Volume 12, Issue 3

Wang G, Huang Y, Yang F, Tian X, Wang K, Liu L, Fan Y, Li X, Li L, Shi B, Hao Y, Xia C, Nie Q, et al, . High expression of SMYD3 indicates poor survival outcome and promotes tumour progression through an IGF-1R/AKT/E2F-1 positive feedback loop in bladder cancer. . 12:2030-2048. https://doi.org/10.18632/aging.102718

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                TY  - JOUR
                AU  - Wang, Guoliang 
                AU  - Huang, Yi 
                AU  - Yang, Feilong 
                AU  - Tian, Xiaojun 
                AU  - Wang, Kun 
                AU  - Liu, Li 
                AU  - Fan, Yidong 
                AU  - Li, Xiaofeng 
                AU  - Li, Luchao 
                AU  - Shi, Benkang 
                AU  - Hao, Yichang 
                AU  - Xia, Chuanyou 
                AU  - Nie, Qingsheng 
                AU  - Xin, Yue 
                AU  - Shi, Zhenfeng 
                AU  - Ma, Lulin 
                AU  - Xu, Dawei 
                AU  - Liu, Cheng 
                TI  - High expression of SMYD3 indicates poor survival outcome and promotes tumour progression through an IGF-1R/AKT/E2F-1 positive feedback loop in bladder cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102718
                DO  - 10.18632/aging.102718
                SP  - 2030
                EP  - 2048
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wang, Guoliang 
                AU  - Huang, Yi 
                AU  - Yang, Feilong 
                AU  - Tian, Xiaojun 
                AU  - Wang, Kun 
                AU  - Liu, Li 
                AU  - Fan, Yidong 
                AU  - Li, Xiaofeng 
                AU  - Li, Luchao 
                AU  - Shi, Benkang 
                AU  - Hao, Yichang 
                AU  - Xia, Chuanyou 
                AU  - Nie, Qingsheng 
                AU  - Xin, Yue 
                AU  - Shi, Zhenfeng 
                AU  - Ma, Lulin 
                AU  - Xu, Dawei 
                AU  - Liu, Cheng 
                TI  - High expression of SMYD3 indicates poor survival outcome and promotes tumour progression through an IGF-1R/AKT/E2F-1 positive feedback loop in bladder cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102718
                DO  - 10.18632/aging.102718
                SP  - 2030
                EP  - 2048
                PY  - 
                AB  - The AKT/mTOR pathway is critical for bladder cancer (BC) pathogenesis and is hyper-activated during BC progression. In the present study, we identified a novel positive feedback loop involving oncogenic factors histone methyltransferase SMYD3, insulin-like growth factor-1 receptor (IGF-1R), AKT, and E2F-1. SMYD3 expression was significantly up-regulated in BC tumors and positively associated with histological grade, lymph node metastasis, and shorter patient survival. Depletion of SMYD3 inhibited BC cell proliferation, colony formation, migration, invasion, and xenograft tumor growth. Mechanistically, SMYD3 inhibition led to the diminished AKT/mTOR signaling activity, thereby triggering deleterious effects on BC cells. Furthermore, SMYD3 directly activates the expression of IGF-1R, a critical activator of AKT in BC, by inducing hyper-methylation of histone H3-K4 and subsequent chromatin remodeling in the IGF-1R promoter region. On the other hand, E2F-1, a downstream factor of the AKT pathway, binds to the E2F-1 binding motifs at the SMYD3 promoter and consequently induces SMYD3 transcription and expression. Thus, SMYD3/IGF-1R/AKT/E2F-1 forms a positive feedback loop leading to the hyper-activated AKT signaling. Our findings provide not only profound insights into SMYD3-mediated oncogenic activity but also present a unique avenue for treating BC by directly disrupting this signaling circuit.
                ER  -

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Targeting of miR-96-5p by catalpol ameliorates oxidative stress and hepatic steatosis in LDLr-/- mice via p66shc/cytochrome C cascade

Yukun Zhang, Changyuan Wang, Jiawei Lu, Yue Jin, Canyao Xu, Qiang Meng, Qi Liu, Deshi Dong, Xiaodong Ma, Kexin Liu, Huijun Sun,

https://doi.org/10.18632/aging.102721 pp 2049—2069

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Zhang Y, Wang C, Lu J, Jin Y, Xu C, Meng Q, Liu Q, Dong D, Ma X, Liu K, Sun H, . Targeting of miR-96-5p by catalpol ameliorates oxidative stress and hepatic steatosis in LDLr-/- mice via p66shc/cytochrome C cascade. . 12:2049-2069. https://doi.org/10.18632/aging.102721

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                TY  - JOUR
                AU  - Zhang, Yukun 
                AU  - Wang, Changyuan 
                AU  - Lu, Jiawei 
                AU  - Jin, Yue 
                AU  - Xu, Canyao 
                AU  - Meng, Qiang 
                AU  - Liu, Qi 
                AU  - Dong, Deshi 
                AU  - Ma, Xiaodong 
                AU  - Liu, Kexin 
                AU  - Sun, Huijun 
                TI  - Targeting of miR-96-5p by catalpol ameliorates oxidative stress and hepatic steatosis in LDLr-/- mice via p66shc/cytochrome C cascade
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102721
                DO  - 10.18632/aging.102721
                SP  - 2049
                EP  - 2069
                PY  - 
                AB  - Hepatic steatosis and oxidative stress are considered to be the sequential steps in the development of non-alcoholic fatty liver disease (NAFLD). We previously found that catalpol, an iridoid glucoside extracted from the root of Romania glutinosa L, protected against diabetes-induced hepatic oxidative stress. Here, we found that the increased expression of p66shc was observed in NAFLD models and catalpol could inhibit p66shc expression to ameliorate NAFLD effectively. However, the underlying mechanisms remained unknown. The aim of the present study was to investigate the p66shc-targeting miRNAs in regulating oxidative stress and hepatic steatosis, also the mechanisms of catalpol inhibiting NAFLD. We found that the effects of catalpol inhibiting hepatic oxidative stress and steasis are dependent on inhibiting P66Shc expression. In addition, miR-96-5p was able to suppress p66shc/cytochrome C cascade via targeting p66shc mRNA 3&#x2019;UTR, and catalpol could lead to suppression of NAFLD via upregulating miR-96-5p level. Thus, catalpol was effective in ameliorating NAFLD, and miR-96-5p/p66shc/cytochrome C cascade might be a potential target.
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Mitochondria and aging in older individuals: an analysis of DNA methylation age metrics, leukocyte telomere length, and mitochondrial DNA copy number in the VA normative aging study

Jacopo Dolcini, Haotian Wu, Jamaji C. Nwanaji-Enwerem, Marianthi-Anna Kiomourtozlogu, Akin Cayir, Marco Sanchez-Guerra, Pantel Vokonas, Joel Schwarz, Andrea A. Baccarelli,

https://doi.org/10.18632/aging.102722 pp 2070—2083

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Dolcini J, Wu H, Nwanaji-Enwerem JC, Kiomourtozlogu M, Cayir A, Sanchez-Guerra M, Vokonas P, Schwarz J, Baccarelli AA, . Mitochondria and aging in older individuals: an analysis of DNA methylation age metrics, leukocyte telomere length, and mitochondrial DNA copy number in the VA normative aging study. . 12:2070-2083. https://doi.org/10.18632/aging.102722

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                TY  - JOUR
                AU  - Dolcini, Jacopo 
                AU  - Wu, Haotian 
                AU  - Nwanaji-Enwerem, Jamaji C. 
                AU  - Kiomourtozlogu, Marianthi-Anna 
                AU  - Cayir, Akin 
                AU  - Sanchez-Guerra, Marco 
                AU  - Vokonas, Pantel 
                AU  - Schwarz, Joel 
                AU  - Baccarelli, Andrea A. 
                TI  - Mitochondria and aging in older individuals: an analysis of DNA methylation age metrics, leukocyte telomere length, and mitochondrial DNA copy number in the VA normative aging study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102722
                DO  - 10.18632/aging.102722
                SP  - 2070
                EP  - 2083
                PY  - 
                AB  - Population aging is a looming global health challenge. New biological aging metrics based on DNA methylation levels have been developed in addition to traditional aging biomarkers. The prospective relationships of aging biomarkers with mitochondrial changes are still not well understood. Here, we examined the prospective associations of mitochondrial copy number (mtDNAcn) with several aging biomarkers &#x2013; DNAm-Age, DNAm-PhenoAge, DNAm-GrimAge, and leukocyte telomere length. We analyzed 812 individuals from Veteran Affairs Normative Aging Study (NAS) with available blood samples from 1999-2013. Whole blood mtDNAcn and relative leukocyte telomere length were measured via qPCR. DNA methylation was assessed and used to calculate DNAm-Age, DNAm-GrimAge, and DNAm-PhenoAge. Linear mixed models were used to quantify the associations of mtDNAcn with DNAm-Age, DNAm-GrimAge, DNAm-PhenoAge, and leukocyte telomere length. In multivariable cross-sectional analyses, mtDNAcn is negatively associated with DNAm-Age PhenoAge and DNAm-PhenoAge. In contrast, mtDNAcn is associated with prospective measures of higher DNAm-PhenoAge and shorter leukocyte telomere length. Our study shows that higher mtDNAcn is associated with prospective measures of greater DNAm-PhenoAge and shorter leukocyte telomere length independent of chronological age. This indicates a role for mitochondrial in aging-related disease and mortality, but not the departure of biological age from chronological age.
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Insulin impedes osteogenesis of BMSCs by inhibiting autophagy and promoting premature senescence via the TGF-β1 pathway

Ping Zhang, Hengguo Zhang, Jialin Lin, Tao Xiao, Rongyao Xu, Yu Fu, Yuchao Zhang, Yifei Du, Jie Cheng, Hongbing Jiang,

https://doi.org/10.18632/aging.102723 pp 2084—2100

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Zhang P, Zhang H, Lin J, Xiao T, Xu R, Fu Y, Zhang Y, Du Y, Cheng J, Jiang H, . Insulin impedes osteogenesis of BMSCs by inhibiting autophagy and promoting premature senescence via the TGF-β1 pathway. . 12:2084-2100. https://doi.org/10.18632/aging.102723

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                TY  - JOUR
                AU  - Zhang, Ping 
                AU  - Zhang, Hengguo 
                AU  - Lin, Jialin 
                AU  - Xiao, Tao 
                AU  - Xu, Rongyao 
                AU  - Fu, Yu 
                AU  - Zhang, Yuchao 
                AU  - Du, Yifei 
                AU  - Cheng, Jie 
                AU  - Jiang, Hongbing 
                TI  - Insulin impedes osteogenesis of BMSCs by inhibiting autophagy and promoting premature senescence via the TGF-β1 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102723
                DO  - 10.18632/aging.102723
                SP  - 2084
                EP  - 2100
                PY  - 
                AB  - The dysfunction of bone marrow stromal cells (BMSCs) may be a core factor in Type 2 diabetes mellitus (T2DM) associated osteoporosis. However, the underlying mechanism is not well understood. Here, we delineated the critical role of insulin impeding osteogenesis of BMSCs in T2DM. Compared with BMSCs from healthy people (H-BMSCs), BMSCs from T2DM patient (DM-BMSCs) showed decreased osteogenic differentiation and autophagy level, and increased senescent phenotype. H-BMSCs incubated in hyperglycemic and hyperinsulinemic conditions similarly showed these phenotypes of DM-BMSCs. Notably, enhanced TGF-&#x3B2;1 expression was detected not only in DM-BMSCs and high-glucose and insulin-treated H-BMSCs, but also in bone callus of streptozocin-induced diabetic rats. Moreover, inhibiting TGF-&#x3B2;1 signaling not only enhanced osteogenic differentiation and autophagy level of DM-BMSCs, but also delayed senescence of DM-BMSCs, as well as promoted mandible defect healing of diabetic rats. Finally, we further verified that it was TGF-&#x3B2; receptor II (T&#x3B2;RII), not T&#x3B2;RI, markedly increased in both DM-BMSCs and insulin-treated H-BMSCs. Our data revealed that insulin impeded osteogenesis of BMSCs by inhibiting autophagy and promoting premature senescence, which it should be responsible for T2DM-induced bone loss, at least in part. These findings suggest that inhibiting TGF-&#x3B2;1 pathway may be a potential therapeutic target for T2DM associated bone disorders.
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CSF1R inhibitor PLX5622 and environmental enrichment additively improve metabolic outcomes in middle-aged female mice

Seemaab Ali, Anthony G. Mansour, Wei Huang, Nicholas J. Queen, Xiaokui Mo, Jacqueline M. Anderson, Quais N. Hassan II, Ripal S. Patel, Ryan K. Wilkins, Michael A. Caligiuri, Lei Cao,

https://doi.org/10.18632/aging.102724 pp 2101—2122

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Ali S, Mansour AG, Huang W, Queen NJ, Mo X, Anderson JM, Hassan II QN, Patel RS, Wilkins RK, Caligiuri MA, Cao L, . CSF1R inhibitor PLX5622 and environmental enrichment additively improve metabolic outcomes in middle-aged female mice. . 12:2101-2122. https://doi.org/10.18632/aging.102724

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                TY  - JOUR
                AU  - Ali, Seemaab 
                AU  - Mansour, Anthony G. 
                AU  - Huang, Wei 
                AU  - Queen, Nicholas J. 
                AU  - Mo, Xiaokui 
                AU  - Anderson, Jacqueline M. 
                AU  - Hassan II, Quais N. 
                AU  - Patel, Ripal S. 
                AU  - Wilkins, Ryan K. 
                AU  - Caligiuri, Michael A. 
                AU  - Cao, Lei 
                TI  - CSF1R inhibitor PLX5622 and environmental enrichment additively improve metabolic outcomes in middle-aged female mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102724
                DO  - 10.18632/aging.102724
                SP  - 2101
                EP  - 2122
                PY  - 
                AB  - As the elderly population grows, chronic metabolic dysfunction including obesity and diabetes are becoming increasingly common comorbidities. Hypothalamic inflammation through CNS resident microglia serves as a common pathway between developing obesity and developing systemic aging pathologies. Despite understanding aging as a life-long process involving interactions between individuals and their environment, limited studies address the dynamics of environment interactions with aging or aging therapeutics. We previously demonstrated environmental enrichment (EE) is an effective model for studying improved metabolic health and overall healthspan in mice, which acts through a brain-fat axis. Here we investigated the CSF1R inhibitor PLX5622 (PLX), which depletes microglia, and its effects on metabolic decline in aging in interaction with EE. PLX in combination with EE substantially improved metabolic outcomes in middle-aged female mice over PLX or EE alone. Chronic PLX treatment depleted 75% of microglia from the hypothalamus and reduced markers of inflammation without affecting brain-derived neurotrophic factor levels induced by EE. Adipose tissue remodeling and adipose tissue macrophage modulation were observed in response to CSF1R inhibition, which may contribute to the combined benefits seen in EE with PLX. Our study suggests benefits exist from combined drug and lifestyle interventions in aged animals.
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Bone morphogenetic protein 9, and its genetic variants contribute to susceptibility of idiopathic pulmonary arterial hypertension

Kefang Guo, Liying Xu, Lin Jin, Huilin Wang, Yun Ren, Yan Hu, Jing Yu, Jing Cang,

https://doi.org/10.18632/aging.102726 pp 2123—2131

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Guo K, Xu L, Jin L, Wang H, Ren Y, Hu Y, Yu J, Cang J, . Bone morphogenetic protein 9, and its genetic variants contribute to susceptibility of idiopathic pulmonary arterial hypertension. . 12:2123-2131. https://doi.org/10.18632/aging.102726

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                TY  - JOUR
                AU  - Guo, Kefang 
                AU  - Xu, Liying 
                AU  - Jin, Lin 
                AU  - Wang, Huilin 
                AU  - Ren, Yun 
                AU  - Hu, Yan 
                AU  - Yu, Jing 
                AU  - Cang, Jing 
                TI  - Bone morphogenetic protein 9, and its genetic variants contribute to susceptibility of idiopathic pulmonary arterial hypertension
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102726
                DO  - 10.18632/aging.102726
                SP  - 2123
                EP  - 2131
                PY  - 
                AB  - Considering the predominant role of rare variants of the Bone morphogenetic protein 9 (BMP9) gene in the occurrence of idiopathic pulmonary arterial hypertension (IPAH), here we conducted a case-control study, together with functional validation, to explore the relationships between variants of the BMP9 gene and development of IPAH. We found minor alleles of rs3740297 (OR: 0.72, 95% CI: 0.59-0.87, P=7.77&#xD7;10-5) and rs7923671 (OR: 0.76, 95% CI: 0.62-0.93, P=0.009) were significantly associated with decreased risk of IPAH. Minor alleles of rs3740297 and rs7923671 were significantly associated with increased plasma level of BMP9 in both IPAH cases and controls (P&lt;0.001). An allele of rs7923671 showed higher relative luciferase activity compared to that containing G allele (P&lt;0.001). Mechanism exploration found that pulmonary artery smooth muscle cells (PASMC) cell line transfected with rs3740297 C allele construct, miR-149 mimic, and antagomir miR-149 showed more sensitive change of the relative luciferase activity and BMP9 expression. This means minor allele T of rs3740297 could significantly decrease susceptibility of IPAH in Chinese population, possibly by increasing BMP9 expression through losing a miR-149 binding site. Our study provides evidence for genetic associations between two specific variants in the BMP9 gene and plasma level of BMP9, occurrence of IPAH.
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EP300 mutation is associated with tumor mutation burden and promotes antitumor immunity in bladder cancer patients

Gongmin Zhu, Lijiao Pei, Yuan Li, Xin Gou,

https://doi.org/10.18632/aging.102728 pp 2132—2141

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Zhu G, Pei L, Li Y, Gou X, . EP300 mutation is associated with tumor mutation burden and promotes antitumor immunity in bladder cancer patients. . 12:2132-2141. https://doi.org/10.18632/aging.102728

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                TY  - JOUR
                AU  - Zhu, Gongmin 
                AU  - Pei, Lijiao 
                AU  - Li, Yuan 
                AU  - Gou, Xin 
                TI  - EP300 mutation is associated with tumor mutation burden and promotes antitumor immunity in bladder cancer patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102728
                DO  - 10.18632/aging.102728
                SP  - 2132
                EP  - 2141
                PY  - 
                AB  - Bladder cancer is a leading cause of morbidity and mortality worldwide. Currently, immunotherapy has become a worthwhile therapy for bladder cancer. Tumor mutation burden (TMB) has been regarded as the most prevalent biomarker to predict immunotherapy. Bladder cancer is reported to have the third highest mutation rate. However, whether these gene mutations are related to TMB and immune response remain unknown. In this study, we downloaded somatic mutation data of bladder cancer from The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) datasets, and found 11 frequently mutated genes were covered by both two cohorts including FGFR3, TTN, XIRP2, CREBBP, PIK3CA, TP53, MUC16, EP300 (E1A binding protein P300), ARID1A, ERBB2, and KDM6A. Among them, EP300 mutation was associated with higher TMB and indicated a favorable clinical prognosis. Furthermore, based on Gene set enrichment analysis (GSEA) and CIBERSORT algorithm, we observed that EP300 mutation upregulated signaling pathways involved in immune system and enhanced antitumor immune response. In conclusion, EP300 is frequently mutated in bladder cancer, and its mutation is associated with increased TMB and promotes antitumor immunity, which may serve as a biomarker to predict immune response.
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Baicalin alleviates benign prostate hyperplasia through androgen-dependent apoptosis

Bo-Ram Jin, Hyo-Jin An,

https://doi.org/10.18632/aging.102731 pp 2142—2155

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Jin B, An H, . Baicalin alleviates benign prostate hyperplasia through androgen-dependent apoptosis. . 12:2142-2155. https://doi.org/10.18632/aging.102731

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                TY  - JOUR
                AU  - Jin, Bo-Ram 
                AU  - An, Hyo-Jin 
                TI  - Baicalin alleviates benign prostate hyperplasia through androgen-dependent apoptosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102731
                DO  - 10.18632/aging.102731
                SP  - 2142
                EP  - 2155
                PY  - 
                AB  - BPH is a disease prevalent among elderly men that is characterized by abnormal proliferation of prostatic epithelial and stromal tissues. No effective treatment exists for BPH owing to lack of a clear understanding of its molecular etiology. Although several studies have reported therapeutic effects of baicalin against numerous diseases, including prostate cancer, its beneficial effects on BPH have not yet been explored. The present study investigated the therapeutic effects of baicalin on the development of BPH and its mechanism of action. We established a testosterone-treated BPH animal model and DHT-stimulated prostate cell lines, including RWPE-1 and WPMY-1. Administration of baicalin ameliorated the pathological prostate enlargement, suppressed the production of DHT, and inhibited the activity of 5&#x3B1;- reductase Type II in the animal model. BC exerted these effects via its anti-proliferative effects by restoring the Bax/Bcl-2 ratio, activating caspase-3 and caspase-8, and inducing the phosphorylation of AMPK. In vitro studies using DHT-stimulated prostate cells demonstrated an up-regulation of BPH-related and proliferation markers, whereas baicalin clearly reduced the overexpression of AR, PSA, PCNA, and Bcl-2. These results suggested that baicalin could suppress androgen-dependent development of BPH both in vivo and in vitro by inducing apoptosis.
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Knockdown of P3H4 inhibits proliferation and invasion of bladder cancer

Lin Hao, Kun Pang, Hui Pang, Junjie Zhang, Zhiguo Zhang, Houguang He, Rongsheng Zhou, Zhenduo Shi, Conghui Han,

https://doi.org/10.18632/aging.102732 pp 2156—2168

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Hao L, Pang K, Pang H, Zhang J, Zhang Z, He H, Zhou R, Shi Z, Han C, . Knockdown of P3H4 inhibits proliferation and invasion of bladder cancer. . 12:2156-2168. https://doi.org/10.18632/aging.102732

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                TY  - JOUR
                AU  - Hao, Lin 
                AU  - Pang, Kun 
                AU  - Pang, Hui 
                AU  - Zhang, Junjie 
                AU  - Zhang, Zhiguo 
                AU  - He, Houguang 
                AU  - Zhou, Rongsheng 
                AU  - Shi, Zhenduo 
                AU  - Han, Conghui 
                TI  - Knockdown of P3H4 inhibits proliferation and invasion of bladder cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102732
                DO  - 10.18632/aging.102732
                SP  - 2156
                EP  - 2168
                PY  - 
                AB  - The prolyl 3-hydroxylase family member 4 (P3H4) (alias SC65) is implicated in a variety of physiological and pathological processes. However, little is known about the role of P3H4 in tumors. This study aimed to investigate the role of P3H4 in bladder cancer (BC) and the regulatory mechanisms that influence its expression. P3H4 was highly expressed in BC tissues. Knockdown of P3H4 inhibited BC cell proliferation, cell cycle, migration and invasion in vitro, and inhibited BC growth in vivo. We also found that ETV4 bound directly to the promoter region of P3H4 and activated its transcription. Furthermore, overexpression of ETV4 rescued the inhibition of proliferation and invasion induced by PH4 silencing. ETV4 was significantly overexpressed in the BC tissues. In conclusion, P3H4 functioned an oncogene role in BC progression, and ETV4 bound directly to the P3H4 promoter region to regulate its transcription.
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Identification of 34 genes conferring genetic and pharmacological risk for the comorbidity of schizophrenia and smoking behaviors

Yunlong Ma, Jingjing Li, Yi Xu, Yan Wang, Yinghao Yao, Qiang Liu, Maiqiu Wang, Xinyi Zhao, Rongli Fan, Jiali Chen, Bin Zhang, Zhen Cai, Haijun Han, Zhongli Yang, Wenji Yuan, Yigang Zhong, Xiangning Chen, Jennie Z. Ma, Thomas J. Payne, Yizhou Xu, Yuping Ning, Wenyan Cui, Ming D. Li,

https://doi.org/10.18632/aging.102735 pp 2169—2225

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Ma Y, Li J, Xu Y, Wang Y, Yao Y, Liu Q, Wang M, Zhao X, Fan R, Chen J, Zhang B, Cai Z, Han H, et al, . Identification of 34 genes conferring genetic and pharmacological risk for the comorbidity of schizophrenia and smoking behaviors. . 12:2169-2225. https://doi.org/10.18632/aging.102735

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                TY  - JOUR
                AU  - Ma, Yunlong 
                AU  - Li, Jingjing 
                AU  - Xu, Yi 
                AU  - Wang, Yan 
                AU  - Yao, Yinghao 
                AU  - Liu, Qiang 
                AU  - Wang, Maiqiu 
                AU  - Zhao, Xinyi 
                AU  - Fan, Rongli 
                AU  - Chen, Jiali 
                AU  - Zhang, Bin 
                AU  - Cai, Zhen 
                AU  - Han, Haijun 
                AU  - Yang, Zhongli 
                AU  - Yuan, Wenji 
                AU  - Zhong, Yigang 
                AU  - Chen, Xiangning 
                AU  - Ma, Jennie Z. 
                AU  - Payne, Thomas J. 
                AU  - Xu, Yizhou 
                AU  - Ning, Yuping 
                AU  - Cui, Wenyan 
                AU  - Li, Ming D. 
                TI  - Identification of 34 genes conferring genetic and pharmacological risk for the comorbidity of schizophrenia and smoking behaviors
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102735
                DO  - 10.18632/aging.102735
                SP  - 2169
                EP  - 2225
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ma, Yunlong 
                AU  - Li, Jingjing 
                AU  - Xu, Yi 
                AU  - Wang, Yan 
                AU  - Yao, Yinghao 
                AU  - Liu, Qiang 
                AU  - Wang, Maiqiu 
                AU  - Zhao, Xinyi 
                AU  - Fan, Rongli 
                AU  - Chen, Jiali 
                AU  - Zhang, Bin 
                AU  - Cai, Zhen 
                AU  - Han, Haijun 
                AU  - Yang, Zhongli 
                AU  - Yuan, Wenji 
                AU  - Zhong, Yigang 
                AU  - Chen, Xiangning 
                AU  - Ma, Jennie Z. 
                AU  - Payne, Thomas J. 
                AU  - Xu, Yizhou 
                AU  - Ning, Yuping 
                AU  - Cui, Wenyan 
                AU  - Li, Ming D. 
                TI  - Identification of 34 genes conferring genetic and pharmacological risk for the comorbidity of schizophrenia and smoking behaviors
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102735
                DO  - 10.18632/aging.102735
                SP  - 2169
                EP  - 2225
                PY  - 
                AB  - The prevalence of smoking is significantly higher in persons with schizophrenia (SCZ) than in the general population. However, the biological mechanisms of the comorbidity of smoking and SCZ are largely unknown. This study aimed to reveal shared biological pathways for the two diseases by analyzing data from two genome-wide association studies with a total sample size of 153,898. With pathway-based analysis, we first discovered 18 significantly enriched pathways shared by SCZ and smoking, which were classified into five groups: postsynaptic density, cadherin binding, dendritic spine, long-term depression, and axon guidance. Then, by using an integrative analysis of genetic, epigenetic, and expression data, we found not only 34 critical genes (e.g., PRKCZ, ARHGEF3, and CDKN1A) but also various risk-associated SNPs in these genes, which convey susceptibility to the comorbidity of the two disorders. Finally, using both in vivo and in vitro data, we demonstrated that the expression profiles of the 34 genes were significantly altered by multiple psychotropic drugs. Together, this multi-omics study not only reveals target genes for new drugs to treat SCZ but also reveals new insights into the shared genetic vulnerabilities of SCZ and smoking behaviors.
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Aucubin exerts anti-osteoporotic effects by promoting osteoblast differentiation

Yutong Li, Yongfeng Zhang, Xinrui Zhang, Wenqian Lu, Xin Liu, Min Hu, Di Wang,

https://doi.org/10.18632/aging.102742 pp 2226—2245

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Li Y, Zhang Y, Zhang X, Lu W, Liu X, Hu M, Wang D, . Aucubin exerts anti-osteoporotic effects by promoting osteoblast differentiation. . 12:2226-2245. https://doi.org/10.18632/aging.102742

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                TY  - JOUR
                AU  - Li, Yutong 
                AU  - Zhang, Yongfeng 
                AU  - Zhang, Xinrui 
                AU  - Lu, Wenqian 
                AU  - Liu, Xin 
                AU  - Hu, Min 
                AU  - Wang, Di 
                TI  - Aucubin exerts anti-osteoporotic effects by promoting osteoblast differentiation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102742
                DO  - 10.18632/aging.102742
                SP  - 2226
                EP  - 2245
                PY  - 
                AB  - Osteoporosis is a metabolic disease characterized by reduced osteoblast differentiation and proliferation. Oxidative stress plays a role in the pathogenesis of osteoporosis. Aucubin (AU), an iridoid glycoside, was previously shown to promote osteoblast differentiation. We investigated the effects of AU on MG63 human osteoblast-like cells treated with dexamethasone (Dex) or hydrogen peroxide (H2O2) to induce oxidative damage. AU protected MG63 cells against apoptosis, and promoted increased expression of cytokines associated with osteoblast differentiation, including collagen I, osteocalcin (OCN), osteopontin (OPN), and osterix. In Dex- and H2O2-treated MG63 cells, AU also enhanced the expression of anti-oxidative stress-associated factors in the nuclear respiratory factor 2 signaling pathway, including superoxide dismutases 1 and 2, heme oxygenases 1 and 2, and catalase. In vivo, using a Dex-induced mouse model of osteoporosis, AU promoted increased cortical bone thickness, increased bone density, and tighter trabecular bone. Additionally, it stimulated an increase in the expression of collagen I, OCN, OPN, osterix, and phosphorylated Akt and Smads in bone tissue. Finally, AU stimulated the expression of cytokines associated with osteoblast differentiation in bone tissue and serum. Our data indicate AU may have therapeutic efficacy in osteoporosis.
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The protein tyrosine kinase inhibitor, Genistein, delays intervertebral disc degeneration in rats by inhibiting the p38 pathway-mediated inflammatory response

Jun Ge, Quan Zhou, Xiaoqiang Cheng, Jiale Qian, Qi Yan, Cenhao Wu, Yufeng Chen, Huilin Yang, Jun Zou,

https://doi.org/10.18632/aging.102743 pp 2246—2260

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Ge J, Zhou Q, Cheng X, Qian J, Yan Q, Wu C, Chen Y, Yang H, Zou J, . The protein tyrosine kinase inhibitor, Genistein, delays intervertebral disc degeneration in rats by inhibiting the p38 pathway-mediated inflammatory response. . 12:2246-2260. https://doi.org/10.18632/aging.102743

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                TY  - JOUR
                AU  - Ge, Jun 
                AU  - Zhou, Quan 
                AU  - Cheng, Xiaoqiang 
                AU  - Qian, Jiale 
                AU  - Yan, Qi 
                AU  - Wu, Cenhao 
                AU  - Chen, Yufeng 
                AU  - Yang, Huilin 
                AU  - Zou, Jun 
                TI  - The protein tyrosine kinase inhibitor, Genistein, delays intervertebral disc degeneration in rats by inhibiting the p38 pathway-mediated inflammatory response
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102743
                DO  - 10.18632/aging.102743
                SP  - 2246
                EP  - 2260
                PY  - 
                AB  - The treatment for intervertebral disc degeneration (IDD) has drawn great attention and recent studies have revealed that the p38 MAPK pathway is a potential therapeutic target for delaying the degeneration of intervertebral discs. In this study, we analyzed a nature-derived protein tyrosine kinase inhibitor, Genistein, and its function in delaying IDD in rats both in vitro and in vivo via the p38 MAPK pathway. Nucleus pulposus cells treated with Genistein showed better function compared with untreated cells. Further study revealed that Genistein could play a protective role in IDD by inhibiting phosphorylation of p38, consequently inhibiting the p38 pathway-mediated inflammatory response. The rat IDD model also demonstrated that Genistein could effectively delay the degeneration of intervertebral disc tissue. The current study reveals new biological functions of Genistein, further demonstrates the effects of the p38 MAPK pathway on intervertebral disc degeneration, and deepens our understanding of the treatment and prevention of IDD.
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TYRO3 facilitates cell growth and metastasis via activation of the Wnt/β-catenin signaling pathway in human gastric cancer cells

Dehu Chen, Qinghong Liu, Gan Cao, Wei Zhang,

https://doi.org/10.18632/aging.102744 pp 2261—2274

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Chen D, Liu Q, Cao G, Zhang W, . TYRO3 facilitates cell growth and metastasis via activation of the Wnt/β-catenin signaling pathway in human gastric cancer cells. . 12:2261-2274. https://doi.org/10.18632/aging.102744

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                TY  - JOUR
                AU  - Chen, Dehu 
                AU  - Liu, Qinghong 
                AU  - Cao, Gan 
                AU  - Zhang, Wei 
                TI  - TYRO3 facilitates cell growth and metastasis via activation of the Wnt/β-catenin signaling pathway in human gastric cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102744
                DO  - 10.18632/aging.102744
                SP  - 2261
                EP  - 2274
                PY  - 
                AB  - It has become increasingly important to identify valuable therapeutic targets to improve the prognosis of cancer patients. Although emerging evidence has suggested TYRO3 as a potential therapeutic target in various types of cancers, less is known about its role in gastric cancer (GC) development. Herein, we investigated the functional and molecular mechanisms by which TYRO3 influenced GC. TYRO3 mRNA and protein were evaluated by quantitative real-time PCR (qRT-PCR), western blotting, and immunohistochemistry. Other methods including stable transfection of TYRO3 into GC cells, wound healing, Transwell assays, CCK-8 assays, colony formation assays, immunocytochemistry in vitro, and tumorigenesis in vivo were also conducted. Our results indicated that high levels of TYRO3 significantly correlated with clinical metastasis and poor prognoses in patients with GC. In addition, TYRO3 silencing distinctively suppressed GC cell growth, invasion, and metastasis both in vitro and in vivo. Conversely, TYRO3 overexpression led to the opposite effects. Mechanistic analyses revealed that the Wnt/&#x3B2;-catenin signaling pathway might be involved in TYRO3-facilitated GC cell behavior. Collectively, we demonstrated that elevated TYRO3 expression contributed to GC cell growth and metastasis via the Wnt/&#x3B2;-catenin pathway, suggesting a novel therapeutic target for GC.
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PAS kinase deficiency reduces aging effects in mice

Pilar Dongil, Ana Pérez-García, Verónica Hurtado-Carneiro, Carmen Herrero-de-Dios, Elvira Álvarez, Carmen Sanz,

https://doi.org/10.18632/aging.102745 pp 2275—2301

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Dongil P, Pérez-García A, Hurtado-Carneiro V, Herrero-de-Dios C, Álvarez E, Sanz C, . PAS kinase deficiency reduces aging effects in mice. . 12:2275-2301. https://doi.org/10.18632/aging.102745

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                TY  - JOUR
                AU  - Dongil, Pilar 
                AU  - Pérez-García, Ana 
                AU  - Hurtado-Carneiro, Verónica 
                AU  - Herrero-de-Dios, Carmen 
                AU  - Álvarez, Elvira 
                AU  - Sanz, Carmen 
                TI  - PAS kinase deficiency reduces aging effects in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102745
                DO  - 10.18632/aging.102745
                SP  - 2275
                EP  - 2301
                PY  - 
                AB  - Several signaling pathways may be affected during aging. All are regulated by nutrient levels leading to a decline in mitochondrial function and autophagy and to an increase in oxidative stress. PAS Domain Kinase (PASK) is a nutrient and bioenergetic sensor. We have previously found that PASK plays a role in the control of hepatic metabolic balance and mitochondrial homeostasis. To investigate PASK&#x2019;s role in hepatic oxidative stress during aging, we analyzed the mitochondrial function, glucose tolerance, insulin resistance, and lipid-related parameters in aged PASK-deficient mice. Hepatic Pask mRNA decreased in step with aging, being undetectable in aged wild-type (WT) mice. Aged PASK-deficient mice recorded lower levels of ROS/RNS compared to aged WT. The regulators of mitochondrial biogenesis, PGC1a, SIRT1 and NRF2, decreased in aged WT, while aged PASK-deficient mice recorded a higher expression of NRF2, GCLm and HO1 proteins and CS activity under fasted conditions. Additionally, aged PASK-deficient mice recorded an overexpression of the longevity gene FoxO3a, and maintained elevated PCNA protein, suggesting that hepatic cell repair mechanisms might be functional. PASK-deficient mice have better insulin sensitivity and no glucose intolerance, as confirmed by a normal HOMA-IR index. PASK may be a good target for reducing damage during aging.
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Identification of an immune-related risk signature for predicting prognosis in clear cell renal cell carcinoma

Xiaoliang Hua, Juan Chen, Yang Su, Chaozhao Liang,

https://doi.org/10.18632/aging.102746 pp 2302—2332

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Hua X, Chen J, Su Y, Liang C, . Identification of an immune-related risk signature for predicting prognosis in clear cell renal cell carcinoma. . 12:2302-2332. https://doi.org/10.18632/aging.102746

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                TY  - JOUR
                AU  - Hua, Xiaoliang 
                AU  - Chen, Juan 
                AU  - Su, Yang 
                AU  - Liang, Chaozhao 
                TI  - Identification of an immune-related risk signature for predicting prognosis in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102746
                DO  - 10.18632/aging.102746
                SP  - 2302
                EP  - 2332
                PY  - 
                AB  - Immune status affects the initiation and progression of clear cell renal cell carcinoma (ccRCC), the most common subtype of renal cell carcinoma. In this study, we identified an immune-related, five-gene signature that improves survival prediction in ccRCC. Patients were classified as high- and low-risk based on the signature risk score. Survival analysis showed differential prognosis, while principal component analysis revealed distinctly different immune phenotypes between the two risk groups. High-risk patients tended to have advanced stage, higher grade disease, and poorer prognoses. Functional enrichment analysis showed that the signature genes were mainly involved in the cytokine-cytokine receptor interaction pathway. Moreover, we found that tumors from high-risk patients had higher relative abundance of T follicular helper cells, regulatory T cells, and M0 macrophages, and higher expression of PD-1, CTLA-4, LAG3, and CD47 than low-risk patients. This suggests our gene signature may not only serve as an indicator of tumor immune status, but may be a promising tool to select high-risk patients who may benefit from immune checkpoint inhibitor therapy. Multivariate Cox regression analysis showed that the signature remained an independent prognostic factor after adjusting for clinicopathological variables, while prognostic accuracy was further improved after integrating clinical parameters into the analysis.
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Long non-coding RNA NNT-AS1 promotes cholangiocarcinoma cells proliferation and epithelial-to-mesenchymal transition through down-regulating miR-203

Yulei Gu, Zhiqiang Zhu, Hui Pei, Dong Xu, Yumin Jiang, Luanluan Zhang, Lili Xiao,

https://doi.org/10.18632/aging.102747 pp 2333—2346

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Gu Y, Zhu Z, Pei H, Xu D, Jiang Y, Zhang L, Xiao L, . Long non-coding RNA NNT-AS1 promotes cholangiocarcinoma cells proliferation and epithelial-to-mesenchymal transition through down-regulating miR-203. . 12:2333-2346. https://doi.org/10.18632/aging.102747

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                TY  - JOUR
                AU  - Gu, Yulei 
                AU  - Zhu, Zhiqiang 
                AU  - Pei, Hui 
                AU  - Xu, Dong 
                AU  - Jiang, Yumin 
                AU  - Zhang, Luanluan 
                AU  - Xiao, Lili 
                TI  - Long non-coding RNA NNT-AS1 promotes cholangiocarcinoma cells proliferation and epithelial-to-mesenchymal transition through down-regulating miR-203
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102747
                DO  - 10.18632/aging.102747
                SP  - 2333
                EP  - 2346
                PY  - 
                AB  - Background: Cholangiocarcinoma (CCA) is a serious malignant tumor. Long non-coding RNA NNT-AS1 (NNT-AS1) takes crucial roles in several tumors. So, we planned to research the roles and underlying mechanism of NNT-AS1 in CCA.Results: NNT-AS1 overexpression was appeared in CCA tissues and cell lines. Proliferation was promoted by NNT-AS1 overexpression in CCLP1 and TFK1 cells. Besides, NNT-AS1 overexpression reduced E-cadherin level and raised levels of N-cadherin, vimentin, Snail and Slug. However, the opposite trend was occurred by NNT-AS1 knockdown. Further, NNT-AS1 overexpression promoted phosphatidylinositol 3 kinase (PI3K)/AKT and extracellular signal-regulated kinase (ERK)1/2 pathways. MiR-203 was sponged by NNT-AS1 and miR-203 mimic reversed the above promoting effects of NNT-AS1. Additionally, insulin-like growth factor type 1 receptor (IGF1R) and zinc finger E-box binding homeobox 1 (ZEB1) were two potential targets of miR-203.Conclusion: NNT-AS1 promoted proliferation, EMT and PI3K/AKT and ERK1/2 pathways in CCLP1 and TFK1 cells through down-regulating miR-203.Methods: CCLP1 and TFK1 cells were co-transfected with pcDNA-NNT-AS1 and miR-203 mimic. Bromodeoxyuridine (BrdU), flow cytometry, quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot were employed to detect roles and mechanism of NNT-AS1. Interaction between NNT-AS1 and miR-203 or miR-203 and target genes was examined through luciferase activity experiment.
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Protein disulfide isomerases are promising targets for predicting the survival and tumor progression in glioma patients

Zhigang Peng, Yu Chen, Hui Cao, Hecun Zou, Xin Wan, Wenjing Zeng, Yanling Liu, Jiaqing Hu, Nan Zhang, Zhiwei Xia, Zhixiong Liu, Quan Cheng,

https://doi.org/10.18632/aging.102748 pp 2347—2372

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Peng Z, Chen Y, Cao H, Zou H, Wan X, Zeng W, Liu Y, Hu J, Zhang N, Xia Z, Liu Z, Cheng Q, . Protein disulfide isomerases are promising targets for predicting the survival and tumor progression in glioma patients. . 12:2347-2372. https://doi.org/10.18632/aging.102748

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                TY  - JOUR
                AU  - Peng, Zhigang 
                AU  - Chen, Yu 
                AU  - Cao, Hui 
                AU  - Zou, Hecun 
                AU  - Wan, Xin 
                AU  - Zeng, Wenjing 
                AU  - Liu, Yanling 
                AU  - Hu, Jiaqing 
                AU  - Zhang, Nan 
                AU  - Xia, Zhiwei 
                AU  - Liu, Zhixiong 
                AU  - Cheng, Quan 
                TI  - Protein disulfide isomerases are promising targets for predicting the survival and tumor progression in glioma patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102748
                DO  - 10.18632/aging.102748
                SP  - 2347
                EP  - 2372
                PY  - 
                AB  - The present study focused on the expression patterns, prognostic values and potential mechanism of the PDI family in gliomas. Most PDI family members&#x2019; mRNA expressions were observed significantly different between gliomas classified by clinical features. Construction of the PDI signature, cluster and risk score models of glioma was done using GSVA, consensus clustering analysis, and LASSO Cox regression analysis respectively. High values of PDI signature/ risk score and cluster 1 in gliomas were associated with malignant clinicopathological characteristics and poor prognosis. Analysis of the distinctive genomic alterations in gliomas revealed that many cases having high PDI signature and risk score were associated with genomic aberrations of driver oncogenes. GSVA analysis showed that PDI family was involved in many signaling pathways in ERAD, apoptosis, and MHC class I among many more. Prognostic nomogram revealed that the risk score was a good prognosis indicator for gliomas. The qRT-PCR and immunohistochemistry confirmed that P4HB, PDIA4 and PDIA5 were overexpressed in gliomas. In summary, this research highlighted the clinical importance of PDI family in tumorigenesis and progression in gliomas.
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UBE2M promotes cell proliferation via the β-catenin/cyclin D1 signaling in hepatocellular carcinoma

Guang-Cong Zhang, Xiang-Nan Yu, Jia-Lei Sun, Ju Xiong, Yi-Jun Yang, Xue-Mei Jiang, Ji-Min Zhu,

https://doi.org/10.18632/aging.102749 pp 2373—2392

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Zhang G, Yu X, Sun J, Xiong J, Yang Y, Jiang X, Zhu J, . UBE2M promotes cell proliferation via the β-catenin/cyclin D1 signaling in hepatocellular carcinoma. . 12:2373-2392. https://doi.org/10.18632/aging.102749

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                TY  - JOUR
                AU  - Zhang, Guang-Cong 
                AU  - Yu, Xiang-Nan 
                AU  - Sun, Jia-Lei 
                AU  - Xiong, Ju 
                AU  - Yang, Yi-Jun 
                AU  - Jiang, Xue-Mei 
                AU  - Zhu, Ji-Min 
                TI  - UBE2M promotes cell proliferation via the β-catenin/cyclin D1 signaling in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102749
                DO  - 10.18632/aging.102749
                SP  - 2373
                EP  - 2392
                PY  - 
                AB  - Upregulated ubiquitin-conjugating enzyme E2M (UBE2M) is associated with poor prognosis in malignancies; However, the phenotype and mechanism of action of UBE2M in hepatocellular carcinoma (HCC) remain elusive. Here, we report that UBE2M is overexpressed and correlated with poor prognosis in HCC patients. The UBE2M level is an independent prognostic factor for HCC patients. UBE2M knockdown inhibits HCC cell proliferation, migration, and invasion, whereas its overexpression has an opposite effect. Mechanistically, upregulated UBE2M exerts oncogenic effects by translocation of accumulated &#x3B2;-catenin from the cytoplasm to the nucleus, thus activating downstream &#x3B2;-catenin/cyclin D1 signaling. In summary, our study demonstrates a notable role of UBE2M in promoting the growth of HCC, providing a novel strategy for HCC prevention and treatment.
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Abnormal overexpression of G9a in melanoma cells promotes cancer progression via upregulation of the Notch1 signaling pathway

Ning-Ning Dang, Jing Jiao, Xianguang Meng, Yunhe An, Chen Han, Shuhong Huang,

https://doi.org/10.18632/aging.102750 pp 2393—2407

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Dang N, Jiao J, Meng X, An Y, Han C, Huang S, . Abnormal overexpression of G9a in melanoma cells promotes cancer progression via upregulation of the Notch1 signaling pathway. . 12:2393-2407. https://doi.org/10.18632/aging.102750

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                TY  - JOUR
                AU  - Dang, Ning-Ning 
                AU  - Jiao, Jing 
                AU  - Meng, Xianguang 
                AU  - An, Yunhe 
                AU  - Han, Chen 
                AU  - Huang, Shuhong 
                TI  - Abnormal overexpression of G9a in melanoma cells promotes cancer progression via upregulation of the Notch1 signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102750
                DO  - 10.18632/aging.102750
                SP  - 2393
                EP  - 2407
                PY  - 
                AB  - Malignant melanoma is a type of very dangerous skin cancer. Histone modifiers usually become dysregulated during the process of carcinoma development, thus there is potential for a histone modifier inhibitor as a useful drug for cancer therapy. There is a multitude of evidence regarding the role of G9a, a histone methyltransferase (HMTase), in tumorigenesis. In this study, we first showed that G9a was significantly upregulated in melanoma patients. Using the TCGA database, we found a significantly higher expression of G9a in primary melanoma samples (n = 461) compared to normal skin samples (n = 551). Next, we knocked down G9a in human M14 and A375 melanoma cell lines in vitro via small interfering RNA (siRNA). This resulted in a significant decrease in cell viability, migration and invasion, and an increase in cell apoptosis. UNC0642 is a small molecule inhibitor of G9a that demonstrates minimal cell toxicity and good in vivo pharmacokinetic characteristics. We investigated the role of UNC0642 in melanoma cells, and detected its anti-cancer effects in vitro and in vivo. Next, we treated cells with UNC0642, and observed a significant decrease in cell viability in M14 and A375 cell lines. Furthermore, treatment with UNC0642 resulted in increased apoptosis. In immunocompetent mice bearing A375 engrafts, treatment with UNC0642 inhibited tumor growth. Results of Western blot analysis revealed that administration of UNC0642 or silencing of G9a expression by siRNA reduced Notch1 expression significantly and decreased the level of Hes1 in A375. All in all, the data from our study demonstrates potential of G9a as a therapeutic target in the treatment of melanoma.
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Integrated analysis of DNA methylation and mRNA expression profiles to identify key genes involved in the regrowth of clinically non-functioning pituitary adenoma

Sen Cheng, Chuzhong Li, Weiyan Xie, Yazhou Miao, Jing Guo, Jichao Wang, Yazhuo Zhang,

https://doi.org/10.18632/aging.102751 pp 2408—2427

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Cheng S, Li C, Xie W, Miao Y, Guo J, Wang J, Zhang Y, . Integrated analysis of DNA methylation and mRNA expression profiles to identify key genes involved in the regrowth of clinically non-functioning pituitary adenoma. . 12:2408-2427. https://doi.org/10.18632/aging.102751

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                TY  - JOUR
                AU  - Cheng, Sen 
                AU  - Li, Chuzhong 
                AU  - Xie, Weiyan 
                AU  - Miao, Yazhou 
                AU  - Guo, Jing 
                AU  - Wang, Jichao 
                AU  - Zhang, Yazhuo 
                TI  - Integrated analysis of DNA methylation and mRNA expression profiles to identify key genes involved in the regrowth of clinically non-functioning pituitary adenoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102751
                DO  - 10.18632/aging.102751
                SP  - 2408
                EP  - 2427
                PY  - 
                AB  - Tumour regrowth is a key characteristic of clinically non-functioning pituitary adenoma (NFPA). No applicable prognosis evaluation method is available for post-operative patients. We aimed to identify DNA methylation biomarkers that can facilitate prognosis evaluation. Genome-wide DNA methylation and mRNA microarray analyses were performed for tumour samples from 71 NFPA patients. Differentially expressed genes and methylated genes were identified based on the regrowth vs non-regrowth grouping. There were 139 genes that showed alterations in methylation status and expression level, and only 13 genes showed a negative correlation. The progression-free analysis found that FAM90A1, ETS2, STAT6, MYT1L, ING2 and KCNK1 are related to tumour regrowth. A prognosis-prediction model was built based on all 13 genes from integrated analysis, and the 6-gene model achieved the best area under the receiver operating characteristic curves (AUC) of 0.820, compared with 0.785 and 0.568 for the 13-gene and 7-gene models, respectively. Our prognostic biomarkers were validated by pyrosequencing and RT-PCR. FAM90A1 and ING2 was found to be independent prognostic factors of tumour regrowth with univariate Cox regression. The DNA methylation and expression levels of FAM90A1 and ING2 are associated with tumour regrowth, and may serve as biomarkers for predicting the prognosis of patients with NFPA.
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A high neutrophil-to-lymphocyte ratio predicts hemorrhagic transformation of large atherosclerotic infarction in patients with acute ischemic stroke

Wen-Bo Zhang, Ya-Ying Zeng, Fang Wang, Lin Cheng, Wen-Jie Tang, Xiao-Qiang Wang,

https://doi.org/10.18632/aging.102752 pp 2428—2439

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Zhang W, Zeng Y, Wang F, Cheng L, Tang W, Wang X, . A high neutrophil-to-lymphocyte ratio predicts hemorrhagic transformation of large atherosclerotic infarction in patients with acute ischemic stroke. . 12:2428-2439. https://doi.org/10.18632/aging.102752

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                TY  - JOUR
                AU  - Zhang, Wen-Bo 
                AU  - Zeng, Ya-Ying 
                AU  - Wang, Fang 
                AU  - Cheng, Lin 
                AU  - Tang, Wen-Jie 
                AU  - Wang, Xiao-Qiang 
                TI  - A high neutrophil-to-lymphocyte ratio predicts hemorrhagic transformation of large atherosclerotic infarction in patients with acute ischemic stroke
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102752
                DO  - 10.18632/aging.102752
                SP  - 2428
                EP  - 2439
                PY  - 
                AB  - Increasing evidence suggests that inflammation is associated with the development of acute ischemic stroke (AIS). The neutrophil-to-lymphocyte ratio (N/L) is an important marker of inflammation and is highly correlated with mortality in stroke patients in recent studies. The N/L of patients who experience hemorrhagic transformation (HT) after AIS is know, but any relationship between N/L and large artery atherosclerosis (LAA) remains unclear, this is our present topic. We enrolled 185 patients with LAA-type HT in the development cohort from a prospective, consecutive, hospital-based stroke registry to this end. We matched these patients to 213 LAA patients who did not develop HT as controls. The incidence of HT after LAA was significantly greater (P&lt;0.01) in patients with higher N/L. We developed a predictive nomogram (incorporating age, systolic blood pressure, the National Institutes of Health Stroke Scale, and the N/L) for LAA patients. The predictive power was good (area under the curve, AUC: 0.832, 95%CI: 0.791&#x2013;0.872). Our findings were further validated in a validation cohort of 202 patients with AIS attributable to LAA (AUC:0.836, 95%CI:0.781&#x2013;0.891). In summary, a high N/L is associated with an increased risk for HT after LAA.
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HO-1 induced autophagy protects against IL-1 β-mediated apoptosis in human nucleus pulposus cells by inhibiting NF-κB

Luetao Zou, Hongyan Lei, Jieliang Shen, Xulin Liu, Xiang Zhang, Longxi Wu, Jie Hao, Wei Jiang, Zhenming Hu,

https://doi.org/10.18632/aging.102753 pp 2440—2452

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Zou L, Lei H, Shen J, Liu X, Zhang X, Wu L, Hao J, Jiang W, Hu Z, . HO-1 induced autophagy protects against IL-1 β-mediated apoptosis in human nucleus pulposus cells by inhibiting NF-κB. . 12:2440-2452. https://doi.org/10.18632/aging.102753

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                TY  - JOUR
                AU  - Zou, Luetao 
                AU  - Lei, Hongyan 
                AU  - Shen, Jieliang 
                AU  - Liu, Xulin 
                AU  - Zhang, Xiang 
                AU  - Wu, Longxi 
                AU  - Hao, Jie 
                AU  - Jiang, Wei 
                AU  - Hu, Zhenming 
                TI  - HO-1 induced autophagy protects against IL-1 β-mediated apoptosis in human nucleus pulposus cells by inhibiting NF-κB
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102753
                DO  - 10.18632/aging.102753
                SP  - 2440
                EP  - 2452
                PY  - 
                AB  - In this study, we investigated the role of heme oxygenase-1 (HO-1) in intervertebral disc degeneration (IDD) by assessing the effects of HO-1 overexpression on IL-1&#x3B2;-induced apoptosis in nucleus pulposus cells (NPCs). Immunohistochemical staining showed HO-1 expression to be lower in NPCs from IDD patients than from patients with lumbar vertebral fractures (LVF). Western blot analysis showed HO-1 and LC3-II/I levels to be lower in NP tissues from IDD patients than from LVF patients, suggesting suppression of autophagy in degenerative intervertebral disc. Consistent with that idea, autophagy was increased in HO-1-overexpressing NPCs while IL-1&#x3B2;-induced apoptosis was reduced. These effects were reversed by treatment with the early autophagy inhibitor 3-methyl adenine, which suggests HO-1-induced autophagy suppresses IL-1&#x3B2;-induced apoptosis in NPCs. HO-1 overexpression promoted autophagy by increasing levels of Beclin-1/PI3KC3 complex. Phospho-P65 levels were lower in HO-1-overexpressing NPCs, suggesting inhibition of NF-&#x3BA;B-mediated apoptosis. Our study thus demonstrates that HO-1 promotes autophagy by enhancing formation of Beclin-1/PI3KC3 complex and suppresses IL-1&#x3B2;-induced apoptosis by inhibiting NF-&#x3BA;B. We suggest that HO-1 is a potential therapeutic target to alleviate IDD.
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The whole transcriptome regulation as a function of mitochondrial polymorphisms and aging in Caenorhabditis elegans

Yuanjian Song, Yuechen Wang, Ying Li, Liang Wang, WenDa Zhang, Jing Cheng, Yao Zhu, Haoyu Zhang, Qiang Zhang, Haichen Niu, Yingwei zheng, Mengyu Liang, Mengqiong Deng, Hao Shi, Hao Wang, Fang Zhang, Zuobin Zhu,

https://doi.org/10.18632/aging.102754 pp 2453—2470

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Song Y, Wang Y, Li Y, Wang L, Zhang W, Cheng J, Zhu Y, Zhang H, Zhang Q, Niu H, zheng Y, Liang M, Deng M, et al, . The whole transcriptome regulation as a function of mitochondrial polymorphisms and aging in Caenorhabditis elegans. . 12:2453-2470. https://doi.org/10.18632/aging.102754

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 TY - JOUR
 AU - Song, Yuanjian 
 AU - Wang, Yuechen 
 AU - Li, Ying 
 AU - Wang, Liang 
 AU - Zhang, WenDa 
 AU - Cheng, Jing 
 AU - Zhu, Yao 
 AU - Zhang, Haoyu 
 AU - Zhang, Qiang 
 AU - Niu, Haichen 
 AU - zheng, Yingwei 
 AU - Liang, Mengyu 
 AU - Deng, Mengqiong 
 AU - Shi, Hao 
 AU - Wang, Hao 
 AU - Zhang, Fang 
 AU - Zhu, Zuobin 
 TI - The whole transcriptome regulation as a function of mitochondrial polymorphisms and aging in Caenorhabditis elegans
 JO - 
 JA - 
 VL - 12
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102754
 DO - 10.18632/aging.102754
 SP - 2453
 EP - 2470
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Song, Yuanjian 
 AU - Wang, Yuechen 
 AU - Li, Ying 
 AU - Wang, Liang 
 AU - Zhang, WenDa 
 AU - Cheng, Jing 
 AU - Zhu, Yao 
 AU - Zhang, Haoyu 
 AU - Zhang, Qiang 
 AU - Niu, Haichen 
 AU - zheng, Yingwei 
 AU - Liang, Mengyu 
 AU - Deng, Mengqiong 
 AU - Shi, Hao 
 AU - Wang, Hao 
 AU - Zhang, Fang 
 AU - Zhu, Zuobin 
 TI - The whole transcriptome regulation as a function of mitochondrial polymorphisms and aging in Caenorhabditis elegans
 JO - 
 JA - 
 VL - 12
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102754
 DO - 10.18632/aging.102754
 SP - 2453
 EP - 2470
 PY - 
 AB - Recently, mitochondrial-nuclear interaction in aging has been widely studied. However, the nuclear genome controlled by natural mitochondrial variations that influence aging has not been comprehensively understood so far. We hypothesized that mitochondrial polymorphisms could play critical roles in the aging process, probably by regulation of the whole-transcriptome expression. Our results showed that mitochondria polymorphisms not only decreased the mitochondrial mass but also miRNA, lncRNA, mRNA, circRNA and metabolite profiles. Furthermore, most genes that are associated with mitochondria show age-related expression features (P = 3.58E-35). We also constructed a differentially expressed circRNA-lncRNA-miRNA-mRNA regulatory network and a ceRNA network affected by the mitochondrial variations. In addition, Kyoto Encyclopedia of Genes and Genomes pathway analyses showed that the genes affected by the mitochondrial variation were enriched in metabolic activity. We finally constructed a multi-level regulatory network with aging which affected by the mitochondrial variation in Caenorhabditis elegans. The interactions between these genes and metabolites have great values for further aging research. In sum, our findings provide new evidence for understanding the molecular mechanisms of how mitochondria influence aging.
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Sepsis induced cognitive impairments by disrupting hippocampal parvalbumin interneuron-mediated inhibitory network via a D4-receptor mechanism

Muhuo Ji, Shuming Li, Ling Zhang, Yuzhu Gao, Qiuting Zeng, Minjie Mao, Jianjun Yang,

https://doi.org/10.18632/aging.102755 pp 2471—2484

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Ji M, Li S, Zhang L, Gao Y, Zeng Q, Mao M, Yang J, . Sepsis induced cognitive impairments by disrupting hippocampal parvalbumin interneuron-mediated inhibitory network via a D4-receptor mechanism. . 12:2471-2484. https://doi.org/10.18632/aging.102755

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                TY  - JOUR
                AU  - Ji, Muhuo 
                AU  - Li, Shuming 
                AU  - Zhang, Ling 
                AU  - Gao, Yuzhu 
                AU  - Zeng, Qiuting 
                AU  - Mao, Minjie 
                AU  - Yang, Jianjun 
                TI  - Sepsis induced cognitive impairments by disrupting hippocampal parvalbumin interneuron-mediated inhibitory network via a D4-receptor mechanism
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102755
                DO  - 10.18632/aging.102755
                SP  - 2471
                EP  - 2484
                PY  - 
                AB  - Patients who suffer sepsis often develop cognitive impairments, yet the underlying mechanisms largely remain to be elucidated. Increasing evidence has suggested that parvalbumin (PV) interneurons are required for the synchronization of neural activities and higher brain processes, whereas its dysfunction is implicated in many psychiatric disorders. In the present study, we examined the role of hippocampal PV interneuron-mediated inhibitory network in a rat model of polymicrobial sepsis induced by cecal ligation and puncture (CLP) and also explored the underlying mechanism. Here we showed that CLP-induced cognitive impairments, which were accompanied by significantly decreased expressions of PV and dopamine 4 (D4) receptor, decreased slow &#x3B3; oscillation band, and reduced frequency of miniature inhibitory postsynaptic currents (mIPSCs). Notably, D4 receptor agonist RO-10-5824 treatment was able to reverse most of these abnormities. In summary, our study suggests that sepsis might disrupt PV interneuron-mediated network function that is dependent on the D4 receptor, leading to abnormal &#x3B3; oscillation and consequent cognitive impairments.
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Circular RNA hsa_circ_0056836 functions an oncogenic gene in hepatocellular carcinoma through modulating miR-766-3p/FOSL2 axis

Zhiqin Li, Yang Liu, Jingya Yan, Qinglei Zeng, Yushu Hu, Hongyan Wang, Hua Li, Juan Li, Zujiang Yu,

https://doi.org/10.18632/aging.102756 pp 2485—2497

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Li Z, Liu Y, Yan J, Zeng Q, Hu Y, Wang H, Li H, Li J, Yu Z, . Circular RNA hsa_circ_0056836 functions an oncogenic gene in hepatocellular carcinoma through modulating miR-766-3p/FOSL2 axis. . 12:2485-2497. https://doi.org/10.18632/aging.102756

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                TY  - JOUR
                AU  - Li, Zhiqin 
                AU  - Liu, Yang 
                AU  - Yan, Jingya 
                AU  - Zeng, Qinglei 
                AU  - Hu, Yushu 
                AU  - Wang, Hongyan 
                AU  - Li, Hua 
                AU  - Li, Juan 
                AU  - Yu, Zujiang 
                TI  - Circular RNA hsa_circ_0056836 functions an oncogenic gene in hepatocellular carcinoma through modulating miR-766-3p/FOSL2 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102756
                DO  - 10.18632/aging.102756
                SP  - 2485
                EP  - 2497
                PY  - 
                AB  - Background: Circular RNA (circRNA) remains a tumour-related factor in various biological cells and plays regulatory roles in gene expression. It is a type of non-coding RNA, whereas the function of human circRNA in hepatocellular carcinoma (HCC) is still not clear yet. Our investigation used the HCC cell line to uncover the biological function of hsa_circ_0056836 in the development and progression of hepatocellular carcinoma.Results: The present study showed that hsa_circ_0056836 revealed high expressions in HCC cell lines and tissues compared with corresponding controls. Silencing of Hsa_circ_0056836 decreased cell migration, proliferation and invasion. Silencing of hsa_circ_0056836 inhibited the development of HCC in xenograft nude mice. Mechanistically, we found that hsa_circ_0056836 directly bound to miR-766-3p, thereby alleviating the targeted inhibition of Fos-related antigen 2 (FOSL2). The results of this study indicated that hsa_circ_0056836 is a novel oncogenic RNA of vast potential as a tumor biomarker.Conclusion: In summary, the hsa_circ_0056836 / miR-766-3p / FOSL2 axis may serve as a promising strategy for HCC treatment.Method: First, the expressions of hsa_circ_0056836 in HCC tissues and corresponding para-cancerous tissues as well as in HCC cell lines and normal hepatocytes THLE-3 were detected by RT-PCR. Subcellular localization of hsa_circ_0056836 was confirmed by FISH. To detect the association between hsa_circ_0056836 and miR-766-3p, AGO2-RIP and Luciferase reporter assay were adopted. Loss of function study was applied to assess the role of hsa_circ_0056836 in HCC and to determine tumorigenesis in nude mice.
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The association between monocyte to high-density lipoprotein ratio and hemorrhagic transformation in patients with acute ischemic stroke

Yanan Wang, Yajun Cheng, Quhong Song, Chenchen Wei, Junfeng Liu, Bo Wu, Ming Liu,

https://doi.org/10.18632/aging.102757 pp 2498—2506

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Wang Y, Cheng Y, Song Q, Wei C, Liu J, Wu B, Liu M, . The association between monocyte to high-density lipoprotein ratio and hemorrhagic transformation in patients with acute ischemic stroke. . 12:2498-2506. https://doi.org/10.18632/aging.102757

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                TY  - JOUR
                AU  - Wang, Yanan 
                AU  - Cheng, Yajun 
                AU  - Song, Quhong 
                AU  - Wei, Chenchen 
                AU  - Liu, Junfeng 
                AU  - Wu, Bo 
                AU  - Liu, Ming 
                TI  - The association between monocyte to high-density lipoprotein ratio and hemorrhagic transformation in patients with acute ischemic stroke
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102757
                DO  - 10.18632/aging.102757
                SP  - 2498
                EP  - 2506
                PY  - 
                AB  - Hemorrhagic transformation (HT) is a common complication in patients with acute ischemic stroke. We investigated whether the monocyte to high-density lipoprotein ratio (MHR) is related to HT. Consecutive patients with ischemic stroke within 24 h of symptom onset were included in this study. HT was diagnosed by follow-up brain imaging after admission, and was classified as asymptomatic or symptomatic according to whether patients showed any neurologic worsening. Logistic regression was performed to estimate the association between MHR and HT. Of the 974 enrolled patients, 148 (15.2%) developed HT, and 24 (2.5%) patients experienced symptomatic HT. Compared to the highest MHR tertile (&gt; 0.37), the lowest MHR tertile (&lt; 0.22) was associated with 1.81-fold increase (95% CI 1.08-3.01, P = 0.024) in the odds of HT and 3.82-fold increase (95% CI 1.04-14.00, P = 0.043) in the odds of symptomatic HT after adjustment for possible confounders. Using a multivariate logistic regression model with restricted cubic spline, we found that elevated MHR was associated with a decreased risk of HT and symptomatic HT. In summary, lower MHR was independently associated with increased risk of HT and symptomatic HT in patients with ischemic stroke.
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PRMT5-TRIM21 interaction regulates the senescence of osteosarcoma cells by targeting the TXNIP/p21 axis

Yu-Hang Li, Kui-Leung Tong, Jun-Lei Lu, Jie-Bin Lin, Zhen-Yan Li, Yuan Sang, Abdelmoumin Ghodbane, Xue-Juan Gao, Man-Seng Tam, Chang-Deng Hu, Huan-Tian Zhang, Zhen-Gang Zha,

https://doi.org/10.18632/aging.102760 pp 2507—2529

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Li Y, Tong K, Lu J, Lin J, Li Z, Sang Y, Ghodbane A, Gao X, Tam M, Hu C, Zhang H, Zha Z, . PRMT5-TRIM21 interaction regulates the senescence of osteosarcoma cells by targeting the TXNIP/p21 axis. . 12:2507-2529. https://doi.org/10.18632/aging.102760

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                TY  - JOUR
                AU  - Li, Yu-Hang 
                AU  - Tong, Kui-Leung 
                AU  - Lu, Jun-Lei 
                AU  - Lin, Jie-Bin 
                AU  - Li, Zhen-Yan 
                AU  - Sang, Yuan 
                AU  - Ghodbane, Abdelmoumin 
                AU  - Gao, Xue-Juan 
                AU  - Tam, Man-Seng 
                AU  - Hu, Chang-Deng 
                AU  - Zhang, Huan-Tian 
                AU  - Zha, Zhen-Gang 
                TI  - PRMT5-TRIM21 interaction regulates the senescence of osteosarcoma cells by targeting the TXNIP/p21 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102760
                DO  - 10.18632/aging.102760
                SP  - 2507
                EP  - 2529
                PY  - 
                AB  - Osteosarcoma (OS) is the most common bone malignancy in adolescents and has poor clinical outcomes. Protein arginine methyltransferase 5 (PRMT5) has recently been shown to be aberrantly expressed in various cancers, yet its role in OS remains elusive. Here, we found that PRMT5 was overexpressed in OS and its overexpression predicted poor clinical outcomes. PRMT5 knockdown significantly triggered pronounced senescence in OS cells, as evidenced by the increase in senescence-associated &#x3B2;-galactosidase (SA-&#x3B2;-gal)-stained cells, induction of p21 expression, and upregulation of senescence-associated secretory phenotype (SASP) gene expression. In addition, we found that PRMT5 plays a key role in regulating DNA damaging agents-induced OS cell senescence, possibly, via affecting the repair of DNA damage. Furthermore, we found that TXNIP acts as a key factor mediating PRMT5 depletion-induced DNA damage and cellular senescence. Mechanistically, TRIM21, which interacts with PRMT5, was essential for the regulation of TXNIP/p21 expression. In summary, we propose a model in which PRMT5, by interaction with TRIM21, plays a key role in regulating the TXNIP/p21 axis during senescence in OS cells. The present findings suggest that PRMT5 overexpression in OS cells might confer resistance to chemotherapy and that targeting the PRMT5/TRIM21/TXNIP signaling may enhance the therapeutic efficacy in OS.
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Circular RNA expression in isoproterenol hydrochloride-induced cardiac hypertrophy

Ming-Hui Yang, Hao Wang, Sheng-Na Han, Xin Jia, Si Zhang, Fei-Fei Dai, Meng-Jiao Zhou, Zhongnan Yin, Tian-Qi Wang, Ming-Xi Zang, Li-Xiang Xue,

https://doi.org/10.18632/aging.102761 pp 2530—2544

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Yang M, Wang H, Han S, Jia X, Zhang S, Dai F, Zhou M, Yin Z, Wang T, Zang M, Xue L, . Circular RNA expression in isoproterenol hydrochloride-induced cardiac hypertrophy. . 12:2530-2544. https://doi.org/10.18632/aging.102761

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                TY  - JOUR
                AU  - Yang, Ming-Hui 
                AU  - Wang, Hao 
                AU  - Han, Sheng-Na 
                AU  - Jia, Xin 
                AU  - Zhang, Si 
                AU  - Dai, Fei-Fei 
                AU  - Zhou, Meng-Jiao 
                AU  - Yin, Zhongnan 
                AU  - Wang, Tian-Qi 
                AU  - Zang, Ming-Xi 
                AU  - Xue, Li-Xiang 
                TI  - Circular RNA expression in isoproterenol hydrochloride-induced cardiac hypertrophy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102761
                DO  - 10.18632/aging.102761
                SP  - 2530
                EP  - 2544
                PY  - 
                AB  - Circular RNA (circRNA) is a novel class of noncoding RNAs, and the roles of circRNAs in the development of cardiac hypertrophy remain to be explored. Here, we investigate the potential roles of circRNAs in cardiac hypertrophy. By circRNA sequencing in left ventricular specimens collected from 8-week-old mice with isoproterenol hydrochloride-induced cardiac hypertrophy, we found 401 out of 3323 total circRNAs were dysregulated in the hypertrophic hearts compared with the controls. Of these, 303 circRNAs were upregulated and 98 were downregulated. Moreover, the GO and KEGG analyses revealed that the majority of parental gene of differentially expressed circRNAs were not only related to biological process such as metabolic process and response to stimulus, but also related to pathway such as circulatory system and cardiovascular diseases. On the other hand, total 1974 miRNAs were predicted to binding to these differentially expressed circRNAs, and the possible target mRNAs of those miRNAs were also predicted and analyzed in terms of functional annotation. Finally, we identified that ANF and miR-23a are downstream targets of circRNA wwp1, suggesting that circRNA wwp1 exerts inhibitory roles of cardiac hypertrophy via down-regulation of ANF and miR-23a, which underlying the potential mechanisms whereby circRNA regulates cardiac hypertrophy.
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Global burden of larynx cancer, 1990-2017: estimates from the global burden of disease 2017 study

Yujiao Deng, Meng Wang, Linghui Zhou, Yi Zheng, Na Li, Tian Tian, Zhen Zhai, Si Yang, Qian Hao, Ying Wu, Dingli Song, Dai Zhang, Jun Lyu, Zhijun Dai,

https://doi.org/10.18632/aging.102762 pp 2545—2583

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Deng Y, Wang M, Zhou L, Zheng Y, Li N, Tian T, Zhai Z, Yang S, Hao Q, Wu Y, Song D, Zhang D, Lyu J, et al, . Global burden of larynx cancer, 1990-2017: estimates from the global burden of disease 2017 study. . 12:2545-2583. https://doi.org/10.18632/aging.102762

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                TY  - JOUR
                AU  - Deng, Yujiao 
                AU  - Wang, Meng 
                AU  - Zhou, Linghui 
                AU  - Zheng, Yi 
                AU  - Li, Na 
                AU  - Tian, Tian 
                AU  - Zhai, Zhen 
                AU  - Yang, Si 
                AU  - Hao, Qian 
                AU  - Wu, Ying 
                AU  - Song, Dingli 
                AU  - Zhang, Dai 
                AU  - Lyu, Jun 
                AU  - Dai, Zhijun 
                TI  - Global burden of larynx cancer, 1990-2017: estimates from the global burden of disease 2017 study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102762
                DO  - 10.18632/aging.102762
                SP  - 2545
                EP  - 2583
                PY  - 
                AB  - Larynx cancer is one of the most common cancers in head and neck. This study aimed to investigate the health burden of larynx cancer at global, regional, and national levels. We collected data of larynx cancer between 1990 and 2017 from the Global Burden of Disease study, including incidence, mortality, and disability adjusted life-years (DALYs). Estimated annual percentage changes (EAPCs) were calculated to assess the changes in age-standardized rate (ASR) of larynx cancer. From 1990 to 2017, LC incident cases increased by 58.67%; however, age-standardized incidence rate (ASIR) decreased, with an EAPC of -0.99. Additionally, the incident cases and ASIR of LC were 6-fold higher for male than those for female in 2017. Over the past 28 years, deaths and DALYs of larynx cancer increased by 33.84% and 25%. Contrarily, age-standardized death and DALY rate showed a downward trend. Incidence, death, and DALYs of larynx cancer were always the highest in people aged 50-69 years. Overall, all the ASRs showed downward trends globally. The majority of larynx cancer burden was observed in men, especially among male aged 50-69 years. South and East Asia carried the heaviest burden of larynx cancer worldwide.
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LDL-C plays a causal role on T2DM: a Mendelian randomization analysis

Wenbin Pan, Weiju Sun, Shuo Yang, He Zhuang, Huijie Jiang, Hong Ju, Donghua Wang, Ying Han,

https://doi.org/10.18632/aging.102763 pp 2584—2594

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Pan W, Sun W, Yang S, Zhuang H, Jiang H, Ju H, Wang D, Han Y, . LDL-C plays a causal role on T2DM: a Mendelian randomization analysis. . 12:2584-2594. https://doi.org/10.18632/aging.102763

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                TY  - JOUR
                AU  - Pan, Wenbin 
                AU  - Sun, Weiju 
                AU  - Yang, Shuo 
                AU  - Zhuang, He 
                AU  - Jiang, Huijie 
                AU  - Ju, Hong 
                AU  - Wang, Donghua 
                AU  - Han, Ying 
                TI  - LDL-C plays a causal role on T2DM: a Mendelian randomization analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102763
                DO  - 10.18632/aging.102763
                SP  - 2584
                EP  - 2594
                PY  - 
                AB  - Diabetic dyslipidemia is a common condition in patients with Type 2 diabetes mellitus (T2DM). However, with the increasing application of statins which mainly decrease low-density lipoprotein cholesterol (LDL-C) levels, clinical trials and meta-analysis showed a clearly increase of the incidence of new-onset DMs, partly due to genetic factors. To determine whether a causal relationship exists between LDL-C and T2DM, we conducted a two-sample Mendelian Randomization (MR) analysis using genetic variations as instrumental variables (IVs). Initially, 29 SNPs significantly related to LDL-C (P&#x2264; 5.0&#xD7;10-8) were selected as based on results from the study of Henry et al, which processed loci data influencing lipids identified by the Global Lipids Genetics Consortium (GLGC) from 188,577 individuals of European ancestry. While 6 SNPs related to T2DM (P value &lt; 5&#xD7;10-2) were deleted, with the remaining 23 SNPs without LD eventually being deemed as IVs. The combined effect of all these 23 SNPs on T2DM, as generated with use of the penalized robust inverse-variance weighted (IVW) method (Beta value 0.24, 95%CI 0.087~0.393, P-value=0.002) demonstrated that elevated LDL-C levels significantly increased the risk of T2DM. The relationship between LDL-C and Type 1 diabetes mellitus (T1DM) with this analysis producing negative pooled results (Beta value -0.202, 95%CI -2.888~2.484, P-value=0.883).
                ER  -

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Notch1/2/3/4 are prognostic biomarker and correlated with immune infiltrates in gastric cancer

Jian Hu, Jianghong Yu, Jun Gan, Ning Song, Liubin Shi, Jie Liu, Ziqiang Zhang, Jianjun Du,

https://doi.org/10.18632/aging.102764 pp 2595—2609

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Hu J, Yu J, Gan J, Song N, Shi L, Liu J, Zhang Z, Du J, . Notch1/2/3/4 are prognostic biomarker and correlated with immune infiltrates in gastric cancer. . 12:2595-2609. https://doi.org/10.18632/aging.102764

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                TY  - JOUR
                AU  - Hu, Jian 
                AU  - Yu, Jianghong 
                AU  - Gan, Jun 
                AU  - Song, Ning 
                AU  - Shi, Liubin 
                AU  - Liu, Jie 
                AU  - Zhang, Ziqiang 
                AU  - Du, Jianjun 
                TI  - Notch1/2/3/4 are prognostic biomarker and correlated with immune infiltrates in gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102764
                DO  - 10.18632/aging.102764
                SP  - 2595
                EP  - 2609
                PY  - 
                AB  - Notch refers to a set of genes encoding a family of transmembrane receptors in mammalian cells. Previous evidence indicated that Notch receptors were implicated in the onset of gastric cancer. However, there is little evidence on the different genetic expression patterns of the four Notch receptors and their values for patient prognosis. Most recently, we investigated the transcriptional data of Notch receptors and related patient survival in patients with GC based on several databases, including ONCOMINE, GEPIA, Kaplan&#x2013;Meier Plotter, cBioPortal and TIMER. According to our findings, gastric cancer tissues, compared with adjacent normal tissues presented a higher level of expression of Notch1/2/3. We also performed a survival analysis and noted that gastric cancer patients with high transcription levels of Notch1/2/3/4 had a low relapse-free survival. In gastric cancer patients, higher levels of infiltration in their CD4+ T cells, macrophages, neutrophils, and dendritic cells were positive associated with the expression of Notch receptors. Notch expression had significant association with diverse immune marker sets in gastric cancer. Overall, this study provides evidence that Notch1/2/3/4 could become the potential targets for precision treatment and new biomarkers in the prognosis of gastric cancer.
                ER  -

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Testicular biopsies microarray analysis reveals circRNAs are involved in the pathogenesis of non-obstructive azoospermia

Hao Bo, Zhizhong Liu, Ruiling Tang, Guanghui Gong, Xingming Wang, Han Zhang, Fang Zhu, Dai Zhou, Wenbing Zhu, Yueqiu Tan, Liqing Fan,

https://doi.org/10.18632/aging.102765 pp 2610—2625

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Bo H, Liu Z, Tang R, Gong G, Wang X, Zhang H, Zhu F, Zhou D, Zhu W, Tan Y, Fan L, . Testicular biopsies microarray analysis reveals circRNAs are involved in the pathogenesis of non-obstructive azoospermia. . 12:2610-2625. https://doi.org/10.18632/aging.102765

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                TY  - JOUR
                AU  - Bo, Hao 
                AU  - Liu, Zhizhong 
                AU  - Tang, Ruiling 
                AU  - Gong, Guanghui 
                AU  - Wang, Xingming 
                AU  - Zhang, Han 
                AU  - Zhu, Fang 
                AU  - Zhou, Dai 
                AU  - Zhu, Wenbing 
                AU  - Tan, Yueqiu 
                AU  - Fan, Liqing 
                TI  - Testicular biopsies microarray analysis reveals circRNAs are involved in the pathogenesis of non-obstructive azoospermia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102765
                DO  - 10.18632/aging.102765
                SP  - 2610
                EP  - 2625
                PY  - 
                AB  - Circular RNAs (circRNAs) have been reported to be involved in many diseases. But there is no report on circRNAs in non-obstructive azoospermia (NOA). The purpose of this paper is to explore the circular RNA expression profile and potential functions of circRNAs in NOA patients. We first preformed circRNA expression profiling analysis using a circRNA microarray in testicular samples from NOA and obstructive azoospermia (OA) patients. CircRNAs were validated by qRT-PCR. Bioinformatics analysis were used to construct the ceRNA network. GO and KEGG enrichment analysis were performed by using DAVID. Microarray analysis identified 82 differentially expressed circRNAs in NOA specimens. The differential expression of hsa_circRNA_402130, hsa_circRNA_072697, hsa_circRNA_030050, hsa_circRNA_100812 and hsa_circRNA_406168 was confirmed by qRT-PCR. Enrichment analysis revealed the association of hsa_circRNA_402130 and hsa_circRNA_072697 with multiple signaling pathways. The data indicated that circRNAs were significantly dysregulated in NOA specimens and might involve in the pathogenesis of NOA.
                ER  -

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Screening and identification of genes associated with cell proliferation in cholangiocarcinoma

Li Guo, Yaodong Zhang, Zibo Yin, Yaya Ji, Guowei Yang, Bowen Qian, Sunjing Li, Jun Wang, Tingming Liang, Changxian Li, Xiangcheng Li,

https://doi.org/10.18632/aging.102766 pp 2626—2646

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Guo L, Zhang Y, Yin Z, Ji Y, Yang G, Qian B, Li S, Wang J, Liang T, Li C, Li X, . Screening and identification of genes associated with cell proliferation in cholangiocarcinoma. . 12:2626-2646. https://doi.org/10.18632/aging.102766

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                TY  - JOUR
                AU  - Guo, Li 
                AU  - Zhang, Yaodong 
                AU  - Yin, Zibo 
                AU  - Ji, Yaya 
                AU  - Yang, Guowei 
                AU  - Qian, Bowen 
                AU  - Li, Sunjing 
                AU  - Wang, Jun 
                AU  - Liang, Tingming 
                AU  - Li, Changxian 
                AU  - Li, Xiangcheng 
                TI  - Screening and identification of genes associated with cell proliferation in cholangiocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102766
                DO  - 10.18632/aging.102766
                SP  - 2626
                EP  - 2646
                PY  - 
                AB  - Cholangiocarcinoma (CCA), an aggressive tumor with poor prognosis, is a malignant cancer with increasing incidence and mortality rates. It is important to survey crucial genes in CCA to find and design potential drug targets, especially for those genes associated with cell proliferation that is a key biological process in tumorgenesis. Herein, we surveyed genes associated with cell proliferation via a comprehensive pan-cancer analysis. Candidate genes were further analyzed using multiple approaches, including cross-analysis from diverse molecular levels, examination of potential function and interactions, and additional experimental validation. We primarily screened 15 potential genes based on 11 validated genes, and these 26 genes were further examined to delineate their biological functions and potential roles in cancer treatment. Several of them were involved synthetically lethal genetic interactions, especially for RECQL4, TOP2A, MKI67 and ASPM, indicating their potential roles in drug design and cancer treatment. Further experimental validation indicated that some genes were significantly upregulated in several cancer cell lines, implying their important roles in tumorigenesis. Our study identifies some genes associated with cell proliferation, which may be potential future targets in molecular targeted therapy.
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Association of serum retinoic acid with depression in patients with acute ischemic stroke

Cai-Di Yang, Ming-Li Cheng, Wen Liu, Ding-Hua Zeng,

https://doi.org/10.18632/aging.102767 pp 2647—2658

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Yang C, Cheng M, Liu W, Zeng D, . Association of serum retinoic acid with depression in patients with acute ischemic stroke. . 12:2647-2658. https://doi.org/10.18632/aging.102767

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                TY  - JOUR
                AU  - Yang, Cai-Di 
                AU  - Cheng, Ming-Li 
                AU  - Liu, Wen 
                AU  - Zeng, Ding-Hua 
                TI  - Association of serum retinoic acid with depression in patients with acute ischemic stroke
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102767
                DO  - 10.18632/aging.102767
                SP  - 2647
                EP  - 2658
                PY  - 
                AB  - Retinoic acid (RA), produced by the metabolism of vitamin A, makes effects on depression and stroke. This study was aimed to evaluate the relationship between RA levels in serum and post-stroke depression (PSD). A single-center (Chengdu, China) prospective cohort study was conducted on patients with acute ischemic stroke. The RA serum level was measured at admission. The PSD was assessed in the 3-month follow-up. The RA-PSD relationship was evaluated with conditional logistic regression. In total, 239 ischemic stroke cases and 100 healthy controls were included. The median RA serum level in patients with ischemic stroke was 2.45 ng/ml (interquartile range [IQR], 0.72-4.33), lower(P&lt;0.001) than 3.89 ng/ml of those in control cases ([IQR]: 2.62-5.39). The crude and adjusted odds ratios [OR] (and 95% confidence intervals [CI]) of PSD associated with an IQR increase for RA were 0.54 (0.44, 0.67) and 0.66 (0.52, 0.79), respectively. Higher ORs of PSD associated with reduced RA levels (&lt;cut-off=2.8ng/ml) were observed (OR=3.01 [95% CI, 2.34-4.98]; P&lt;0.001). This study revealed that, in patients with ischemic stroke, reduced RA serum level was related to higher risk of PSD at 3 months, which may be applied as a predictive indicator.
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Effects of resveratrol, granulocyte-macrophage colony-stimulating factor or dichloroacetic acid in the culture media on embryonic development and pregnancy rates in aged mice

Jeong Yoon, Kyoung-Mi Juhn, Eun-Hye Jung, Hye-Jeong Park, San-Hyun Yoon, Yong Ko, Chang-Young Hur, Jin-Ho Lim,

https://doi.org/10.18632/aging.102768 pp 2659—2669

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Yoon J, Juhn K, Jung E, Park H, Yoon S, Ko Y, Hur C, Lim J, . Effects of resveratrol, granulocyte-macrophage colony-stimulating factor or dichloroacetic acid in the culture media on embryonic development and pregnancy rates in aged mice. . 12:2659-2669. https://doi.org/10.18632/aging.102768

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                TY  - JOUR
                AU  - Yoon, Jeong 
                AU  - Juhn, Kyoung-Mi 
                AU  - Jung, Eun-Hye 
                AU  - Park, Hye-Jeong 
                AU  - Yoon, San-Hyun 
                AU  - Ko, Yong 
                AU  - Hur, Chang-Young 
                AU  - Lim, Jin-Ho 
                TI  - Effects of resveratrol, granulocyte-macrophage colony-stimulating factor or dichloroacetic acid in the culture media on embryonic development and pregnancy rates in aged mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102768
                DO  - 10.18632/aging.102768
                SP  - 2659
                EP  - 2669
                PY  - 
                AB  - The success rate of assisted reproductive technology is closely correlated with maternal age. Reproductive aging pathologies are frequently caused by impaired DNA repair, genomic instability, and mitochondrial dysfunction. Several reports have shown that resveratrol can prevent age-related diseases by improving mitochondrial function. Improved blastocyst development and mitochondrial output by dichloroacetic acid (DCA) supplementation were reported in aged mice. Granulocyte-macrophage colony-stimulating factor (GM-CSF) has significant effects on implantation rates in women with previous miscarriages. Therefore, this study was conducted to observe how those compounds influence the developmental and the reproductive potential of aged oocytes. BDF1 female mice at 58&#x2013;62 weeks old were used for this study. MII oocytes were fertilized and cultured in MRC media supplemented with or without resveratrol (0.5 &#x3BC;M), GM-CSF (2 ng/ml) or DCA (1.0 mM). The addition of resveratrol, GM-CSF or DCA tended to increase blastocyst development and pregnancy rates. Supplementation with resveratrol significantly increased the pregnancy and implantation rates (p &lt; 0.05). Moreover, resveratrol decreased reactive oxygen species production and increased mitochondrial membrane potential. These results suggest that the addition of resveratrol can increase pregnancy outcomes in women of advanced maternal age.
                ER  -

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Determinants and indicators of successful ageing associated with mortality: a 4-year population-based study

Wei-Ju Lee, Li-Ning Peng, Ming-Hsien Lin, Ching-Hui Loh, Liang-Kung Chen,

https://doi.org/10.18632/aging.102769 pp 2670—2679

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Lee W, Peng L, Lin M, Loh C, Chen L, . Determinants and indicators of successful ageing associated with mortality: a 4-year population-based study. . 12:2670-2679. https://doi.org/10.18632/aging.102769

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                TY  - JOUR
                AU  - Lee, Wei-Ju 
                AU  - Peng, Li-Ning 
                AU  - Lin, Ming-Hsien 
                AU  - Loh, Ching-Hui 
                AU  - Chen, Liang-Kung 
                TI  - Determinants and indicators of successful ageing associated with mortality: a 4-year population-based study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102769
                DO  - 10.18632/aging.102769
                SP  - 2670
                EP  - 2679
                PY  - 
                AB  - Successful aging may be a solution to the major challenges that population aging poses to healthcare systems, financial security, and labor force supply. Hence, we studied the value of factors discovered by exploratory factor analysis in predicting four main indicators of successful aging, and their association with mortality. We followed-up a nationally representative sample of 1284 older adults for a median of 50 months. Successful aging was defined by fast walking, independence, emotional vitality, and self-rated health. Exploratory factor analysis revealed five determinants: physical activity, life satisfaction and financial status, health status, stress, and cognitive function. Physical activity and health status were significant factors in living independently. Life satisfaction and financial status were associated with walking speed. Stress was solely associated with emotional vitality. Life satisfaction and financial status, and health status, were important predictors of self-rated health. Compared to people without any successful aging indicators, those with one, two, three, or four showed dose-dependent lessening of mortality risk, with respective hazard ratios of 0.39 (95% CI 0.25&#x2013;0.59), 0.29 (95% CI 0.17&#x2013;0.50), 0.23 (95% CI 0.11&#x2013;0.51), and 0.09 (95% CI 0.01&#x2013;0.66). These associations were stronger in males, older adults, smokers, and drinkers, than in their counterparts.
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Methionine increases yolk production to offset the negative effect of caloric restriction on reproduction without affecting longevity in C. elegans

Gaojian Zhou, Chuan Huang, Liu Xing, Le Li, Yan Jiang, Yuehua Wei,

https://doi.org/10.18632/aging.102770 pp 2680—2697

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Zhou G, Huang C, Xing L, Li L, Jiang Y, Wei Y, . Methionine increases yolk production to offset the negative effect of caloric restriction on reproduction without affecting longevity in C. elegans. . 12:2680-2697. https://doi.org/10.18632/aging.102770

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Provider: 
 TY - JOUR
 AU - Zhou, Gaojian 
 AU - Huang, Chuan 
 AU - Xing, Liu 
 AU - Li, Le 
 AU - Jiang, Yan 
 AU - Wei, Yuehua 
 TI - Methionine increases yolk production to offset the negative effect of caloric restriction on reproduction without affecting longevity in C. elegans
 JO - 
 JA - 
 VL - 12
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102770
 DO - 10.18632/aging.102770
 SP - 2680
 EP - 2697
 PY - 
 AB - Caloric restriction (CR) or Dietary restriction (DR) is known to improve health and in many cases increases lifespan. However, its negative effect on reproduction has not been fully studied. Practicing CR/DR without adequate knowledge on its side effect may risk complications such as infertility, birth defect, or malnutrition. In this study, by using several CR strategies in C. elegans, we examine key functions of reproduction including embryonic development and larvae growth. We find that CR significantly decreases the survival of embryos and slows the growth of the offspring. We further determine that defect in oocyte but not sperm is responsible for the compromised reproduction under CR. Interestingly, adding methionine to the medium reverses the reproduction defects, but does not affect the long lifespan resulted from CR. The beneficial effect of methionine on reproduction requires the yolk protein vitellogenin. CR down-regulates vitellogenin expression, which can be reversed by supplementing methionine in the food. Lacking the yolk protein transport due to rme-2 mutation blocks methionine&#x2019;s beneficial effects. Our study has revealed a novel, methionine-mediated genetic pathway linking nutrient sensing to reproduction and suggested methionine as a potential food supplement to mitigate the side effect of CR.
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Relationship between plasma S-Klotho and cardiometabolic risk in sedentary adults

Francisco J. Amaro-Gahete, Lucas Jurado-Fasoli, Guillermo Sanchez-Delgado, José V. García-Lario, Manuel J. Castillo, Jonatan R. Ruiz,

https://doi.org/10.18632/aging.102771 pp 2698—2710

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Amaro-Gahete FJ, Jurado-Fasoli L, Sanchez-Delgado G, García-Lario JV, Castillo MJ, Ruiz JR, . Relationship between plasma S-Klotho and cardiometabolic risk in sedentary adults. . 12:2698-2710. https://doi.org/10.18632/aging.102771

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                TY  - JOUR
                AU  - Amaro-Gahete, Francisco J. 
                AU  - Jurado-Fasoli, Lucas 
                AU  - Sanchez-Delgado, Guillermo 
                AU  - García-Lario, José V. 
                AU  - Castillo, Manuel J. 
                AU  - Ruiz, Jonatan R. 
                TI  - Relationship between plasma S-Klotho and cardiometabolic risk in sedentary adults
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102771
                DO  - 10.18632/aging.102771
                SP  - 2698
                EP  - 2710
                PY  - 
                AB  - This cross-sectional study investigates the relationship between the shed form of the Klotho protein (S-Klotho) in plasma, and cardiometabolic risk in healthy, sedentary adults. The study subjects were 214 healthy, sedentary adults (~64% women). Data were collected during the baseline assessments of two randomized controlled trials: The FIT-AGEING study (n=74 [~50% women] middle-aged adults aged 40-65 years) and the ACTIBATE study (n=140 [~70% women] young adults aged 18-25 years). A sex-specific cardiometabolic risk score was calculated for each subject based on waist circumference, systolic and diastolic blood pressure, and plasma glucose, high-density lipoprotein cholesterol and triglycerides. A significant inverse relationship was detected between S-Klotho and the cardiometabolic risk score of both the middle-aged men and women (&#x3B2;=-0.658, R2=0.433, P&lt;0.001 and &#x3B2;=-0.442, R2=0.195, P=0.007) which persisted after adjusting for actual age, energy intake, and VO2max. No significant association was found between S-Klotho and cardiometabolic risk score for the young, healthy adults (P&gt;0.5), nor for the young, healthy men and women when analysed separately (all P&gt;0.1). In conclusion, in healthy, sedentary, middle-aged adults, but not in young, healthy, sedentary adults, higher plasma S-Klotho concentrations are associated with a lower cardiometabolic risk score.
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Dasatinib plus quercetin prevents uterine age-related dysfunction and fibrosis in mice

Marcelo B. Cavalcante, Tatiana D. Saccon, Allancer D.C. Nunes, James L. Kirkland, Tamara Tchkonia, Augusto Schneider, Michal M. Masternak,

https://doi.org/10.18632/aging.102772 pp 2711—2722

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Cavalcante MB, Saccon TD, Nunes AD, Kirkland JL, Tchkonia T, Schneider A, Masternak MM, . Dasatinib plus quercetin prevents uterine age-related dysfunction and fibrosis in mice. . 12:2711-2722. https://doi.org/10.18632/aging.102772

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                TY  - JOUR
                AU  - Cavalcante, Marcelo B. 
                AU  - Saccon, Tatiana D. 
                AU  - Nunes, Allancer D.C. 
                AU  - Kirkland, James L. 
                AU  - Tchkonia, Tamara 
                AU  - Schneider, Augusto 
                AU  - Masternak, Michal M. 
                TI  - Dasatinib plus quercetin prevents uterine age-related dysfunction and fibrosis in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102772
                DO  - 10.18632/aging.102772
                SP  - 2711
                EP  - 2722
                PY  - 
                AB  - The uterine fibrosis contributes to gestational outcomes. Collagen deposition in the uterus is related to uterine aging. Senolytic therapies are an option for reducing health complications related to aging. We investigated effects of aging and the senolytic drug combination of dasatinib plus quercetin (D+Q) on uterine fibrosis. Forty mice, 20 young females (03-months) and 20 old females (18-months), were analyzed. Young (Y) and old (O) animals were divided into groups of 10 mice, with one treatment (T) group (YT and OT) and another control &#xA9; group (YC and OC). Comparative analysis of Pi3k/Akt1/mTor and p53 gene expression and related microRNAs (miR34a, miR34b, miR34c, miR146a, miR449a, miR21a, miR126a, and miR181b) among groups was performed to test effects of age and treatment on collagen deposition pathways. Aging promoted downregulation of the Pi3k/Akt1/mTor signaling pathway (P = 0.005, P = 0.031, and P = 0.028, respectively) as well as a reduction in expression of miR34c (P = 0.029), miR126a (P = 0.009), and miR181b (P = 0.007). D+Q treatment increased p53 gene expression (P = 0.041) and decreased miR34a (P = 0.016). Our results demonstrate a role for the Pi3k/Akt1/mTor signaling pathway in uterine aging and suggest for the first time a possible anti-fibrotic effect in the uterus of D+Q senolytic therapy.
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Meta-analytic evidence for the anti-aging effect of hormesis on Caenorhabditis elegans

Tao Sun, Huifeng Wu, Ming Cong, Junfei Zhan, Fei Li,

https://doi.org/10.18632/aging.102773 pp 2723—2746

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Sun T, Wu H, Cong M, Zhan J, Li F, . Meta-analytic evidence for the anti-aging effect of hormesis on Caenorhabditis elegans. . 12:2723-2746. https://doi.org/10.18632/aging.102773

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 TY - JOUR
 AU - Sun, Tao 
 AU - Wu, Huifeng 
 AU - Cong, Ming 
 AU - Zhan, Junfei 
 AU - Li, Fei 
 TI - Meta-analytic evidence for the anti-aging effect of hormesis on Caenorhabditis elegans
 JO - 
 JA - 
 VL - 12
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102773
 DO - 10.18632/aging.102773
 SP - 2723
 EP - 2746
 PY - 
 AB - Mild stress-induced hormesis, as a promising strategy to improve longevity and healthy aging, meets both praise and criticism. To comprehensively assess the applicability of hormesis in aging intervention, this meta-analysis was conducted focusing on the effect of hormesis on Caenorhabditis elegans. Twenty-six papers involving 198 effect size estimates met the inclusion criteria. Meta-analytic results indicated that hormesis could significantly extend the mean lifespan of C. elegans by 16.7% and 25.1% under normal and stress culture conditions (p &lt; 0.05), respectively. The healthspan assays showed that hormesis remarkably enhanced the bending frequency and pumping rate of worms by 28.9% and 7.0% (p &lt; 0.05), respectively, while effectively reduced the lipofuscin level by 15.9% (p &lt; 0.05). The obviously increased expression of dauer formation protein-16 (1.66-fold) and its transcriptional targets, including superoxide dismutase-3 (2.46-fold), catalase-1 (2.32-fold) and small heat shock protein-16.2 (2.88-fold) (p &lt; 0.05), was one of the molecular mechanisms underlying these positive effects of hormesis. This meta-analysis provided strong evidence for the anti-aging role of hormesis, highlighting its lifespan-prolonging, healthspan-enhancing and resistance-increasing effects on C. elegans. Given that dauer formation protein-16 was highly conservative, hormesis offered the theoretical possibility of delaying intrinsic aging through exogenous intervention among humans.
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Single-cell RNA sequencing of immune cells in gastric cancer patients

Kai Fu, Bingqing Hui, Qian Wang, Chen Lu, Weihong Shi, Zhigang Zhang, Dawei Rong, Betty Zhang, Zhaofeng Tian, Weiwei Tang, Hongyong Cao, Xuehao Wang, Ziyi Chen,

https://doi.org/10.18632/aging.102774 pp 2747—2763

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Fu K, Hui B, Wang Q, Lu C, Shi W, Zhang Z, Rong D, Zhang B, Tian Z, Tang W, Cao H, Wang X, Chen Z, . Single-cell RNA sequencing of immune cells in gastric cancer patients. . 12:2747-2763. https://doi.org/10.18632/aging.102774

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                TY  - JOUR
                AU  - Fu, Kai 
                AU  - Hui, Bingqing 
                AU  - Wang, Qian 
                AU  - Lu, Chen 
                AU  - Shi, Weihong 
                AU  - Zhang, Zhigang 
                AU  - Rong, Dawei 
                AU  - Zhang, Betty 
                AU  - Tian, Zhaofeng 
                AU  - Tang, Weiwei 
                AU  - Cao, Hongyong 
                AU  - Wang, Xuehao 
                AU  - Chen, Ziyi 
                TI  - Single-cell RNA sequencing of immune cells in gastric cancer patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102774
                DO  - 10.18632/aging.102774
                SP  - 2747
                EP  - 2763
                PY  - 
                AB  - Cancer immunotherapy has achieved positive clinical responses in the treatment of various cancers, including gastric cancer (GC). In this study, we characterized the heterogeneity of T cells isolated from GC patients at the single-cell level using single-cell RNA sequencing. We identified different immune cell subtypes and their heterogeneous transcription factors and depicted their developmental trajectories. In particular, we focused on exhausted CD8+ cells and Tregs and discovered that, as compared to control, the IRF8 transcription factor was downregulated in CD8+ tumour-infiltrating lymphocytes (TILs) from GC tissues, and that GC patients with lower IRF8 levels in blood CD8+ T cells tended to be a at a more advanced disease stage. These findings provide a theoretical basis for targeted immune therapy in GC.
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Age-specific differential changes on gut microbiota composition in patients with major depressive disorder

Jian-Jun Chen, Sirong He, Liang Fang, Bin Wang, Shun-Jie Bai, Jing Xie, Chan-Juan Zhou, Wei Wang, Peng Xie,

https://doi.org/10.18632/aging.102775 pp 2764—2776

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Chen J, He S, Fang L, Wang B, Bai S, Xie J, Zhou C, Wang W, Xie P, . Age-specific differential changes on gut microbiota composition in patients with major depressive disorder. . 12:2764-2776. https://doi.org/10.18632/aging.102775

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                TY  - JOUR
                AU  - Chen, Jian-Jun 
                AU  - He, Sirong 
                AU  - Fang, Liang 
                AU  - Wang, Bin 
                AU  - Bai, Shun-Jie 
                AU  - Xie, Jing 
                AU  - Zhou, Chan-Juan 
                AU  - Wang, Wei 
                AU  - Xie, Peng 
                TI  - Age-specific differential changes on gut microbiota composition in patients with major depressive disorder
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102775
                DO  - 10.18632/aging.102775
                SP  - 2764
                EP  - 2776
                PY  - 
                AB  - Emerging evidence has shown the age-related changes in gut microbiota, but few studies were conducted to explore the effects of age on the gut microbiota in patients with major depressive disorder (MDD). This study was performed to identify the age-specific differential gut microbiota in MDD patients. In total, 70 MDD patients and 71 healthy controls (HCs) were recruited and divided into two groups: young group (age 18-29 years) and middle-aged group (age 30-59 years). The 16S rRNA gene sequences were extracted from the collected fecal samples. Finally, we found that the relative abundances of Firmicutes and Bacteroidetes were significantly decreased and increased, respectively, in young MDD patients as compared with young HCs, and the relative abundances of Bacteroidetes and Actinobacteria were significantly decreased and increased, respectively, in middle-aged MDD patients as compared with middle-aged HCs. Meanwhile, six and 25 differentially abundant bacterial taxa responsible for the differences between MDD patients (young and middle-aged, respectively) and their respective HCs were identified. Our results demonstrated that there were age-specific differential changes on gut microbiota composition in patients with MDD. Our findings would provide a novel perspective to uncover the pathogenesis underlying MDD.
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TP53/miR-34a-associated signaling targets SERPINE1 expression in human pancreatic cancer

Shaw M. Akula, Peter P. Ruvolo, James A. McCubrey,

https://doi.org/10.18632/aging.102776 pp 2777—2797

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Akula SM, Ruvolo PP, McCubrey JA, . TP53/miR-34a-associated signaling targets SERPINE1 expression in human pancreatic cancer. . 12:2777-2797. https://doi.org/10.18632/aging.102776

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 TY - JOUR
 AU - Akula, Shaw M. 
 AU - Ruvolo, Peter P. 
 AU - McCubrey, James A. 
 TI - TP53/miR-34a-associated signaling targets SERPINE1 expression in human pancreatic cancer
 JO - 
 JA - 
 VL - 12
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102776
 DO - 10.18632/aging.102776
 SP - 2777
 EP - 2797
 PY - 
 AB - Pancreatic ductal adenocarcinoma (PDAC) is a disease of aging. The TP53 gene product regulates cell growth, aging, and cancer. To determine the important targets of TP53 in PDAC, we examined the expression of 440 proteins on a reverse phase protein array (RPPA) in PDAC-derived MIA-PaCa-2 cells which either had WT-TP53 or lacked WT-TP53. MIA-PaCa-2 cells have a TP53 mutation as well as mutant KRAS and represent a good in vitro model to study PDAC. RPPA analysis demonstrated expression of tumor promoting proteins in cells that lacked WT-TP53; and this feature could be reversed significantly when the cells were transfected with vector encoding WT-TP53 or treated with berberine or a modified berberine (BBR). Expression of miR-34a-associated signaling was elevated in cells expressing WT-TP53 compared to cells expressing mTP53. Results from in vivo studies using human PDAC specimens confirmed the in vitro results as the expression of miR-34a and associated signaling was significantly decreased in PDAC specimens compared to non-cancerous tissues. This study determined SERPINE1 as a miR-34a target with relevance to the biology of PDAC. Thus, we have identified a key target (SERPINE1) of the TP53/miR-34a axis that may serve as a potential biomarker for early detection of pancreatic cancer.
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Functional lncRNA-miRNA-mRNA networks in rabbit carotid atherosclerosis

Yingnan Wu, Feng Zhang, Rui Lu, Yanan Feng, Xiaoying Li, Shuang Zhang, Wenying Hou, Jiawei Tian, Xianchao Kong, Litao Sun,

https://doi.org/10.18632/aging.102778 pp 2798—2813

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Wu Y, Zhang F, Lu R, Feng Y, Li X, Zhang S, Hou W, Tian J, Kong X, Sun L, . Functional lncRNA-miRNA-mRNA networks in rabbit carotid atherosclerosis. . 12:2798-2813. https://doi.org/10.18632/aging.102778

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                TY  - JOUR
                AU  - Wu, Yingnan 
                AU  - Zhang, Feng 
                AU  - Lu, Rui 
                AU  - Feng, Yanan 
                AU  - Li, Xiaoying 
                AU  - Zhang, Shuang 
                AU  - Hou, Wenying 
                AU  - Tian, Jiawei 
                AU  - Kong, Xianchao 
                AU  - Sun, Litao 
                TI  - Functional lncRNA-miRNA-mRNA networks in rabbit carotid atherosclerosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102778
                DO  - 10.18632/aging.102778
                SP  - 2798
                EP  - 2813
                PY  - 
                AB  - Atherosclerosis is one of the most common clinical cardiovascular disorders. Accumulating evidence indicates that lncRNAs exert critical functions in atherosclerosis; however, their functional roles and regulatory mechanisms remain unclear. In this study, we induced atherosclerotic plaques in three rabbit carotid arteries through an atherogenic diet and balloon injury; three age-matched rabbits were fed normal chow and served as controls. We thoroughly investigated the RNA (mRNA, lncRNA and miRNA) expression profiles in atherosclerotic rabbit carotid models with deep RNA sequencing. We identified several significantly differentially expressed RNAs. The corresponding lncRNA-miRNA-mRNA network was constructed, and the significantly dysregulated network was selected. Furthermore, Gene Ontology and &#x2002;Kyoto Encyclopedia of Genes and Genomes analyses indicated that the mRNAs in the network were involved in leukocyte activation, cell proliferation, cell adhesion molecules and cytokine-cytokine receptor interaction. After rigorous screening, we obtained a differentially expressed lncRNA-miRNA-mRNA interaction network associated with atherosclerosis. In the network, XLOC_054118 and XLOC_030217 upregulate the CHI3L1, SOAT, CTSB and CAPG genes by competitively binding to the miRNA ocu-miR-96-5p. XLOC_062719 and XLOC_063297 upregulate CTSS, CTSB and EDNRA genes by competitively binding to the miRNA ocu-miR-185-5p.
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Cerebral small vessel disease is associated with gait disturbance among community-dwelling elderly individuals: the Taizhou imaging study

Peixi Li, Yingzhe Wang, Yanfeng Jiang, Kexun Zhang, Qi Yang, Ziyu Yuan, Zhen Zhu, Weijun Tang, Min Fan, Weimin Ye, Qiang Dong, Li Jin, Ding Ding, Mei Cui, Xingdong Chen,

https://doi.org/10.18632/aging.102779 pp 2814—2824

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Li P, Wang Y, Jiang Y, Zhang K, Yang Q, Yuan Z, Zhu Z, Tang W, Fan M, Ye W, Dong Q, Jin L, Ding D, et al, . Cerebral small vessel disease is associated with gait disturbance among community-dwelling elderly individuals: the Taizhou imaging study. . 12:2814-2824. https://doi.org/10.18632/aging.102779

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                TY  - JOUR
                AU  - Li, Peixi 
                AU  - Wang, Yingzhe 
                AU  - Jiang, Yanfeng 
                AU  - Zhang, Kexun 
                AU  - Yang, Qi 
                AU  - Yuan, Ziyu 
                AU  - Zhu, Zhen 
                AU  - Tang, Weijun 
                AU  - Fan, Min 
                AU  - Ye, Weimin 
                AU  - Dong, Qiang 
                AU  - Jin, Li 
                AU  - Ding, Ding 
                AU  - Cui, Mei 
                AU  - Chen, Xingdong 
                TI  - Cerebral small vessel disease is associated with gait disturbance among community-dwelling elderly individuals: the Taizhou imaging study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102779
                DO  - 10.18632/aging.102779
                SP  - 2814
                EP  - 2824
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, Peixi 
                AU  - Wang, Yingzhe 
                AU  - Jiang, Yanfeng 
                AU  - Zhang, Kexun 
                AU  - Yang, Qi 
                AU  - Yuan, Ziyu 
                AU  - Zhu, Zhen 
                AU  - Tang, Weijun 
                AU  - Fan, Min 
                AU  - Ye, Weimin 
                AU  - Dong, Qiang 
                AU  - Jin, Li 
                AU  - Ding, Ding 
                AU  - Cui, Mei 
                AU  - Chen, Xingdong 
                TI  - Cerebral small vessel disease is associated with gait disturbance among community-dwelling elderly individuals: the Taizhou imaging study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102779
                DO  - 10.18632/aging.102779
                SP  - 2814
                EP  - 2824
                PY  - 
                AB  - Gait disturbance is considered to be a significant clinical manifestation of cerebral small vessel disease (CSVD). We aimed to investigate the association between different imaging markers of CSVD or total CSVD burden and gait disturbance in a community-dwelling population. In the cross-sectional Taizhou Imaging Study (TIS), 314 participants free of neurological disorders underwent MRI scanning and gait assessment with quantitative wearable devices as well as clinical rating scales. In linear regression, after adjustment for demographics and vascular risks, total CSVD burden was associated with prolonged 3-m walking (&#x3B2;=0.118, P=0.035), shorter stride length (&#x3B2;=-0.106, P=0.042), and poorer Timed-Up-and-Go (TUG) performance (&#x3B2;=0.146, P=0.009). Lacunes were positively associated with 3-m walking (&#x3B2;=0.118, P=0.037) and duration of TUG test (&#x3B2;=0.112, P=0.047). White matter hyperintensities and cerebral microbleeds were associated with prolonged stride time (&#x3B2;=0.134, P=0.024) and increased stance phase time percentage (&#x3B2;=0.115, P=0.038), respectively. Logistic regression revealed that participants with high CSVD burden or more lacunes were more likely to have an impaired gait velocity and an impaired TUG test. These results suggest that total CSVD burden and CSVD imaging markers are associated with gait disturbance among community-dwelling elderly people. Different CSVD imaging markers may cause gait disturbance through different pathways.
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Immune-related key gene CLDN10 correlates with lymph node metastasis but predicts favorable prognosis in papillary thyroid carcinoma

Zhaolan Xiang, Cheng Zhong, Aoshuang Chang, Junjun Ling, Houyu Zhao, Wei Zhou, Xianlu Zhuo,

https://doi.org/10.18632/aging.102780 pp 2825—2839

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Xiang Z, Zhong C, Chang A, Ling J, Zhao H, Zhou W, Zhuo X, . Immune-related key gene CLDN10 correlates with lymph node metastasis but predicts favorable prognosis in papillary thyroid carcinoma. . 12:2825-2839. https://doi.org/10.18632/aging.102780

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                TY  - JOUR
                AU  - Xiang, Zhaolan 
                AU  - Zhong, Cheng 
                AU  - Chang, Aoshuang 
                AU  - Ling, Junjun 
                AU  - Zhao, Houyu 
                AU  - Zhou, Wei 
                AU  - Zhuo, Xianlu 
                TI  - Immune-related key gene CLDN10 correlates with lymph node metastasis but predicts favorable prognosis in papillary thyroid carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102780
                DO  - 10.18632/aging.102780
                SP  - 2825
                EP  - 2839
                PY  - 
                AB  - The functions of immune cells in lymph node metastasis (LNM) have attracted considerable attention. This study aimed to screen the key immune-related and LNM-related genes in PTC. In the discovery phase, the immune-related genes in LNM were screened by using bioinformatics methods. In the validation phases, the association of the genes with LNM was first confirmed in a cohort from The Cancer Genome Atlas and a cohort based on a tissue chip. Then, the relationship of the genes with immune cell infiltration was further explored. Consequently, CLDN10 was identified, and its high expression was correlated with the presence of LNM in PTC but predicted a favorable prognosis. High CLDN10 expression was positively correlated with the infiltration of several immune cells, such as B cells, CD8+T cells, and macrophages. High CLDN10 expression may improve the outcomes of patients with PTC by increasing immune cell infiltration, although it might be associated with LNM. In conclusion, although CLDN1 might be correlated with LNM, it may also increase the infiltration of immune cells, including CD8+T cells and macrophages, and improve the clinical outcomes of patients with PTC. The effects of tumor purity and immune cell infiltration need to be considered in prognosis evaluation.
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Uric acid induces stress resistance and extends the life span through activating the stress response factor DAF-16/FOXO and SKN-1/NRF2

Qin-Li Wan, Xiaodie Fu, Wenyu Dai, Jing Yang, Zhenhuan Luo, Xiao Meng, Xiao Liu, Ruowei Zhong, Hengwen Yang, Qinghua Zhou,

https://doi.org/10.18632/aging.102781 pp 2840—2856

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Wan Q, Fu X, Dai W, Yang J, Luo Z, Meng X, Liu X, Zhong R, Yang H, Zhou Q, . Uric acid induces stress resistance and extends the life span through activating the stress response factor DAF-16/FOXO and SKN-1/NRF2. . 12:2840-2856. https://doi.org/10.18632/aging.102781

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                TY  - JOUR
                AU  - Wan, Qin-Li 
                AU  - Fu, Xiaodie 
                AU  - Dai, Wenyu 
                AU  - Yang, Jing 
                AU  - Luo, Zhenhuan 
                AU  - Meng, Xiao 
                AU  - Liu, Xiao 
                AU  - Zhong, Ruowei 
                AU  - Yang, Hengwen 
                AU  - Zhou, Qinghua 
                TI  - Uric acid induces stress resistance and extends the life span through activating the stress response factor DAF-16/FOXO and SKN-1/NRF2
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102781
                DO  - 10.18632/aging.102781
                SP  - 2840
                EP  - 2856
                PY  - 
                AB  - Uric acid is a common metabolite found in mammals&#x2019; serum. Recently, several metabolites have been identified that modulate aging, and uric acid levels are positively correlated with mammals&#x2019; lifespan. However, the molecular mechanisms underlying this are largely undefined. Here we show that uric acid, an end product of purine metabolism, enhances the resistance of oxidative stress and extends the life span of Caenorhabditis elegans (C. elegans). We show that uric acid enhances a variety of pathways and leads to the upregulation of genes that are required for uric acid-mediated life span extension. We find that the transcription factors DAF-16/FOXO, SKN-1/NRF2 and HSF-1 contribute to the beneficial longevity conferred by uric acid. We also show that uric acid induced life span extension by regulating the reproductive signaling and insulin/IGF-1 signaling (IIS) pathways. In addition, we find that mitochondrial function plays an important role in uric acid-mediated life span extension. Taken together, these data suggest that uric acid prolongs the life span of C. elegans, in part, because of its antioxidative activity, which in turn regulates the IIS and the reproductive signaling pathways, thereby activating the function of the transcription factors DAF-16, HSF-1 and SKN-1.
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A nomogram combining long non-coding RNA expression profiles and clinical factors predicts survival in patients with bladder cancer

Yifan Wang, Lutao Du, Xuemei Yang, Juan Li, Peilong Li, Yinghui Zhao, Weili Duan, Yingjie Chen, Yunshan Wang, Haiting Mao, Chuanxin Wang,

https://doi.org/10.18632/aging.102782 pp 2857—2879

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Wang Y, Du L, Yang X, Li J, Li P, Zhao Y, Duan W, Chen Y, Wang Y, Mao H, Wang C, . A nomogram combining long non-coding RNA expression profiles and clinical factors predicts survival in patients with bladder cancer. . 12:2857-2879. https://doi.org/10.18632/aging.102782

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                TY  - JOUR
                AU  - Wang, Yifan 
                AU  - Du, Lutao 
                AU  - Yang, Xuemei 
                AU  - Li, Juan 
                AU  - Li, Peilong 
                AU  - Zhao, Yinghui 
                AU  - Duan, Weili 
                AU  - Chen, Yingjie 
                AU  - Wang, Yunshan 
                AU  - Mao, Haiting 
                AU  - Wang, Chuanxin 
                TI  - A nomogram combining long non-coding RNA expression profiles and clinical factors predicts survival in patients with bladder cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102782
                DO  - 10.18632/aging.102782
                SP  - 2857
                EP  - 2879
                PY  - 
                AB  - Bladder cancer (BCa) is a heterogeneous disease with various tumorigenic mechanisms and clinical behaviors. The current tumor-node-metastasis (TNM) staging system is inadequate to predict overall survival (OS) in BCa patients. We developed a BCa-specific, long-non-coding-RNA (lncRNA)-based nomogram to improve survival prediction in BCa. We obtained the large-scale gene expression profiles of samples from 414 BCa patients in The Cancer Genome Atlas database. Using an lncRNA-mining computational framework, we identified three OS-related lncRNAs among 826 lncRNAs that were differentially expressed between BCa and normal samples. We then constructed a three-lncRNA signature, which efficiently distinguished high-risk from low-risk patients and was even viable in the TNM stage-II, TNM stage-III and &#x2265;65-year-old subgroups (all P&lt;0.05). Using clinical risk factors, we developed a signature-based nomogram, which performed better than the molecular signature or clinical factors alone for prognostic prediction. A bioinformatical analysis revealed that the three OS-related lncRNAs were co-expressed with genes involved in extracellular matrix organization. Functional assays demonstrated that RNF144A-AS1, one of the three OS-related lncRNAs, promoted BCa cell migration and invasion in vitro. Our three-lncRNA signature-based nomogram effectively predicts the prognosis of BCa patients, and could potentially be used for individualized management of such patients.
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In vivo protective effect of adipsin-deficiency on spontaneous knee osteoarthritis in aging mice

Frédéric Paré, Ginette Tardif, Hassan Fahmi, Yassine Ouhaddi, Jean-Pierre Pelletier, Johanne Martel-Pelletier,

https://doi.org/10.18632/aging.102784 pp 2880—2896

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Paré F, Tardif G, Fahmi H, Ouhaddi Y, Pelletier J, Martel-Pelletier J, . In vivo protective effect of adipsin-deficiency on spontaneous knee osteoarthritis in aging mice. . 12:2880-2896. https://doi.org/10.18632/aging.102784

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 TY - JOUR
 AU - Paré, Frédéric 
 AU - Tardif, Ginette 
 AU - Fahmi, Hassan 
 AU - Ouhaddi, Yassine 
 AU - Pelletier, Jean-Pierre 
 AU - Martel-Pelletier, Johanne 
 TI - In vivo protective effect of adipsin-deficiency on spontaneous knee osteoarthritis in aging mice
 JO - 
 JA - 
 VL - 12
 IS - 3
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.102784
 DO - 10.18632/aging.102784
 SP - 2880
 EP - 2896
 PY - 
 AB - The adipokine adipsin is an emerging mediator of human osteoarthritis (OA) progression. Here, we investigated its in vivo role in the development of spontaneous OA in aging mice. We compared articular knee joint morphology, histology in knee cartilage, synovial membrane, subchondral bone, meniscus, and anterior cruciate ligament (ACL); and chondrogenesis in the ACL from adipsin-deficient (Df-/-) and wild-type (Df+/+) 20-week- and 20-month-old mice. Serum levels of a panel of adipokines, inflammatory factors, and metalloproteases known to be implicated in OA were investigated. Data first revealed that the early manifestation of OA appeared in the ACL of 20-week-old mice, progressing to severe alterations in the 20 month-old wild-type mice. Further results demonstrated that adipsin-deficiency protected the articular tissues from spontaneous OA progression and triggered significantly higher serum levels of the adipokines adiponectin and FGF-21 while lowering levels of the inflammatory factor interleukin 6 (IL-6) in both young and old mice. This work further underlines the clinical relevance of adipsin as a novel therapeutic approach of human OA. Moreover, this study shows the potential beneficial effect of the adipokine FGF-21 against OA, and provides support for this factor to be a new biomarker and/or target of primary OA therapeutic avenues.
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Identifying lncRNA–miRNA–mRNA networks to investigate Alzheimer’s disease pathogenesis and therapy strategy

Nana Ma, Changrui Tie, Bo Yu, Wei Zhang, Jun Wan,

https://doi.org/10.18632/aging.102785 pp 2897—2920

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Ma N, Tie C, Yu B, Zhang W, Wan J, . Identifying lncRNA–miRNA–mRNA networks to investigate Alzheimer’s disease pathogenesis and therapy strategy. . 12:2897-2920. https://doi.org/10.18632/aging.102785

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                TY  - JOUR
                AU  - Ma, Nana 
                AU  - Tie, Changrui 
                AU  - Yu, Bo 
                AU  - Zhang, Wei 
                AU  - Wan, Jun 
                TI  - Identifying lncRNA–miRNA–mRNA networks to investigate Alzheimer’s disease pathogenesis and therapy strategy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102785
                DO  - 10.18632/aging.102785
                SP  - 2897
                EP  - 2920
                PY  - 
                AB  - Alzheimer&#x2019;s disease (AD), the most common cause of dementia, leads to neuronal damage and deterioration of cognitive functions in aging brains. There is evidence suggesting the participation of noncoding RNAs in AD-associated pathophysiology. A potential linkage between AD and lncRNA-associated competing endogenous RNA (ceRNA) networks has been revealed. Nevertheless, there are still no genome-wide studies which have identified the lncRNA-associated ceRNA pairs involved in AD. For this reason, deep RNA-sequencing was performed to systematically investigate lncRNA-associated ceRNA mechanisms in AD model mice (APP/PS1) brains. Our results identified 487, 89, and 3,025 significantly dysregulated lncRNAs, miRNAs, and mRNAs, respectively, and the most comprehensive lncRNA-associated ceRNA networks to date are constructed in the APP/PS1 brain. GO analysis revealed the involvement of the identified networks in regulating AD development from distinct origins, such as synapses and dendrites. Following rigorous selection, the lncRNA-associated ceRNA networks in this AD mouse model were found to be mainly involved in synaptic plasticity as well as memory (Akap5) and regulation of amyloid-&#x3B2; (A&#x3B2;)-induced neuroinflammation (Klf4). This study presents the first systematic dissection of lncRNA-associated ceRNA profiles in the APP/PS1 mouse brain. The identified lncRNA-associated ceRNA networks could provide insights that facilitate AD diagnosis and future treatment strategies.
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The nuclear localization signal-mediated nuclear targeting of herpes simplex virus 1 early protein UL2 is important for efficient viral production

Meili Li, Xingmei Zou, Yuanfang Wang, Zuo Xu, Xiaowen Ou, Yiwen Li, Delong Liu, Yingjie Guo, Yangxi Deng, Si Jiang, Tong Li, Shaoxuan Shi, Yilong Bao, Tao Peng, Mingsheng Cai,

https://doi.org/10.18632/aging.102786 pp 2921—2938

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Li M, Zou X, Wang Y, Xu Z, Ou X, Li Y, Liu D, Guo Y, Deng Y, Jiang S, Li T, Shi S, Bao Y, et al, . The nuclear localization signal-mediated nuclear targeting of herpes simplex virus 1 early protein UL2 is important for efficient viral production. . 12:2921-2938. https://doi.org/10.18632/aging.102786

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                TY  - JOUR
                AU  - Li, Meili 
                AU  - Zou, Xingmei 
                AU  - Wang, Yuanfang 
                AU  - Xu, Zuo 
                AU  - Ou, Xiaowen 
                AU  - Li, Yiwen 
                AU  - Liu, Delong 
                AU  - Guo, Yingjie 
                AU  - Deng, Yangxi 
                AU  - Jiang, Si 
                AU  - Li, Tong 
                AU  - Shi, Shaoxuan 
                AU  - Bao, Yilong 
                AU  - Peng, Tao 
                AU  - Cai, Mingsheng 
                TI  - The nuclear localization signal-mediated nuclear targeting of herpes simplex virus 1 early protein UL2 is important for efficient viral production
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102786
                DO  - 10.18632/aging.102786
                SP  - 2921
                EP  - 2938
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Li, Meili 
                AU  - Zou, Xingmei 
                AU  - Wang, Yuanfang 
                AU  - Xu, Zuo 
                AU  - Ou, Xiaowen 
                AU  - Li, Yiwen 
                AU  - Liu, Delong 
                AU  - Guo, Yingjie 
                AU  - Deng, Yangxi 
                AU  - Jiang, Si 
                AU  - Li, Tong 
                AU  - Shi, Shaoxuan 
                AU  - Bao, Yilong 
                AU  - Peng, Tao 
                AU  - Cai, Mingsheng 
                TI  - The nuclear localization signal-mediated nuclear targeting of herpes simplex virus 1 early protein UL2 is important for efficient viral production
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102786
                DO  - 10.18632/aging.102786
                SP  - 2921
                EP  - 2938
                PY  - 
                AB  - Herpes simplex virus 1 (HSV-1) is a representative alphaherpesvirus that can provoke a series of severe diseases to human being, but its exact pathogenesis is not perfectly understood. UL2, a uracil-DNA glycosylase involved in the process of HSV-1 DNA replication, has been shown to be predominantly targeted to the nuclei in our previous study, yet little is established regarding the subcellular localization signal or its related function of UL2 during HSV-1 propagation. Here, by creating a number of UL2 variants merged with enhanced yellow fluorescent protein, an authentic nuclear localization signal (NLS) of UL2 was, for the first time, identified and profiled to amino acids (aa) 1 to 17 (MKRACSRSPSPRRRPSS), and 12RRR14 was indispensable for its nuclear accumulation. Besides, the predicted nuclear export signal (aa 225 to 240) of UL2 was determined to be nonfunctional. Based on the HSV-1 bacterial artificial chromosome and homologous recombination technique, three recombinant viruses with mutations of the identified NLS, deletion and revertant of UL2 were constructed to assess the effect of UL2 nuclear targeting on HSV-1 replication. Compared to the wild type HSV-1, UL2 deletion remarkably restrained viral production, and mutation of NLS targeting UL2 to cytoplasm (pan-cellular distribution) in recombinant virus-infected cells showed a certain degree of deficiency in HSV-1 proliferation. Moreover, recombinant virus with UL2 deletion exhibited serious damages of viral DNA synthesis and mRNA expression, and these processes were partially disrupted in the recombinant virus with UL2 NLS mutation. Collectively, we had established a functional NLS in UL2 and showed that the NLS-mediated nuclear translocation of UL2 was important for efficient production of HSV-1. These data were of significance for further clarifying the biological function of UL2 during HSV-1 infection.
                ER  -

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Atorvastatin reduces cerebral vasospasm and infarction after aneurysmal subarachnoid hemorrhage in elderly Chinese adults

Junhui Chen, Mingchang Li, Xun Zhu, Lei Chen, Shuo Yang, Chunlei Zhang, Ting Wu, Xiaoyan Feng, Yuhai Wang, Qianxue Chen,

https://doi.org/10.18632/aging.102788 pp 2939—2951

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Chen J, Li M, Zhu X, Chen L, Yang S, Zhang C, Wu T, Feng X, Wang Y, Chen Q, . Atorvastatin reduces cerebral vasospasm and infarction after aneurysmal subarachnoid hemorrhage in elderly Chinese adults. . 12:2939-2951. https://doi.org/10.18632/aging.102788

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                TY  - JOUR
                AU  - Chen, Junhui 
                AU  - Li, Mingchang 
                AU  - Zhu, Xun 
                AU  - Chen, Lei 
                AU  - Yang, Shuo 
                AU  - Zhang, Chunlei 
                AU  - Wu, Ting 
                AU  - Feng, Xiaoyan 
                AU  - Wang, Yuhai 
                AU  - Chen, Qianxue 
                TI  - Atorvastatin reduces cerebral vasospasm and infarction after aneurysmal subarachnoid hemorrhage in elderly Chinese adults
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102788
                DO  - 10.18632/aging.102788
                SP  - 2939
                EP  - 2951
                PY  - 
                AB  - We explored whether acute atorvastatin treatment would improve clinical outcomes and reduce the incidence of cerebral vasospasm after aneurysmal subarachnoid hemorrhage in elderly Chinese adults. Patients (60 to 90 years old) were admitted to intensive care units after surgery to clip or embolize their aneurysms. We assessed 592 patients and assigned 159 to receive atorvastatin (20 mg/day) and 158 to receive placebo once daily for up to 14 days. The primary outcome was the Glasgow outcome scale at 6 months, and secondary outcomes were cerebral vasospasm, 30-days all-cause mortality, cerebral infarction, and delayed ischemic neurological deficit. The incidence of postoperative cerebral vasospasm (39.3% vs 56%, P =0.004) and cerebral infarction (18.7% vs 27.3%, P=0.027) were significantly lower in the atorvastatin group. The study did not detect benefits in the use of atorvastatin for 6 months clinical outcome or 30-day all-cause mortality, but it suggests that atorvastatin together with nimodipine can reduce cerebral vasospasm and cerebral infarction after subarachnoid hemorrhage.
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Tfh cell subset biomarkers and inflammatory markers are associated with frailty status and frailty subtypes in the community-dwelling older population: a cross-sectional study

Ming-Juan Yin, Yong-Zhen Xiong, Xiu-Juan Xu, Ling-Feng Huang, Yan Zhang, Xiao-Jun Wang, Liang-Chang Xiu, Jing-Xiao Huang, Ting-Yu Lian, Dong-Mei Liang, Jin-Mei Zen, Jin-Dong Ni,

https://doi.org/10.18632/aging.102789 pp 2952—2973

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Yin M, Xiong Y, Xu X, Huang L, Zhang Y, Wang X, Xiu L, Huang J, Lian T, Liang D, Zen J, Ni J, . Tfh cell subset biomarkers and inflammatory markers are associated with frailty status and frailty subtypes in the community-dwelling older population: a cross-sectional study. . 12:2952-2973. https://doi.org/10.18632/aging.102789

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                TY  - JOUR
                AU  - Yin, Ming-Juan 
                AU  - Xiong, Yong-Zhen 
                AU  - Xu, Xiu-Juan 
                AU  - Huang, Ling-Feng 
                AU  - Zhang, Yan 
                AU  - Wang, Xiao-Jun 
                AU  - Xiu, Liang-Chang 
                AU  - Huang, Jing-Xiao 
                AU  - Lian, Ting-Yu 
                AU  - Liang, Dong-Mei 
                AU  - Zen, Jin-Mei 
                AU  - Ni, Jin-Dong 
                TI  - Tfh cell subset biomarkers and inflammatory markers are associated with frailty status and frailty subtypes in the community-dwelling older population: a cross-sectional study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102789
                DO  - 10.18632/aging.102789
                SP  - 2952
                EP  - 2973
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Yin, Ming-Juan 
                AU  - Xiong, Yong-Zhen 
                AU  - Xu, Xiu-Juan 
                AU  - Huang, Ling-Feng 
                AU  - Zhang, Yan 
                AU  - Wang, Xiao-Jun 
                AU  - Xiu, Liang-Chang 
                AU  - Huang, Jing-Xiao 
                AU  - Lian, Ting-Yu 
                AU  - Liang, Dong-Mei 
                AU  - Zen, Jin-Mei 
                AU  - Ni, Jin-Dong 
                TI  - Tfh cell subset biomarkers and inflammatory markers are associated with frailty status and frailty subtypes in the community-dwelling older population: a cross-sectional study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102789
                DO  - 10.18632/aging.102789
                SP  - 2952
                EP  - 2973
                PY  - 
                AB  - We conducted a cross-sectional study investigating community-dwelling older population to determine association between immunoscenescence marker, inflammatory cytokines and frailty. Frailty status was classified with 33-item modified frailty index and latent class analysis was applied to explore the latent classes (subtypes) of frailty. In multivariable analysis, higher Tfh2 cells were associated with a higher risk of frailty [1.13(1.03&#x2013;1.25)] in females, but a lower risk of cognitive and functional frail [0.92(0.86&#x2013;0.99)] and physiological frail [0.92(0.87&#x2013;0.98)]. Additionally, a greater risk of multi-frail and physiological frail correlated with low Tfh1 [0.77(0.60&#x2013;0.99); 0.87(0.79&#x2013;0.96)] and Tfh17 cells [0.79(0.65&#x2013;0.96); 0.86(0.78&#x2013;0.94)], respectively. Higher B cells were associated with decreased frailty/pre-frailty both in females [0.89(0.81&#x2013;0.98)] and males [0.82(0.71&#x2013;0.96)], but did not correlate with frailty subtypes. Regarding inflammatory markers, participants in the TGF-&#x3B2; 2nd quartile showed a decreased risk of pre-frailty/frailty in females [0.39(0.17&#x2013;0.89)] and psychological frail [0.37(0.16&#x2013;0.88)], compared with those in the top tertile. Moreover, we found participants in the 2nd tertile for IL-12 levels showed a decreased risk of physiological frail [0.40 (0.17&#x2013;0.97)]. Our study highlights the importance of Tfh cell subsets and inflammatory markers in frailty in a sex-specific manner, particularly in terms of frailty subtype.
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Long non-coding RNA TUSC8 inhibits breast cancer growth and metastasis via miR-190b-5p/MYLIP axis

Luqing Zhao, Yangying Zhou, Yuelong Zhao, Qingling Li, Jianhua Zhou, Yitao Mao,

https://doi.org/10.18632/aging.102791 pp 2974—2991

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Zhao L, Zhou Y, Zhao Y, Li Q, Zhou J, Mao Y, . Long non-coding RNA TUSC8 inhibits breast cancer growth and metastasis via miR-190b-5p/MYLIP axis. . 12:2974-2991. https://doi.org/10.18632/aging.102791

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                TY  - JOUR
                AU  - Zhao, Luqing 
                AU  - Zhou, Yangying 
                AU  - Zhao, Yuelong 
                AU  - Li, Qingling 
                AU  - Zhou, Jianhua 
                AU  - Mao, Yitao 
                TI  - Long non-coding RNA TUSC8 inhibits breast cancer growth and metastasis via miR-190b-5p/MYLIP axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102791
                DO  - 10.18632/aging.102791
                SP  - 2974
                EP  - 2991
                PY  - 
                AB  - The lncRNA tumor suppressor candidate 8 (TUSC8) plays a critical role in the development of several cancers. However, the biological functions and underlying molecular mechanisms of TUSC8 with respect to breast cancer remain largely unclear. Here, we found that TUSC8 was significantly down-regulated in breast cancer tissues and its high expression predicted better prognosis of breast cancer patients. Functionally, knock-down of TUSC8 drastically promoted the proliferation, migration and invasion of breast cancer cells in vitro and facilitated tumorigenicity and metastasis in vivo. Mechanistically, the results of luciferase reporter, RIP and RNA pull-down assays proved that TUSC8 functioned as molecular sponge for miR-190b-5p. Furthermore, we showed that TUSC8 served as a competing endogenous RNA (ceRNA) of myosin regulatory light chain interacting protein (MYLIP) through competitively binding with miR-190b-5p and suppressed breast cancer metastasis through regulating the expression of epithelial&#x2013;mesenchymal transition (EMT) related markers. Clinically, the receiver operating characteristic curve (ROC) analyses revealed that the combination usage of TUSC8 and MYLIP might become novel promising diagnostic biomarkers for breast cancer. Taken together, these results suggested that TUSC8 inhibited breast cancer growth and metastasis via miR-190b-5p/MYLIP axis, providing us new insights into developing potential therapeutic targets for breast cancer patients.
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EGF released from human placental mesenchymal stem cells improves premature ovarian insufficiency via NRF2/HO-1 activation

Chenyue Ding, Qinyan Zou, Yifei Wu, Jiafeng Lu, Chunfeng Qian, Hong Li, Boxian Huang,

https://doi.org/10.18632/aging.102794 pp 2992—3009

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Ding C, Zou Q, Wu Y, Lu J, Qian C, Li H, Huang B, . EGF released from human placental mesenchymal stem cells improves premature ovarian insufficiency via NRF2/HO-1 activation. . 12:2992-3009. https://doi.org/10.18632/aging.102794

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                TY  - JOUR
                AU  - Ding, Chenyue 
                AU  - Zou, Qinyan 
                AU  - Wu, Yifei 
                AU  - Lu, Jiafeng 
                AU  - Qian, Chunfeng 
                AU  - Li, Hong 
                AU  - Huang, Boxian 
                TI  - EGF released from human placental mesenchymal stem cells improves premature ovarian insufficiency via NRF2/HO-1 activation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102794
                DO  - 10.18632/aging.102794
                SP  - 2992
                EP  - 3009
                PY  - 
                AB  - Human placental mesenchymal stem cells (hPMSCs) have the ability to release cytokines and to differentiate into the three germ layers. To date, the relevance of hPMSCs for the treatment of premature ovarian insufficiency (POI) disease through the regulation of oxidative stress is still unclear. Therefore, to evaluate the therapeutic efficiency and investigate the mechanism of hPMSCs, we generated a mouse model of POI and collected human ovarian granule cells (hGCs) from patients with POI. hPMSCs displayed therapeutic effects on POI ovarian function, including recovered follicular numbers and increased expression of oocyte markers. Furthermore, secretion of the cytokine EGF (epidermal growth factor) was higher from hPMSCs than it was from other cells. FACS and Western blot analyses showed that EGF elevated the proliferation and reduced the apoptosis in hGCs. hPMSCs and EGF inhibited oxidative stress levels. Protein assays demonstrated that EGF suppressed oxidative stress by dose-dependently upregulating the expression of the NRF2/HO-1 pathway, and it inhibited the apoptosis by regulating the PTEN/PI3K/AKT pathway. These findings provide an experimental foundation for hPMSCs in improving ovarian function through the secretion of EGF. The mechanism of action of EGF is related to protection from oxidative stress by activation of the NRF2/HO-1.
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microRNA-1203 targets and silences cyclophilin D to protect human endometrial cells from oxygen and glucose deprivation-re-oxygenation

Hong-Bin Xu, Yu-Fan Zheng, Di Wu, Ya Li, Li-Na Zhou, You-Guo Chen,

https://doi.org/10.18632/aging.102795 pp 3010—3024

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Xu H, Zheng Y, Wu D, Li Y, Zhou L, Chen Y, . microRNA-1203 targets and silences cyclophilin D to protect human endometrial cells from oxygen and glucose deprivation-re-oxygenation. . 12:3010-3024. https://doi.org/10.18632/aging.102795

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                TY  - JOUR
                AU  - Xu, Hong-Bin 
                AU  - Zheng, Yu-Fan 
                AU  - Wu, Di 
                AU  - Li, Ya 
                AU  - Zhou, Li-Na 
                AU  - Chen, You-Guo 
                TI  - microRNA-1203 targets and silences cyclophilin D to protect human endometrial cells from oxygen and glucose deprivation-re-oxygenation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102795
                DO  - 10.18632/aging.102795
                SP  - 3010
                EP  - 3024
                PY  - 
                AB  - Oxygen and glucose deprivation (OGD)-re-oxygenation (OGDR) stimulation to the human endometrial cells mimics ischemia-reperfusion injury. Cyclophilin D (CypD)-dependent programmed necrosis pathway mediates OGDR-induced cytotoxicity to human endometrial cells. We here identified a novel CypD-targeting miRNA, microRNA-1203 (miR-1203). In T-HESC and primary human endometrial cells, ectopic overexpression of miR-1203, using a lentiviral construct, potently downregulated the CypD 3&#x2019;-untranslated region (3&#x2019;-UTR) activity and its expression. Both were however upregulated in endometrial cells with forced miR-1203 inhibition by its anti-sense sequence. Functional studies demonstrated that ectopic miR-1203 overexpression in endometrial cells alleviated OGDR-induced programmed necrosis, inhibiting mitochondrial CypD-p53-adenine nucleotide translocator 1 association, mitochondrial depolarization, reactive oxygen species production, and medium lactate dehydrogenase release. Contrarily OGDR-induced programmed necrosis and cytotoxicity were intensified with forced miR-1203 inhibition in endometrial cells. Significantly, ectopic miR-1203 overexpression or inhibition failed to change OGDR-induced cytotoxicity in CypD-knockout T-HESC cells. Furthermore, ectopic miR-1203 overexpression was unable to protect T-HESC endometrial cells from OGDR when CypD was restored by an UTR-depleted CypD construct. Collectively, these results show that miR-1203 targets and silences CypD to protect human endometrial cells from OGDR
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Obg-like ATPase 1 (OLA1) overexpression predicts poor prognosis and promotes tumor progression by regulating P21/CDK2 in hepatocellular carcinoma

Shanzhou Huang, Chuanzhao Zhang, Chengjun Sun, Yuchen Hou, Yixi Zhang, Nga Lei Tam, Zekang Wang, Jia Yu, Bowen Huang, Hongkai Zhuang, Zixuan Zhou, Zuyi Ma, Zhonghai Sun, Xiaoshun He, Qi Zhou, Baohua Hou, Linwei Wu,

https://doi.org/10.18632/aging.102797 pp 3025—3041

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Huang S, Zhang C, Sun C, Hou Y, Zhang Y, Tam NL, Wang Z, Yu J, Huang B, Zhuang H, Zhou Z, Ma Z, Sun Z, et al, . Obg-like ATPase 1 (OLA1) overexpression predicts poor prognosis and promotes tumor progression by regulating P21/CDK2 in hepatocellular carcinoma. . 12:3025-3041. https://doi.org/10.18632/aging.102797

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                TY  - JOUR
                AU  - Huang, Shanzhou 
                AU  - Zhang, Chuanzhao 
                AU  - Sun, Chengjun 
                AU  - Hou, Yuchen 
                AU  - Zhang, Yixi 
                AU  - Tam, Nga Lei 
                AU  - Wang, Zekang 
                AU  - Yu, Jia 
                AU  - Huang, Bowen 
                AU  - Zhuang, Hongkai 
                AU  - Zhou, Zixuan 
                AU  - Ma, Zuyi 
                AU  - Sun, Zhonghai 
                AU  - He, Xiaoshun 
                AU  - Zhou, Qi 
                AU  - Hou, Baohua 
                AU  - Wu, Linwei 
                TI  - Obg-like ATPase 1 (OLA1) overexpression predicts poor prognosis and promotes tumor progression by regulating P21/CDK2 in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102797
                DO  - 10.18632/aging.102797
                SP  - 3025
                EP  - 3041
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Huang, Shanzhou 
                AU  - Zhang, Chuanzhao 
                AU  - Sun, Chengjun 
                AU  - Hou, Yuchen 
                AU  - Zhang, Yixi 
                AU  - Tam, Nga Lei 
                AU  - Wang, Zekang 
                AU  - Yu, Jia 
                AU  - Huang, Bowen 
                AU  - Zhuang, Hongkai 
                AU  - Zhou, Zixuan 
                AU  - Ma, Zuyi 
                AU  - Sun, Zhonghai 
                AU  - He, Xiaoshun 
                AU  - Zhou, Qi 
                AU  - Hou, Baohua 
                AU  - Wu, Linwei 
                TI  - Obg-like ATPase 1 (OLA1) overexpression predicts poor prognosis and promotes tumor progression by regulating P21/CDK2 in hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102797
                DO  - 10.18632/aging.102797
                SP  - 3025
                EP  - 3041
                PY  - 
                AB  - Background: Obg-like ATPase 1 (OLA1) has been found to have a dual role in cancers. However, the relationship between OLA1 and hepatocellular carcinoma (HCC) remains unclear.Results: High expression of OLA1 in HCC was detected in public datasets and clinical samples, and correlated with poor prognosis. Downregulation of OLA1 significantly inhibited the proliferation, migration, invasion and tumorigenicity of HCC cells. Mechanistically, GSEA showed that OLA1 might promote tumor progression by regulating the cell cycle and apoptosis. In addition, OLA1 knockdown resulted in G0/G1 phase arrest and high levels of apoptosis. OLA1 could bind with P21 and upregulate CDK2 expression to promote HCC progression.Conclusions: Overall, these findings uncover a role for OLA1 in regulating the proliferation and apoptosis of HCC cells.Materials and methods: The Cancer Genome Atlas and Gene Expression Omnibus datasets were analyzed to identify gene expression. Immunohistochemistry staining, western blot and real-time polymerase chain reaction were performed to evaluate OLA1 expression in samples. Cell count Kit-8, wound-healing, transwell and flow cytometry assays were used to analyze HCC cell progression. Subcutaneous xenotransplantation models were used to investigate the role of OLA1 in vivo. Coimmunoprecipitation was used to analyze protein interactions.
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Entorhinal cortex-based metabolic profiling of chronic restraint stress mice model of depression

Xi Chen, Tianlan Lan, Yue Wang, Yong He, Zhonghao Wu, Yu Tian, Yan Li, Mengge Bai, Wei Zhou, Hanping Zhang, Ke Cheng, Peng Xie,

https://doi.org/10.18632/aging.102798 pp 3042—3052

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Chen X, Lan T, Wang Y, He Y, Wu Z, Tian Y, Li Y, Bai M, Zhou W, Zhang H, Cheng K, Xie P, . Entorhinal cortex-based metabolic profiling of chronic restraint stress mice model of depression. . 12:3042-3052. https://doi.org/10.18632/aging.102798

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                TY  - JOUR
                AU  - Chen, Xi 
                AU  - Lan, Tianlan 
                AU  - Wang, Yue 
                AU  - He, Yong 
                AU  - Wu, Zhonghao 
                AU  - Tian, Yu 
                AU  - Li, Yan 
                AU  - Bai, Mengge 
                AU  - Zhou, Wei 
                AU  - Zhang, Hanping 
                AU  - Cheng, Ke 
                AU  - Xie, Peng 
                TI  - Entorhinal cortex-based metabolic profiling of chronic restraint stress mice model of depression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102798
                DO  - 10.18632/aging.102798
                SP  - 3042
                EP  - 3052
                PY  - 
                AB  - Despite that millions of people suffer from major depressive disorder (MDD), the mechanism underlying MDD remains elusive. Recently, it has been reported that entorhinal cortex (EC) functions on the regulation of depressive-like phenotype relying on the stimulation of glutamatergic afferent from EC to hippocampus. Based on this, we used liquid chromatography-tandem mass spectrometry method to explore metabolic alterations in the EC of mice after exposed to chronic restraint stress (CRS). Molecular validation was conducted via the application of western blot and RT-qPCR. Through this study, we found significant upregulation of glutamate, ornithine aspartic acid, 5-hydroxytryptophan, L-tyrosine and norepinephrine in CRS group, accompanied with downregulation of homovanillic acid. Focusing on these altered metabolic pathways in EC, we found that gene levels of GAD1, GLUL and SNAT1 were increased. Upregulation of SERT and EAAT2 in protein expression level were also validated, while no significant changes were found in TH, AADC, MAOA, VMAT2, GAD1, GLUL and SNAT1. Our findings firstly provide evidence about the alteration of metabolites and related molecules in the EC of mice model of depression, implying the potential mechanism in MDD pathology.
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New landscapes and horizons in hepatocellular carcinoma therapy

Melchiorre Cervello, Maria R. Emma, Giuseppa Augello, Antonella Cusimano, Lydia Giannitrapani, Maurizio Soresi, Shaw M. Akula, Stephen L. Abrams, Linda S. Steelman, Alessandro Gulino, Beatrice Belmonte, Giuseppe Montalto, James A. McCubrey,

https://doi.org/10.18632/aging.102777 pp 3053—3094

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Cervello M, Emma MR, Augello G, Cusimano A, Giannitrapani L, Soresi M, Akula SM, Abrams SL, Steelman LS, Gulino A, Belmonte B, Montalto G, McCubrey JA, . New landscapes and horizons in hepatocellular carcinoma therapy. . 12:3053-3094. https://doi.org/10.18632/aging.102777

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                TY  - JOUR
                AU  - Cervello, Melchiorre 
                AU  - Emma, Maria R. 
                AU  - Augello, Giuseppa 
                AU  - Cusimano, Antonella 
                AU  - Giannitrapani, Lydia 
                AU  - Soresi, Maurizio 
                AU  - Akula, Shaw M. 
                AU  - Abrams, Stephen L. 
                AU  - Steelman, Linda S. 
                AU  - Gulino, Alessandro 
                AU  - Belmonte, Beatrice 
                AU  - Montalto, Giuseppe 
                AU  - McCubrey, James A. 
                TI  - New landscapes and horizons in hepatocellular carcinoma therapy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102777
                DO  - 10.18632/aging.102777
                SP  - 3053
                EP  - 3094
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Cervello, Melchiorre 
                AU  - Emma, Maria R. 
                AU  - Augello, Giuseppa 
                AU  - Cusimano, Antonella 
                AU  - Giannitrapani, Lydia 
                AU  - Soresi, Maurizio 
                AU  - Akula, Shaw M. 
                AU  - Abrams, Stephen L. 
                AU  - Steelman, Linda S. 
                AU  - Gulino, Alessandro 
                AU  - Belmonte, Beatrice 
                AU  - Montalto, Giuseppe 
                AU  - McCubrey, James A. 
                TI  - New landscapes and horizons in hepatocellular carcinoma therapy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102777
                DO  - 10.18632/aging.102777
                SP  - 3053
                EP  - 3094
                PY  - 
                AB  - Hepatocellular carcinoma (HCC), is the sixth most frequent form of cancer and leads to the fourth highest number of deaths each year. HCC results from a combination of environmental factors and aging as there are driver mutations at oncogenes which occur during aging. Most of HCCs are diagnosed at advanced stage preventing curative therapies. Treatment in advanced stage is a challenging and pressing problem, and novel and well-tolerated therapies are urgently needed. We will discuss further advances beyond sorafenib that target additional signaling pathways and immune checkpoint proteins. The scenario of possible systemic therapies for patients with advanced HCC has changed dramatically in recent years. Personalized genomics and various other omics approaches may identify actionable biochemical targets, which are activated in individual patients, which may enhance therapeutic outcomes. Further studies are needed to identify predictive biomarkers and aberrantly activated signaling pathways capable of guiding the clinician in choosing the most appropriate therapy for the individual patient.
                ER  -

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Riluzole: a therapeutic strategy in Alzheimer’s disease by targeting the WNT/β-catenin pathway

Alexandre Vallée, Jean-Noël Vallée, Rémy Guillevin, Yves Lecarpentier,

https://doi.org/10.18632/aging.102830 pp 3095—3113

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Vallée A, Vallée J, Guillevin R, Lecarpentier Y, . Riluzole: a therapeutic strategy in Alzheimer’s disease by targeting the WNT/β-catenin pathway. . 12:3095-3113. https://doi.org/10.18632/aging.102830

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Provider: 
                TY  - JOUR
                AU  - Vallée, Alexandre 
                AU  - Vallée, Jean-Noël 
                AU  - Guillevin, Rémy 
                AU  - Lecarpentier, Yves 
                TI  - Riluzole: a therapeutic strategy in Alzheimer’s disease by targeting the WNT/β-catenin pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102830
                DO  - 10.18632/aging.102830
                SP  - 3095
                EP  - 3113
                PY  - 
                AB  - Alzheimer&#x2019;s disease (AD) is a neurodegenerative disease, where the etiology remains unclear. AD is characterized by amyloid-(A&#x3B2;) protein aggregation and neurofibrillary plaques deposits. Oxidative stress and chronic inflammation have been suggested as causes of AD. Glutamatergic pathway dysregulation is also mainly associated with AD process. In AD, the canonical WNT/&#x3B2;-catenin pathway is downregulated. Downregulation of WNT/&#x3B2;-catenin, by activation of GSK-3&#x3B2;-induced A&#x3B2;, and inactivation of PI3K/Akt pathway involve oxidative stress in AD. The downregulation of the WNT/&#x3B2;-catenin pathway decreases the activity of EAAT2, the glutamate receptors, and leads to neuronal death. In AD, oxidative stress, neuroinflammation and glutamatergic pathway operate in a vicious circle driven by the dysregulation of the WNT/&#x3B2;-catenin pathway. Riluzole is a glutamate modulator and used as treatment in amyotrophic lateral sclerosis. Recent findings have highlighted its use in AD and its potential increase power on the WNT pathway. Nevertheless, the mechanism by which Riluzole can operate in AD remains unclear and should be better determine. The focus of our review is to highlight the potential action of Riluzole in AD by targeting the canonical WNT/&#x3B2;-catenin pathway to modulate glutamatergic pathway, oxidative stress and neuroinflammation
                ER  -

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Correction for: Resveratrol alleviates chemotherapy-induced oogonial stem cell apoptosis and ovarian aging in mice

Meng Wu, Lingwei Ma, Liru Xue, Wenlei Ye, Zhiyong Lu, Xiang Li, Yan Jin, Xian Qin, Dan Chen, Weicheng Tang, Yingying Chen, Zixin Hong, Jinjin Zhang, Aiyue Luo, Shixuan Wang,

https://doi.org/10.18632/aging.102852 pp 3114—3116

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Wu M, Ma L, Xue L, Ye W, Lu Z, Li X, Jin Y, Qin X, Chen D, Tang W, Chen Y, Hong Z, Zhang J, et al, . Correction for: Resveratrol alleviates chemotherapy-induced oogonial stem cell apoptosis and ovarian aging in mice. . 12:3114-3116. https://doi.org/10.18632/aging.102852

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                TY  - JOUR
                AU  - Wu, Meng 
                AU  - Ma, Lingwei 
                AU  - Xue, Liru 
                AU  - Ye, Wenlei 
                AU  - Lu, Zhiyong 
                AU  - Li, Xiang 
                AU  - Jin, Yan 
                AU  - Qin, Xian 
                AU  - Chen, Dan 
                AU  - Tang, Weicheng 
                AU  - Chen, Yingying 
                AU  - Hong, Zixin 
                AU  - Zhang, Jinjin 
                AU  - Luo, Aiyue 
                AU  - Wang, Shixuan 
                TI  - Correction for: Resveratrol alleviates chemotherapy-induced oogonial stem cell apoptosis and ovarian aging in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102852
                DO  - 10.18632/aging.102852
                SP  - 3114
                EP  - 3116
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wu, Meng 
                AU  - Ma, Lingwei 
                AU  - Xue, Liru 
                AU  - Ye, Wenlei 
                AU  - Lu, Zhiyong 
                AU  - Li, Xiang 
                AU  - Jin, Yan 
                AU  - Qin, Xian 
                AU  - Chen, Dan 
                AU  - Tang, Weicheng 
                AU  - Chen, Yingying 
                AU  - Hong, Zixin 
                AU  - Zhang, Jinjin 
                AU  - Luo, Aiyue 
                AU  - Wang, Shixuan 
                TI  - Correction for: Resveratrol alleviates chemotherapy-induced oogonial stem cell apoptosis and ovarian aging in mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 3
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102852
                DO  - 10.18632/aging.102852
                SP  - 3114
                EP  - 3116
                PY  - 
                AB  - 
                ER  -

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Volume 12, Issue 3

About the Cover

Editorials

George M. Martin, Martin Poot, Thomas Haaf,

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Faisal J. Alibhai, Ren-Ke Li,

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Ramon Velazquez, Wendy Winslow, Marc A. Mifflin,

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Michael Simons, Pei-Yu Chen, Thomas W. Chittenden,

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Research Papers

Guoliang Wang, Yi Huang, Feilong Yang, Xiaojun Tian, Kun Wang, Li Liu, Yidong Fan, Xiaofeng Li, Luchao Li, Benkang Shi, Yichang Hao, Chuanyou Xia, Qingsheng Nie, Yue Xin, Zhenfeng Shi, Lulin Ma, Dawei Xu, Cheng Liu,

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Yukun Zhang, Changyuan Wang, Jiawei Lu, Yue Jin, Canyao Xu, Qiang Meng, Qi Liu, Deshi Dong, Xiaodong Ma, Kexin Liu, Huijun Sun,

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Jacopo Dolcini, Haotian Wu, Jamaji C. Nwanaji-Enwerem, Marianthi-Anna Kiomourtozlogu, Akin Cayir, Marco Sanchez-Guerra, Pantel Vokonas, Joel Schwarz, Andrea A. Baccarelli,

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Ping Zhang, Hengguo Zhang, Jialin Lin, Tao Xiao, Rongyao Xu, Yu Fu, Yuchao Zhang, Yifei Du, Jie Cheng, Hongbing Jiang,

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Seemaab Ali, Anthony G. Mansour, Wei Huang, Nicholas J. Queen, Xiaokui Mo, Jacqueline M. Anderson, Quais N. Hassan II, Ripal S. Patel, Ryan K. Wilkins, Michael A. Caligiuri, Lei Cao,

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Kefang Guo, Liying Xu, Lin Jin, Huilin Wang, Yun Ren, Yan Hu, Jing Yu, Jing Cang,

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Gongmin Zhu, Lijiao Pei, Yuan Li, Xin Gou,

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Bo-Ram Jin, Hyo-Jin An,

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Lin Hao, Kun Pang, Hui Pang, Junjie Zhang, Zhiguo Zhang, Houguang He, Rongsheng Zhou, Zhenduo Shi, Conghui Han,

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Yunlong Ma, Jingjing Li, Yi Xu, Yan Wang, Yinghao Yao, Qiang Liu, Maiqiu Wang, Xinyi Zhao, Rongli Fan, Jiali Chen, Bin Zhang, Zhen Cai, Haijun Han, Zhongli Yang, Wenji Yuan, Yigang Zhong, Xiangning Chen, Jennie Z. Ma, Thomas J. Payne, Yizhou Xu, Yuping Ning, Wenyan Cui, Ming D. Li,

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Yutong Li, Yongfeng Zhang, Xinrui Zhang, Wenqian Lu, Xin Liu, Min Hu, Di Wang,

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Jun Ge, Quan Zhou, Xiaoqiang Cheng, Jiale Qian, Qi Yan, Cenhao Wu, Yufeng Chen, Huilin Yang, Jun Zou,

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Dehu Chen, Qinghong Liu, Gan Cao, Wei Zhang,

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Pilar Dongil, Ana Pérez-García, Verónica Hurtado-Carneiro, Carmen Herrero-de-Dios, Elvira Álvarez, Carmen Sanz,

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Xiaoliang Hua, Juan Chen, Yang Su, Chaozhao Liang,

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