experience. . 12:16597-16608. https://doi.org/10.18632/aging.103862

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                TY  - JOUR
                AU  - Mantovani, Francesca 
                AU  - Clavel, Marie-Annick 
                AU  - Potenza, Antonella 
                AU  - Leuzzi, Chiara 
                AU  - Grimaldi, Teresa 
                AU  - Vignali, Luigi 
                AU  - Navazio, Alessandro 
                AU  - Guiducci, Vincenzo 
                TI  - Balloon aortic valvuloplasty as a palliative treatment in patients with severe aortic stenosis and limited life expectancy: a single center experience
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103862
                DO  - 10.18632/aging.103862
                SP  - 16597
                EP  - 16608
                PY  - 
                AB  - Whether balloon aortic valvuloplasty (BAV) may provide an effective palliation in symptomatic high-risk patients is uncertain. Therefore, we aimed to evaluate outcomes in symptomatic high-risk patients with severe aortic stenosis (AS), who underwent BAV. All-cause mortality and length of hospitalization for heart failure (HF) up to death or to 1-year follow up were collected after BAV. One hundred thirty-two (132) patients (62% women), mean age 85&#xB1;7 years, underwent BAV with a substantial reduction of the peak-to-peak aortic gradient from 53&#xB1;21 to 29&#xB1;15 mmHg (p&lt;0.001). The median of days of HF hospitalization prior to BAV was 9 (0-19), and decreased after BAV to 0 (0-9), p&lt;0.001. During 1-year follow-up patients with untreated CAD (85, 64%) had a higher mortality compared to patients with insignificant/treated CAD (47, 36%): 1-year survival: 45&#xB1;7% vs. 66&#xB1; 7%; p=0.02. After adjustment for STS risk score and severity of residual AS, patients with untreated CAD remained at higher risk of mortality (adjusted HR 1.74 [1.01-2.91]; p=0.04). Thus, in this series of symptomatic high-risk patients, BAV was associated with a significant reduction in aortic valve gradient and hospitalization time for HF post-BAV. In patients with significant CAD, percutaneous intervention might be considered in order to improve survival.
                ER  -

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Autoantibodies against M₅-muscarinic and beta₁-adrenergic receptors in periodontitis patients

Isabel Scherbaum, Harald Heidecke, Kübra Bunte, Ulrike Peters, Thomas Beikler, Fritz Boege,

https://doi.org/10.18632/aging.103864 pp 16609—16620

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Scherbaum I, Heidecke H, Bunte K, Peters U, Beikler T, Boege F, . Autoantibodies against M₅-muscarinic and beta₁-adrenergic receptors in periodontitis patients. . 12:16609-16620. https://doi.org/10.18632/aging.103864

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Provider: 
 TY - JOUR
 AU - Scherbaum, Isabel 
 AU - Heidecke, Harald 
 AU - Bunte, Kübra 
 AU - Peters, Ulrike 
 AU - Beikler, Thomas 
 AU - Boege, Fritz 
 TI - Autoantibodies against M5-muscarinic and beta1-adrenergic receptors in periodontitis patients
 JO - 
 JA - 
 VL - 12
 IS - 16
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103864
 DO - 10.18632/aging.103864
 SP - 16609
 EP - 16620
 PY - 
 AB - Autoantibodies against muscarinic and beta1-adrenergic receptors are considered a potential cause and/or risk factor for chronic heart failure. Association of periodontitis with such autoantibodies and with impaired heart function has been observed in patients exposed to endemic Chagas&apos; disease, which triggers by itself cardiomyopathy and receptor immunization.Here we studied the association between periodontitis, markers of cardiac injury and receptor autoimmunization in periodontitis patients (n = 147) not exposed to Chagas&apos; disease. The autoantibodies were determined by IgG binding to native intact muscarinic and beta1-adrenergic receptors or to a cyclic peptide mimicking the disease-relevant conformational autoepitope presented by the active beta1-adrenergic receptor. Possible cardiac injury and inflammatory status were judged by serum levels of proBNP/Troponin I and CRP/IL-6, respectively. These parameters were analysed in healthy and periodontally diseased individuals as well as before and after periodontal therapy.Patients with periodontitis had significantly (p &lt; 0.001) higher levels of autoantibodies against M5-muscarinic and beta1-adrenergic receptors, which further increased following periodontal therapy. Receptor autoantibodies were associated with increased inflammatory status but not with increased markers of cardiac injury. Thus, our data indicate that periodontitis triggers systemic inflammation, which is associated with receptor autoimmunization, and, independently thereof, with cardiac injury.
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Prolonged treatment with Y-27632 promotes the senescence of primary human dermal fibroblasts by increasing the expression of IGFBP-5 and transforming them into a CAF-like phenotype

Xiangyong Li, Qian Zhou, Shuangshuang Wang, Ping Wang, Juan Li, Zhiwei Xie, Chang Liu, Jie Wen, Xunwei Wu,

https://doi.org/10.18632/aging.103910 pp 16621—16646

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Li X, Zhou Q, Wang S, Wang P, Li J, Xie Z, Liu C, Wen J, Wu X, . Prolonged treatment with Y-27632 promotes the senescence of primary human dermal fibroblasts by increasing the expression of IGFBP-5 and transforming them into a CAF-like phenotype. . 12:16621-16646. https://doi.org/10.18632/aging.103910

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                TY  - JOUR
                AU  - Li, Xiangyong 
                AU  - Zhou, Qian 
                AU  - Wang, Shuangshuang 
                AU  - Wang, Ping 
                AU  - Li, Juan 
                AU  - Xie, Zhiwei 
                AU  - Liu, Chang 
                AU  - Wen, Jie 
                AU  - Wu, Xunwei 
                TI  - Prolonged treatment with Y-27632 promotes the senescence of primary
                human dermal fibroblasts by increasing the expression of IGFBP-5 and transforming them into a CAF-like phenotype
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103910
                DO  - 10.18632/aging.103910
                SP  - 16621
                EP  - 16646
                PY  - 
                AB  - The Rho-kinases (ROCK) inhibitor Y-27632 has been shown to promote the growth of epidermal cells, however, its potential effects on human dermal fibroblasts (HDFs) need to be clarified. Here we show that prolonged treatment of HDFs with Y-27632 decreased their growth by inducing senescence, which was associated with induction of the senescence markers p16 and p21, and downmodulation of the ERK pathways. The senescent HDFs induced by Y-27632 acquired a cancer-associated-fibroblast (CAF)-like phenotype to promote squamous cell carcinoma (SCC) cell growth in vitro. Expression of a newly identified target of Y-27632 by RNA-seq, insulin growth factor binding protein 5 (IGFBP-5), was dramatically increased after 24 h of treatment with Y-27632. Adding recombinant IGFBP-5 protein to the culture medium produced similar phenotypes of HDFs as did treatment with Y-27632, and knockdown of IGFBP-5 blocked the Y-27632-induced senescence. Furthermore, Y-27632 induced the expression of an IGFBP-5 upstream gene, GATA4, and knockdown of GATA4 also reduced the Y-27632-induced senescence. In summary, these results demonstrate for the first time that Y-27632 promotes cellular senescence in primary HDFs by inducing the expression of IGFBP-5 and that prolonged treatment with Y-27632 potentially transforms primary HDFs into CAF-like cells.
                ER  -

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ATP synthase and Alzheimer’s disease: putting a spin on the mitochondrial hypothesis

Brad Ebanks, Thomas L Ingram, Lisa Chakrabarti,

https://doi.org/10.18632/aging.103867 pp 16647—16662

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Ebanks B, Ingram TL, Chakrabarti L, . ATP synthase and Alzheimer’s disease: putting a spin on the mitochondrial hypothesis. . 12:16647-16662. https://doi.org/10.18632/aging.103867

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                TY  - JOUR
                AU  - Ebanks, Brad 
                AU  - Ingram, Thomas L 
                AU  - Chakrabarti, Lisa 
                TI  - ATP synthase and Alzheimer’s disease: putting a spin on the
                mitochondrial hypothesis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 16
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103867
                DO  - 10.18632/aging.103867
                SP  - 16647
                EP  - 16662
                PY  - 
                AB  - It is estimated that over 44 million people across the globe have dementia, and half of these cases are believed to be Alzheimer&#x2019;s disease (AD). As the proportion of the global population which is over the age 60 increases so will the number of individuals living with AD. This will result in ever-increasing demands on healthcare systems and the economy. AD can be either sporadic or familial, but both present with similar pathobiology and symptoms. Three prominent theories about the cause of AD are the amyloid, tau and mitochondrial hypotheses. The mitochondrial hypothesis focuses on mitochondrial dysfunction in AD, however little attention has been given to the potential dysfunction of the mitochondrial ATP synthase in AD. ATP synthase is a proton pump which harnesses the chemical potential energy of the proton gradient across the inner mitochondrial membrane (IMM), generated by the electron transport chain (ETC), in order to produce the cellular energy currency ATP. This review presents the evidence accumulated so far that demonstrates dysfunction of ATP synthase in AD, before highlighting two potential pharmacological interventions which may modulate ATP synthase.
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Correction for: 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.104045 pp 16663—16664

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Lin J, Kuo W, Baskaran R, Kuo C, Chen Y, Chen WS, Ho T, Day CH, Mahalakshmi B, Huang C, . Correction for: Swimming exercise stimulates IGF1/PI3K/Akt and AMPK/SIRT1/PGC1α survival signaling to suppress apoptosis and inflammation in aging hippocampus. . 12:16663-16664. https://doi.org/10.18632/aging.104045

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Volume 12, Issue 16

About the Cover

Editorials

Irena Manov, Amani Odeh, Imad Shams,

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Andrés Moya, Susana Ruiz-Ruiz, Manuel Ferrer,

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J. Matthew Hinkley, Paul M. Coen,

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Priority Research Papers

Marta Varela-Eirín, Paula Carpintero-Fernández, Agustín Sánchez-Temprano, Adrián Varela-Vázquez, Carlos Luis Paíno, Antonio Casado-Díaz, Alfonso Calañas Continente, Virginia Mato, Eduardo Fonseca, Mustapha Kandouz, Alfonso Blanco, José Ramón Caeiro, María D. Mayán,

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Paweł Kordowitzki, Isabel López de Silanes, Ana Guío-Carrión, Maria A. Blasco,

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Research Papers

COVID-19 Early coagulation tests predict risk stratification and prognosis of COVID-19

Lili Luo, Min Xu, Mengyi Du, Haiming Kou, Danying Liao, Zhipeng Cheng, Heng Mei, Yu Hu,

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COVID-19 Clinical characteristics of chronic liver disease with coronavirus disease 2019 (COVID-19): a cohort study in Wuhan, China

Chaowei Li, Qingshi Chen, Jianwen Wang, Huasong Lin, Yalan Lin, Jinhuang Lin, Fangzhan Peng, Jiangmu Chen, Zhirong Yang,

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COVID-19 Clinical course and characteristics of patients with coronavirus disease 2019 in Wuhan, China: a single-centered, retrospective, observational study

Yanfang Liu, Lina Liu, Ye Wang, Xinyang Du, Hong Ma, Jing Yao,

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COVID-19 COVID-19: a probable role of the anticoagulant Protein S in managing COVID-19-associated coagulopathy

Sabyasachi Chatterjee, Tanusree Sengupta, Samarpan Majumder, Rinku Majumder,

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Zixia Huang, Conor V. Whelan, Dina Dechmann, Emma C. Teeling,

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Francesca Lessi, Nicole Grandi, Chiara Maria Mazzanti, Prospero Civita, Cristian Scatena, Paolo Aretini, Pasquale Bandiera, Antonio Fornaciari, Valentina Giuffra, Gino Fornaciari, Antonio Giuseppe Naccarato, Enzo Tramontano, Generoso Bevilacqua,

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Hengbing Wang, Xiaobing Niu, Hesong Jiang, Fei Mao, Bing Zhong, Xi Jiang, Guangbo Fu,

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Chien-Cheng Chen, Tzyy-Yue Wong, Tzu-Yun Chin, Wen-Hsien Lee, Chan-Yen Kuo, Yi-Chiung Hsu,

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Chao Zhang, Guijun Xu, Yao Xu, Haixiao Wu, Xu Guo, Min Mao, Vladimir P. Baklaushev, Vladimir P. Chekhonin, Karl Peltzer, Ye Bai, Guowen Wang, Wenjuan Ma, Xin Wang,

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Chunhui Yang, Yiqing Qiu, Yuan Qing, Jinyu Xu, Wei Dai, Xiaowu Hu, Xi Wu,

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Yaoxin Fan, Lin Wang, Yang Ding, Qiuju Sheng, Chong Zhang, Yanwei Li, Chao Han, Xiaoguang Dou,

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Yi-Lin Kong, Bi-Hui Pan, Jin-Hua Liang, Hua-Yuan Zhu, Li Wang, Yi Xia, Jia-Zhu Wu, Lei Fan, Jian-Yong Li, Wei Xu,

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COVID-19
Early coagulation tests predict risk stratification and prognosis of COVID-19

COVID-19
Clinical characteristics of chronic liver disease with coronavirus disease 2019 (COVID-19): a cohort study in Wuhan, China

COVID-19
Clinical course and characteristics of patients with coronavirus disease 2019 in Wuhan, China: a single-centered, retrospective, observational study

COVID-19
COVID-19: a probable role of the anticoagulant Protein S in managing COVID-19-associated coagulopathy