Volume 12, Issue 10

COVID-19
Metformin and SARS-CoV-2: mechanistic lessons on air pollution to weather the cytokine/thrombotic storm in COVID-19

Javier A. Menendez,

https://doi.org/10.18632/aging.103347 pp 8760—8765

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Menendez JA, . Metformin and SARS-CoV-2: mechanistic lessons on air pollution to weather the cytokine/thrombotic storm in COVID-19. . 12:8760-8765. https://doi.org/10.18632/aging.103347

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                TY  - JOUR
                AU  - Menendez, Javier A. 
                TI  - Metformin and SARS-CoV-2: mechanistic lessons on air pollution to weather the cytokine/thrombotic storm in COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103347
                DO  - 10.18632/aging.103347
                SP  - 8760
                EP  - 8765
                PY  - 
                AB  - Pathological signaling in the lung induced by particulate matter (PM) air pollution partially overlaps with that provoked by COVID-19, the pandemic disease caused by infection with the novel coronavirus SARS-CoV-2. Metformin is capable of suppressing one of the molecular triggers of the proinflammatory and prothrombotic processes of urban PM air pollution, namely the mitochondrial ROS/Ca2+ release-activated Ca2+ channels (CRAC)/IL-6 cascade. Given the linkage between mitochondrial functionality, ion channels, and inflamm-aging, the ability of metformin to target mitochondrial electron transport and prevent ROS/CRAC-mediated IL-6 release might illuminate new therapeutic avenues to quell the raging of the cytokine and thrombotic-like storms that are the leading causes of COVID-19 morbidity and mortality in older people. The incorporation of infection rates, severity and lethality of SARS-CoV-2 infections as new outcomes of metformin usage in elderly populations at risk of developing severe COVID-19, together with the assessment of bronchial/serological titers of inflammatory cytokines and D-dimers, could provide a novel mechanistic basis for the consideration of metformin as a therapeutic strategy against the inflammatory and thrombotic states underlying the gerolavic traits of SARS-CoV-2 infection.
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Muscle-dependent regulation of adipose tissue function in long-lived growth hormone-mutant mice

Xinna Li, Jacquelyn A. Frazier, Edward Spahiu, Madaline McPherson, Richard A. Miller,

https://doi.org/10.18632/aging.103380 pp 8766—8789

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Li X, Frazier JA, Spahiu E, McPherson M, Miller RA, . Muscle-dependent regulation of adipose tissue function in long-lived growth hormone-mutant mice. . 12:8766-8789. https://doi.org/10.18632/aging.103380

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                TY  - JOUR
                AU  - Li, Xinna 
                AU  - Frazier, Jacquelyn A. 
                AU  - Spahiu, Edward 
                AU  - McPherson, Madaline 
                AU  - Miller, Richard A. 
                TI  - Muscle-dependent regulation of adipose tissue function in long-lived growth hormone-mutant mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103380
                DO  - 10.18632/aging.103380
                SP  - 8766
                EP  - 8789
                PY  - 
                AB  - Altered adipose tissue may contribute to the longevity of Snell dwarf and growth hormone receptor (GHR) knock-out mice. We report here that white (WAT) and brown (BAT) fat have elevated UCP1 in both kinds of mice, and that adipocytes in WAT depots turn beige/brown. These imply increased thermogenesis and are expected to lead to improved glucose control. Both kinds of long-lived mice show lower levels of inflammatory M1 macrophages and higher levels of anti-inflammatory M2 macrophages in BAT and WAT, with correspondingly lower levels of TNF&#x3B1;, IL-6, and MCP1. Experiments with mice with tissue-specific disruption of GHR showed that these adipocyte and macrophage changes were not due to hepatic IGF1 production nor to direct GH effects on adipocytes, but instead reflect GH effects on muscle. Muscles deprived of GH signals, either globally (GKO) or in muscle only (MKO), produce higher levels of circulating irisin and its precursor FNDC5. The data thus suggest that the changes in adipose tissue differentiation and inflammatory status seen in long-lived mutant mice reflect interruption of GH-dependent irisin inhibition, with consequential effects on metabolism and thermogenesis.
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Rejuvenation of three germ layers tissues by exchanging old blood plasma with saline-albumin

Melod Mehdipour, Colin Skinner, Nathan Wong, Michael Lieb, Chao Liu, Jessy Etienne, Cameron Kato, Dobri Kiprov, Michael J. Conboy, Irina M. Conboy,

https://doi.org/10.18632/aging.103418 pp 8790—8819

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Mehdipour M, Skinner C, Wong N, Lieb M, Liu C, Etienne J, Kato C, Kiprov D, Conboy MJ, Conboy IM, . Rejuvenation of three germ layers tissues by exchanging old blood plasma with saline-albumin. . 12:8790-8819. https://doi.org/10.18632/aging.103418

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                TY  - JOUR
                AU  - Mehdipour, Melod 
                AU  - Skinner, Colin 
                AU  - Wong, Nathan 
                AU  - Lieb, Michael 
                AU  - Liu, Chao 
                AU  - Etienne, Jessy 
                AU  - Kato, Cameron 
                AU  - Kiprov, Dobri 
                AU  - Conboy, Michael J. 
                AU  - Conboy, Irina M. 
                TI  - Rejuvenation of three germ layers tissues by exchanging old blood plasma with saline-albumin
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103418
                DO  - 10.18632/aging.103418
                SP  - 8790
                EP  - 8819
                PY  - 
                AB  - Heterochronic blood sharing rejuvenates old tissues, and most of the studies on how this works focus on young plasma, its fractions, and a few youthful systemic candidates. However, it was not formally established that young blood is necessary for this multi-tissue rejuvenation. Here, using our recently developed small animal blood exchange process, we replaced half of the plasma in mice with saline containing 5% albumin (terming it a &#x201C;neutral&#x201D; age blood exchange, NBE) thus diluting the plasma factors and replenishing the albumin that would be diminished if only saline was used. Our data demonstrate that a single NBE suffices to meet or exceed the rejuvenative effects of enhancing muscle repair, reducing liver adiposity and fibrosis, and increasing hippocampal neurogenesis in old mice, all the key outcomes seen after blood heterochronicity. Comparative proteomic analysis on serum from NBE, and from a similar human clinical procedure of therapeutic plasma exchange (TPE), revealed a molecular re-setting of the systemic signaling milieu, interestingly, elevating the levels of some proteins, which broadly coordinate tissue maintenance and repair and promote immune responses. Moreover, a single TPE yielded functional blood rejuvenation, abrogating the typical old serum inhibition of progenitor cell proliferation. Ectopically added albumin does not seem to be the sole determinant of such rejuvenation, and levels of albumin do not decrease with age nor are increased by NBE/TPE. A model of action (supported by a large body of published data) is that significant dilution of autoregulatory proteins that crosstalk to multiple signaling pathways (with their own feedback loops) would, through changes in gene expression, have long-lasting molecular and functional effects that are consistent with our observations. This work improves our understanding of the systemic paradigms of multi-tissue rejuvenation and suggest a novel and immediate use of the FDA approved TPE for improving the health and resilience of older people.
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LncRNA H19 diminishes dopaminergic neuron loss by mediating microRNA-301b-3p in Parkinson’s disease via the HPRT1-mediated Wnt/β-catenin signaling pathway

Jingjing Jiang, Xuanyu Piao, Siying Hu, Jingbo Gao, Min Bao,

https://doi.org/10.18632/aging.102877 pp 8820—8836

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Jiang J, Piao X, Hu S, Gao J, Bao M, . LncRNA H19 diminishes dopaminergic neuron loss by mediating microRNA-301b-3p in Parkinson’s disease via the HPRT1-mediated Wnt/β-catenin signaling pathway. . 12:8820-8836. https://doi.org/10.18632/aging.102877

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                TY  - JOUR
                AU  - Jiang, Jingjing 
                AU  - Piao, Xuanyu 
                AU  - Hu, Siying 
                AU  - Gao, Jingbo 
                AU  - Bao, Min 
                TI  - LncRNA H19 diminishes dopaminergic neuron loss by mediating microRNA-301b-3p in Parkinson’s disease via the HPRT1-mediated Wnt/β-catenin signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102877
                DO  - 10.18632/aging.102877
                SP  - 8820
                EP  - 8836
                PY  - 
                AB  - Long non-coding RNAs (lncRNA) and microRNAs (miRNAs) are a subject of active investigation in neurodegenerative disorders including Parkinson&#x2019;s disease (PD). We hypothesized a regulatory role of lncRNA H19 with involvement of hypoxanthine phosphoribosyltransferase 1 (HPRT1) in dopaminergic neuron loss in PD model mice obtained by 6-hydroxydopamine (6-OHDA) lesions. We predicted the differentially expressed genes and related mechanisms by microarray analysis. We measured the expression of tyrosine hydroxylase (TH) and proneural genes in the substantia nigra of lesioned mice before and after treatment with lentiviral oe-HPRT1, agomir-miR-301b-3p and inhibition of the Wnt/&#x3B2;-catenin pathway. We also evaluated the relationship among lncRNA H19, HPRT1 and miR-301b-3p as well as the Wnt/&#x3B2;-catenin signaling pathway in these mice. The obtained results predicted and further confirmed a low level of HPRT1 in lesioned mice. We found low expression of lncRNA H19 and showed that its forced overexpression regulated HPRT1 by binding to miR-301b-3p. The overexpression of HPRT1 increased TH expression and inhibited dopaminergic neuron loss via activating the Wnt/&#x3B2;-catenin pathway, as reflected by increased expressions of Nurr-1, Pitx-3, Ngn-2 and NeuroD1. Thus, overexpressed lncRNA H19 protects against dopaminergic neuron loss in this PD model through activating the Wnt/&#x3B2;-catenin pathway via impairing miR-301b-3p-targeted inhibition of HPRT1 expression.
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The TβR II-targeted aptamer S58 prevents fibrosis after glaucoma filtration surgery

Xueru Li, Yu Leng, Xiangji Li, Yawei Wang, Peng Luo, Chi Zhang, Ziwen Wang, Xiaofeng Yue, Chongxing Shen, Long Chen, Zujuan Liu, Chunmeng Shi, Lin Xie,

https://doi.org/10.18632/aging.102997 pp 8837—8857

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Li X, Leng Y, Li X, Wang Y, Luo P, Zhang C, Wang Z, Yue X, Shen C, Chen L, Liu Z, Shi C, Xie L, . The TβR II-targeted aptamer S58 prevents fibrosis after glaucoma filtration surgery. . 12:8837-8857. https://doi.org/10.18632/aging.102997

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                TY  - JOUR
                AU  - Li, Xueru 
                AU  - Leng, Yu 
                AU  - Li, Xiangji 
                AU  - Wang, Yawei 
                AU  - Luo, Peng 
                AU  - Zhang, Chi 
                AU  - Wang, Ziwen 
                AU  - Yue, Xiaofeng 
                AU  - Shen, Chongxing 
                AU  - Chen, Long 
                AU  - Liu, Zujuan 
                AU  - Shi, Chunmeng 
                AU  - Xie, Lin 
                TI  - The TβR II-targeted aptamer S58 prevents fibrosis after glaucoma filtration surgery
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102997
                DO  - 10.18632/aging.102997
                SP  - 8837
                EP  - 8857
                PY  - 
                AB  - Glaucoma filtration surgery (GFS) is an effective clinical treatment for glaucoma when intraocular pressure (IOP) control is poor. However, the occurrence of conjunctival scarring at the surgical site is the main reason for failure of the surgery. In a previous study, we isolated and developed S58, a novel nucleic acid aptamer targeting T&#x3B2;R II, by systematic evolution of ligands by exponential enrichment (SELEX). Here, we show how S58 sterically inhibits the T&#x3B2;R II interaction with TGF-&#x3B2;. The effects of topical S58 treatment were studied in a rabbit model of GFS. At 6 postoperative weeks, S58 reduced fibrosis and prolonged bleb survival in rabbits after GFS. Further in vitro tests showed that the levels of fibrosis in S58 treated-Human Conjunctival Fibroblasts (HConFs) were decreased and that antioxidant defense was increased. In addition, the loss of nuclear factor erythroid 2-related factor 2 (Nrf2) or the inhibition of phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) reversed the anti-fibrotic effects of S58. The present work suggests that S58 could effectively improve GFS surgical outcomes by activating the intracellular antioxidant defense PI3K/Akt/Nrf2 signaling pathway.
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GSG2 (Haspin) promotes development and progression of bladder cancer through targeting KIF15 (Kinase-12)

Yuhao Chen, Dian Fu, Hai Zhao, Wen Cheng, Feng Xu,

https://doi.org/10.18632/aging.103005 pp 8858—8879

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Chen Y, Fu D, Zhao H, Cheng W, Xu F, . GSG2 (Haspin) promotes development and progression of bladder cancer through targeting KIF15 (Kinase-12). . 12:8858-8879. https://doi.org/10.18632/aging.103005

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                TY  - JOUR
                AU  - Chen, Yuhao 
                AU  - Fu, Dian 
                AU  - Zhao, Hai 
                AU  - Cheng, Wen 
                AU  - Xu, Feng 
                TI  - GSG2 (Haspin) promotes development and progression of bladder cancer through targeting KIF15 (Kinase-12)
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103005
                DO  - 10.18632/aging.103005
                SP  - 8858
                EP  - 8879
                PY  - 
                AB  - Bladder cancer is the most commonly diagnosed malignant tumor in urological system worldwide. The relationship between GSG2 and bladder cancer has not been demonstrated and remains unclear. In this study, it was demonstrated that GSG2 was up-regulated in bladder cancer tissues compared with the normal tissues and its high expression was correlated with more advanced malignant grade and lower survival rate. Further investigations indicated that the overexpression/knockdown of GSG2 could promote/inhibit proliferation, colony formation and migration of bladder cancer cells, while inhibiting/promoting cell apoptosis. Moreover, knockdown of GSG2 could also suppress tumorigenicity of bladder cancer cells in vivo. RNA-sequencing followed by Ingenuity pathway analysis (IPA) was performed for exploring downstream of GSG2 and identified KIF15 as the potential target. Furthermore, our study revealed that knockdown of KIF15 could inhibit development of bladder cancer in vitro, and alleviate the GSG2 overexpression induced promotion of bladder cancer. In conclusion, our study showed, as the first time, GSG2 as a prognostic indicator and tumor promotor for bladder cancer, whose function was carried out probably through the regulation of KIF15.
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lncRNA OGFRP1 functions as a ceRNA to promote the progression of prostate cancer by regulating SARM1 level via miR-124-3p

Keqiang Yan, Lifang Hou, Tiantian Liu, Wei Jiao, Qian Ma, Zhiqing Fang, Shimin Zhang, Daoqing Song, Jikai Liu, Xinghua Gao, Yidong Fan,

https://doi.org/10.18632/aging.103007 pp 8880—8892

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Yan K, Hou L, Liu T, Jiao W, Ma Q, Fang Z, Zhang S, Song D, Liu J, Gao X, Fan Y, . lncRNA OGFRP1 functions as a ceRNA to promote the progression of prostate cancer by regulating SARM1 level via miR-124-3p. . 12:8880-8892. https://doi.org/10.18632/aging.103007

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                TY  - JOUR
                AU  - Yan, Keqiang 
                AU  - Hou, Lifang 
                AU  - Liu, Tiantian 
                AU  - Jiao, Wei 
                AU  - Ma, Qian 
                AU  - Fang, Zhiqing 
                AU  - Zhang, Shimin 
                AU  - Song, Daoqing 
                AU  - Liu, Jikai 
                AU  - Gao, Xinghua 
                AU  - Fan, Yidong 
                TI  - lncRNA OGFRP1 functions as a ceRNA to promote the progression of prostate cancer by regulating SARM1 level via miR-124-3p
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103007
                DO  - 10.18632/aging.103007
                SP  - 8880
                EP  - 8892
                PY  - 
                AB  - lncRNA can interact with miRNA as a ceRNA to participate in the regulation of target gene expression, thus playing an important role in the development of malignant tumors. In this research, we found that OGFRP1 was up-regulated in prostate cancer (PCa) clinical samples and cell lines. Additionally, OGFRP1 is significantly associated with TNM stages III and IV and perineural invasion. Knockdown of OGFRP1 inhibited the growth of PCa cells, suggesting a promotional effect of OGFRP1 in tumor progression. Interestingly, OGFRP1 primarily localized in the cytoplasm, while miR-124-3p was found to bind to OGFRP1. Therefore, we further analyzed the downstream target of miR-124-3p using TargetScan. The result of the luciferase reporter gene assay displayed that SARM1 was a downstream target of miR-124-3p in two PCa cell lines. The overexpression of SARM1 promoted growth and metastasis in PCa cells. Knockdown of OGFRP1 and overexpression of miR-124-3p markedly restored the promotion of SARM1 to PCa cells. In conclusion, lncRNA OGFRP1 completely bound to miR-124-3p and relieved their inhibition on SARM1, thus promoting the growth of PCa cells. This report extended our understanding of the underlying molecular mechanisms of lncRNAs in PCa, which could help us find novel diagnostic and therapeutic targets.
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Long noncoding RNA lnc-LOC645166 promotes adriamycin resistance via NF-κB/GATA3 axis in breast cancer

Ruinian Zheng, Jun Jia, Ling Guan, Huiling Yuan, Kejun Liu, Chun Liu, Weibiao Ye, Yuting Liao, Shunhuan Lin, Ou Huang,

https://doi.org/10.18632/aging.103012 pp 8893—8912

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Zheng R, Jia J, Guan L, Yuan H, Liu K, Liu C, Ye W, Liao Y, Lin S, Huang O, . Long noncoding RNA lnc-LOC645166 promotes adriamycin resistance via NF-κB/GATA3 axis in breast cancer. . 12:8893-8912. https://doi.org/10.18632/aging.103012

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                TY  - JOUR
                AU  - Zheng, Ruinian 
                AU  - Jia, Jun 
                AU  - Guan, Ling 
                AU  - Yuan, Huiling 
                AU  - Liu, Kejun 
                AU  - Liu, Chun 
                AU  - Ye, Weibiao 
                AU  - Liao, Yuting 
                AU  - Lin, Shunhuan 
                AU  - Huang, Ou 
                TI  - Long noncoding RNA lnc-LOC645166 promotes adriamycin resistance via NF-κB/GATA3 axis in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103012
                DO  - 10.18632/aging.103012
                SP  - 8893
                EP  - 8912
                PY  - 
                AB  - Chemoresistance remains a significant obstacle for effective adriamycin (ADR) treatment in breast cancer. Recent efforts have revealed that long noncoding RNAs (lncRNAs) play a crucial role in cancer biology, including chemoresistance. We identified the lncRNA LOC645166 was upregulated in adriamycin resistant-breast cancer cells by Microarray analysis, which was further confirmed in the tissues of nonresponsive patients by reverse transcription-quantitative polymerase chain reaction (RT&#x2013;qPCR), western blotting, and immunohistochemical assays. Downregulation of lncRNA LOC645166 increased cell sensitivity to adriamycin both in vitro and in vivo. In contrast, upregulation of lncRNA LOC645166 strengthened the tolerance of breast cancer cells to adriamycin. Chromatin immunoprecipitation (ChIP) and RNA binding protein immunoprecipitation (RIP) demonstrated that lncRNA LOC645166 could increase the expression of GATA binding protein 3 (GATA3) via binding with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-&#x3BA;B), leading to the activation of STAT3 and promoting chemoresistance in breast cancer. Together, the present study suggested that lncRNA LOC645166 mediated adriamycin chemoresistance in breast cancer by regulating GATA3 via NF-&#x3BA;B.
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HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089

Xiaofeng Shi, Shuang Pan, Li Li, Yongqi Li, Wei Ma, Han Wang, Caiming Xu, Lei Li, Dong Wang,

https://doi.org/10.18632/aging.103079 pp 8913—8922

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Shi X, Pan S, Li L, Li Y, Ma W, Wang H, Xu C, Li L, Wang D, . HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089. . 12:8913-8922. https://doi.org/10.18632/aging.103079

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                TY  - JOUR
                AU  - Shi, Xiaofeng 
                AU  - Pan, Shuang 
                AU  - Li, Li 
                AU  - Li, Yongqi 
                AU  - Ma, Wei 
                AU  - Wang, Han 
                AU  - Xu, Caiming 
                AU  - Li, Lei 
                AU  - Wang, Dong 
                TI  - HIX003209 promotes vascular smooth muscle cell migration and proliferation through modulating miR-6089
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103079
                DO  - 10.18632/aging.103079
                SP  - 8913
                EP  - 8922
                PY  - 
                AB  - Accumulating references have showed that long noncoding RNAs (lncRNAs) act important roles in the development of human diseases. The role and expression of HIX003209 remains unclear in the pathogenesis of atherosclerosis. We showed that HIX003209 expression was upregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. HIX003209 was overexpressed in vascular smooth muscle cells (VSMCs) induced by inflammatory mediators including tumor necrosis factor-&#x3B1;(TNF-&#x3B1;), ox-LDL and latelet-derived growth factor-BB (PDGF-BB). Ectopic expression of HIX003209 enhanced cell growth and migration and induced inflammatory mediators secretion such as interleukin 6 (IL-6), TNF-&#x3B1; and IL-1&#x3B2; in VSMCs. Furthermore, we showed that miR-6089 was downregulated in atherosclerotic coronary tissues compared to normal coronary artery samples. There was a negative association between expression of HIX003209 and miR-6089 in atherosclerotic coronary tissues. MiR-6089 expression was decreased in VSMCs induced by inflammatory mediators including TNF-&#x3B1;, ox-LDL and PDGF-BB. Dual luciferase analysis showed that miR-6089 overexpression decreased luciferase activity of HIX003209 WT-type 3&#x2019;-UTR but not the mut-type 3&#x2019;-UTR. Overexpression of HIX003209 suppressed the expression of miR-6089 in VSMCs. Ectopic expression of HIX003209 induced cell growth, migration and the secretion of inflammatory mediators via regulating miR-6089 expression. These data suggested that HIX003209 promoted VSMCs proliferation, migration and the secretion of inflammatory mediators partly via regulating miR-6089.
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Influence of human amylin on the membrane stability of rat primary hippocampal neurons

Nan Zhang, Yuan Xing, Yongzhou Yu, Chao Liu, Baohua Jin, Lifang Huo, Dezhi Kong, Zuxiao Yang, Xiangjian Zhang, Ruimao Zheng, Zhanfeng Jia, Lin Kang, Wei Zhang,

https://doi.org/10.18632/aging.103105 pp 8923—8938

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Zhang N, Xing Y, Yu Y, Liu C, Jin B, Huo L, Kong D, Yang Z, Zhang X, Zheng R, Jia Z, Kang L, Zhang W, . Influence of human amylin on the membrane stability of rat primary hippocampal neurons. . 12:8923-8938. https://doi.org/10.18632/aging.103105

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                TY  - JOUR
                AU  - Zhang, Nan 
                AU  - Xing, Yuan 
                AU  - Yu, Yongzhou 
                AU  - Liu, Chao 
                AU  - Jin, Baohua 
                AU  - Huo, Lifang 
                AU  - Kong, Dezhi 
                AU  - Yang, Zuxiao 
                AU  - Zhang, Xiangjian 
                AU  - Zheng, Ruimao 
                AU  - Jia, Zhanfeng 
                AU  - Kang, Lin 
                AU  - Zhang, Wei 
                TI  - Influence of human amylin on the membrane stability of rat primary hippocampal neurons
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103105
                DO  - 10.18632/aging.103105
                SP  - 8923
                EP  - 8938
                PY  - 
                AB  - The two most common aging-related diseases, Alzheimer&#x2019;s disease and type 2 diabetes mellitus, are associated with accumulation of amyloid proteins (&#x3B2;-amyloid and amylin, respectively). This amylin aggregation is reportedly cytotoxic to neurons. We found that aggregation of human amylin (hAmylin) induced neuronal apoptosis without obvious microglial infiltration in vivo. High concentrations of hAmylin irreversibly aggregated on the surface of the neuronal plasma membrane. Long-term incubation with hAmylin induced morphological changes in neurons. Moreover, hAmylin permeabilized the neuronal membrane within 1 min in a manner similar to Triton X-100, allowing impermeable fluorescent antibodies to enter the neurons and stain intracellular antigens. hAmylin also permeabilized the cell membrane of astrocytes, though more slowly. Under scanning electron microscopy, we observed that hAmylin destroyed the integrity of the cell membranes of both neurons and astrocytes. Additionally, it increased intracellular reactive oxygen species generation and reduced the mitochondrial membrane potential. Thus, by aggregating on the surface of neurons, hAmylin impaired the cell membrane integrity, induced reactive oxygen species production, reduced the mitochondrial membrane potential, and ultimately induced neuronal apoptosis.
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miR-378a-3p inhibits ischemia/reperfusion-induced apoptosis in H9C2 cardiomyocytes by targeting TRIM55 via the DUSP1-JNK1/2 signaling pathway

Jiaying Tan, Jun Shen, Huigeng Zhu, Ye Gong, Hechen Zhu, Junping Li, Shan Lin, Gang Wu, Tao Sun,

https://doi.org/10.18632/aging.103106 pp 8939—8952

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Tan J, Shen J, Zhu H, Gong Y, Zhu H, Li J, Lin S, Wu G, Sun T, . miR-378a-3p inhibits ischemia/reperfusion-induced apoptosis in H9C2 cardiomyocytes by targeting TRIM55 via the DUSP1-JNK1/2 signaling pathway. . 12:8939-8952. https://doi.org/10.18632/aging.103106

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                TY  - JOUR
                AU  - Tan, Jiaying 
                AU  - Shen, Jun 
                AU  - Zhu, Huigeng 
                AU  - Gong, Ye 
                AU  - Zhu, Hechen 
                AU  - Li, Junping 
                AU  - Lin, Shan 
                AU  - Wu, Gang 
                AU  - Sun, Tao 
                TI  - miR-378a-3p inhibits ischemia/reperfusion-induced apoptosis in H9C2 cardiomyocytes by targeting TRIM55 via the DUSP1-JNK1/2 signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103106
                DO  - 10.18632/aging.103106
                SP  - 8939
                EP  - 8952
                PY  - 
                AB  - MicroRNAs (miRNAs) are involved in many pathological and biological processes, such as ischemia/reperfusion (I/R) injury by modulating gene expression. Increasing evidence indicates that miR-378a-3p might provide a potential cardioprotective effect against ischemic heart disease. Cell apoptosis is a crucial mechanism in I/R injury. As such, this study evaluated the protective effects and underlying mechanisms of action of miR-378a-3p on H9C2 cardiomyocyte apoptosis following I/R injury. We found that I/R-induced H9C2 cardiomyocytes exhibited a decrease in miR-378a-3p expression, while treatment with a miR-378a-3p mimic suppressed cell apoptosis, JNK1/2 activation, cleavage of PARP and caspase-3, and Bax/Bcl-2 ratio but increased DUSP1 expression, which subsequently inhibited JNK1/2 phosphorylation. TRIM55 was shown to be a target of miR-378a-3p and its downregulation inhibited the miR-378a-3p inhibitor-induced increase in cell apoptosis and JNK1/2 activation. TRIM55 inhibited DUSP1 protein expression through ubiquitination of DUSP1. Moreover, DUSP1 overexpression inhibited the TRIM55 overexpression-induced increase in cell apoptosis and JNK1/2 activation. The protective effect of miR-378a-3p was subsequently confirmed in a rat myocardial I/R model, as evidenced by a decrease in cardiomyocyte apoptosis of cardiomyocytes, TRIM55 expression, and JNK1/2 activation. Taken together, these results suggest that miR-378a-3p may protect against I/R-induced cardiomyocyte apoptosis via TRIM55/DUSP1/JNK signaling.
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Valproic acid-labeled chitosan nanoparticles promote recovery of neuronal injury after spinal cord injury

Dimin Wang, Kai Wang, Zhenlei Liu, Zonglin Wang, Hao Wu,

https://doi.org/10.18632/aging.103125 pp 8953—8967

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Wang D, Wang K, Liu Z, Wang Z, Wu H, . Valproic acid-labeled chitosan nanoparticles promote recovery of neuronal injury after spinal cord injury. . 12:8953-8967. https://doi.org/10.18632/aging.103125

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                TY  - JOUR
                AU  - Wang, Dimin 
                AU  - Wang, Kai 
                AU  - Liu, Zhenlei 
                AU  - Wang, Zonglin 
                AU  - Wu, Hao 
                TI  - Valproic acid-labeled chitosan nanoparticles promote recovery of neuronal injury after spinal cord injury
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103125
                DO  - 10.18632/aging.103125
                SP  - 8953
                EP  - 8967
                PY  - 
                AB  - Chitosan nanoparticles have been recognized as a new type of biomaterials for treatment of spinal cord injury (SCI). To develop a novel treatment method targeted delivery injured spinal cord, valproic acid labeled chitosan nanoparticles (VA-CN) were constructed and evaluated in the treatment of SCI. Our results demonstrated that administration of VA-CN significantly promoted the recovery of the function and tissue repair after SCI. Moreover, we found treatment of VA-CN inhibited the reactive astrocytes after SCI. Furthermore, administration of VA-CN enhanced immunoreactions of neuronal related marker NF160, which suggested that VA-CN could promote the neuroprotective function in rats of SCI. The production of IL-1&#x3B2;, IL-6 and TNF-&#x3B1; were significantly decreased following treatment of VA-CN. Meanwhile, administration of VA-CN effectively improved the blood spinal cord barrier (BSCB) disruption after SCI. Administration of VA-CN could enhance the recovery of neuronal injury, suppress the reactive astrocytes and inflammation, and improve the blood spinal cord barrier disruption after SCI in rats. These results provided a novel and promising therapeutic manner for SCI.
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Inhibition of circulating exosomal microRNA-15a-3p accelerates diabetic wound repair

Yuan Xiong, Lang Chen, Tao Yu, Chenchen Yan, Wu Zhou, Faqi Cao, Xiaomeng You, Yingqi Zhang, Yun Sun, Jing Liu, Hang Xue, Yiqiang Hu, Dong Chen, Bobin Mi, Guohui Liu,

https://doi.org/10.18632/aging.103143 pp 8968—8986

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Xiong Y, Chen L, Yu T, Yan C, Zhou W, Cao F, You X, Zhang Y, Sun Y, Liu J, Xue H, Hu Y, Chen D, et al, . Inhibition of circulating exosomal microRNA-15a-3p accelerates diabetic wound repair. . 12:8968-8986. https://doi.org/10.18632/aging.103143

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                TY  - JOUR
                AU  - Xiong, Yuan 
                AU  - Chen, Lang 
                AU  - Yu, Tao 
                AU  - Yan, Chenchen 
                AU  - Zhou, Wu 
                AU  - Cao, Faqi 
                AU  - You, Xiaomeng 
                AU  - Zhang, Yingqi 
                AU  - Sun, Yun 
                AU  - Liu, Jing 
                AU  - Xue, Hang 
                AU  - Hu, Yiqiang 
                AU  - Chen, Dong 
                AU  - Mi, Bobin 
                AU  - Liu, Guohui 
                TI  - Inhibition of circulating exosomal microRNA-15a-3p accelerates diabetic wound repair
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103143
                DO  - 10.18632/aging.103143
                SP  - 8968
                EP  - 8986
                PY  - 
                AB  - Diabetic foot ulcers are a common complication of diabetes, and are usually incurable in the clinic. Exosomes (carriers that transfer endogenous molecules) from diabetic patients&#x2019; blood have been demonstrated to suppress diabetic wound repair. In this study, we investigated the effects of circulating exosomal microRNA-15a-3p (miR-15a-3p) on diabetic wound repair. Exosomes were extracted from diabetic patients&#x2019; blood, and were found to inhibit diabetic wound repair in vitro and in vivo. miR-15a-3p was upregulated in diabetic exosomes, and impaired wound healing. When miR-15a-3p was knocked down in diabetic exosomes, their negative effects were partially reversed both in vitro and in vivo. NADPH oxidase 5 (NOX5) was identified as a potential target of miR-15a-3p, and the inhibition of NOX5 reduced the release of reactive oxygen species, thereby impairing the functionality of human umbilical vein endothelial cells. In summary, inhibition of circulating exosomal miR-15a-3p accelerated diabetic wound repair by activating NOX5, providing a novel therapeutic target for diabetic foot ulcer therapy.
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in vivo cellular evidence of autophagic associated spermiophagy within the principal cells during sperm storage in epididymis of the turtle

Imran Tarique, Yonghong Shi, Noor Samad Gandahi, Baitao Ding, Ping Yang, Chang Chen, Waseem Ali Vistro, Quisheng Chen,

https://doi.org/10.18632/aging.103144 pp 8987—8999

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Tarique I, Shi Y, Gandahi NS, Ding B, Yang P, Chen C, Vistro WA, Chen Q, . in vivo cellular evidence of autophagic associated spermiophagy within the principal cells during sperm storage in epididymis of the turtle. . 12:8987-8999. https://doi.org/10.18632/aging.103144

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Provider: 
 TY - JOUR
 AU - Tarique, Imran 
 AU - Shi, Yonghong 
 AU - Gandahi, Noor Samad 
 AU - Ding, Baitao 
 AU - Yang, Ping 
 AU - Chen, Chang 
 AU - Vistro, Waseem Ali 
 AU - Chen, Quisheng 
 TI - in vivo cellular evidence of autophagic associated spermiophagy within the principal cells during sperm storage in epididymis of the turtle
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103144
 DO - 10.18632/aging.103144
 SP - 8987
 EP - 8999
 PY - 
 AB - The epididymis plays a significant role as a quality control organ for long-term sperm storage, maturation, and fertilizing ability and perform filtration function to eliminate abnormal or residual spermatozoa by phagocytosis. However, the role of autophagy in spermiophagy during sperm storage in turtle epididymis still needs to be studied. In this study, we reported in vivo spermiophagy via the cellular evidence of lysosome engulfment and autophagy within the principal cells during sperm storage in the turtle epididymis. Using immunofluorescence, Lysosome associated membrane protein-1 (LAMP1) and microtubule-associate protein light chain 3 (LC3) showed strong immunosignals within the apical cytoplasm of epididymal epithelia during hibernation than non-hibernation. Co-immunolabeling of LAMP1 and LC3 was strong around the phagocytosed spermatozoa in the epididymal epithelia and protein signaling of LAMP1 and LC3 was confirmed by western blotting. During hibernation, ultrastructure showed epididymal principal cells were involved in spermiophagy and characterized by the membrane&#x2019;s concentric layers around phagocytosed segments of spermatozoa, degenerative changes in the sperm head and lysosome direct attachment, and with the existence of cellular components related to autophagy (autophagosome, autolysosome). In conclusion, spermiophagy occurs by lysosomal engulfment and autophagic activity within the principal cells of the turtle epididymis during sperm storage.
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The role of SIRT1 in BMP2-induced chondrogenic differentiation and cartilage maintenance under oxidative stress

Yang Lu, Li Zhou, Lijun Wang, Shan He, Honglei Ren, Nian Zhou, Zhenming Hu,

https://doi.org/10.18632/aging.103161 pp 9000—9013

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Lu Y, Zhou L, Wang L, He S, Ren H, Zhou N, Hu Z, . The role of SIRT1 in BMP2-induced chondrogenic differentiation and cartilage maintenance under oxidative stress. . 12:9000-9013. https://doi.org/10.18632/aging.103161

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                TY  - JOUR
                AU  - Lu, Yang 
                AU  - Zhou, Li 
                AU  - Wang, Lijun 
                AU  - He, Shan 
                AU  - Ren, Honglei 
                AU  - Zhou, Nian 
                AU  - Hu, Zhenming 
                TI  - The role of SIRT1 in BMP2-induced chondrogenic differentiation and cartilage maintenance under oxidative stress
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103161
                DO  - 10.18632/aging.103161
                SP  - 9000
                EP  - 9013
                PY  - 
                AB  - Articular cartilage defects are common in the clinic but difficult to treat. Exploring the chondrogenic molecular mechanisms of mesenchymal stem cells (MSCs) is of great theoretical interest and industrial significance. Bone morphogenetic protein 2 (BMP2) is a key factor that induces cartilage differentiation and can induce stem cell chondrogenic differentiation. However, the oxidative stress in the microenvironment during cartilage injury and degeneration inhibits cartilage regeneration and homeostasis. Silent mating type information regulator 2 homolog-1 (SIRT1) is an important histone deacetylase that regulates proliferation, differentiation, aging, and inflammation processes; moreover, it is an essential factor for chondrogenesis. The specific mechanism of SIRT1 in cartilage differentiation and homeostasis is still unclear. First, we investigated whether SIRT1 could coordinate BMP2-induced chondrogenic differentiation. Second, we investigated the protective effect of SIRT1 on BMP2-induced MSCs under oxidative stress. The results showed that SIRT1 could promote BMP2-induced chondrogenic differentiation of MSCs, and reduce the apoptosis and decomposition of extracellular matrix under oxidative stress. In summary, these results suggested that SIRT1 plays an important coordination role in BMP2-induced chondrogenic differentiation of stem cells and cartilage maintenance under oxidative stress, establishing the experimental basis for exploring the use of SIRT1 in cartilage defect repair.
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miR-125a-5p inhibits glycolysis by targeting hexokinase-II to improve pulmonary arterial hypertension

Li Luo, Lusheng Xiao, Guili Lian, Huajun Wang, Liangdi Xie,

https://doi.org/10.18632/aging.103163 pp 9014—9030

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Luo L, Xiao L, Lian G, Wang H, Xie L, . miR-125a-5p inhibits glycolysis by targeting hexokinase-II to improve pulmonary arterial hypertension. . 12:9014-9030. https://doi.org/10.18632/aging.103163

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                TY  - JOUR
                AU  - Luo, Li 
                AU  - Xiao, Lusheng 
                AU  - Lian, Guili 
                AU  - Wang, Huajun 
                AU  - Xie, Liangdi 
                TI  - miR-125a-5p inhibits glycolysis by targeting hexokinase-II to improve pulmonary arterial hypertension
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103163
                DO  - 10.18632/aging.103163
                SP  - 9014
                EP  - 9030
                PY  - 
                AB  - Purpose: The aim of this study was to investigate the effect of microRNAs on the proliferation of pulmonary arterial smooth muscle cells (PASMCs) as a result of targeting hexokinase-II (HK-II) and its mechanism of action.Results: Differences in metabolic patterns were found between the normal group and monocrotaline-induced pulmonary arterial hypertension (MCT-PH) group. miR-125a-5p decreased glycolysis levels of monocrotaline (MCT)-induced PASMCs by targeting HK-II and inhibiting its proliferation. In vivo experiments found that miR-125a-5p agomir upregulated HK-II expression in the MCT-PH. Right ventricular hypertrophy was reversed and cardiac function improved as a result of decreased mean pulmonary artery pressure (mPAP).Conclusion: In vitro and in vivo experiments both confirmed that miR-125a-5p could inhibit cell glycolysis and PASMC proliferation to improve PAH by targeting HK-II.Methods: HK-II overexpression was constructed, and differentially expressed microRNAs were screened for using microarrays. Serum metabolites were detected using Nuclear Magnetic Resonance (NMR). Through screening for characteristic metabolites in rat body fluids and by analyzing biological functions, disordered metabolic pathways were identified. Activity of the miR-125a-5p target HK-II was measured using a luciferase reporter assay. Expression of downstream molecules was measured by RT&#x2013;qPCR and/or western blot. Glucose consumption and lactic acid production were analyzed and used as a reflection of glycolysis.
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Role of Citicoline in an in vitro AMD model

Sonali Nashine, M. Cristina Kenney,

https://doi.org/10.18632/aging.103164 pp 9031—9040

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Nashine S, Kenney MC, . Role of Citicoline in an in vitro AMD model. . 12:9031-9040. https://doi.org/10.18632/aging.103164

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 TY - JOUR
 AU - Nashine, Sonali 
 AU - Kenney, M. Cristina 
 TI - Role of Citicoline in an in vitro AMD model
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103164
 DO - 10.18632/aging.103164
 SP - 9031
 EP - 9040
 PY - 
 AB - Citicoline is the exogenous form of the nootropic, Cytidine 5&apos;-diphosphate-choline that exerts its neuroprotective effects in the brain as well as in the eye. The current study characterized the cytoprotective effects of purified Citicoline in transmitochondrial AMD (Age-related Macular Degeneration) RPE cybrid cells which carry diseased mitochondria from clinically characterized AMD patients. The effects of Citicoline were examined via flow cytometry analysis of AnnexinV/ PI-stained cells, IncuCyte live-cell imaging analysis to quantify cells undergoing caspase-3/7-mediated apoptosis, analyses of gene expression profiles of apoptosis, hypoxia, and angiogenesis markers, and measurement of ROS levels and cell viability. Our results demonstrated that Citicoline when added exogenously alleviates apoptotic effects as evidenced by diminished AnnexinV/PI and Caspase-3/7 staining, downregulation of apoptosis genes, enhanced cell viability, and reduced oxidative stress in AMD RPE cybrid cells. In conclusion, our study identified Citicoline as a protector in AMD RPE cybrid cells in vitro. However, further studies are required to establish the merit of Citicoline as a cytoprotective molecule in AMD and to decipher the molecular underpinnings of its mechanism of action in AMD.
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Sigma-1 receptor is involved in diminished ovarian reserve possibly by influencing endoplasmic reticulum stress-mediated granulosa cells apoptosis

Lile Jiang, Jinquan Cui, Cuilian Zhang, Juanke Xie, Shaodi Zhang, Dongjun Fu, Wei Duo,

https://doi.org/10.18632/aging.103166 pp 9041—9065

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Jiang L, Cui J, Zhang C, Xie J, Zhang S, Fu D, Duo W, . Sigma-1 receptor is involved in diminished ovarian reserve possibly by influencing endoplasmic reticulum stress-mediated granulosa cells apoptosis. . 12:9041-9065. https://doi.org/10.18632/aging.103166

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                TY  - JOUR
                AU  - Jiang, Lile 
                AU  - Cui, Jinquan 
                AU  - Zhang, Cuilian 
                AU  - Xie, Juanke 
                AU  - Zhang, Shaodi 
                AU  - Fu, Dongjun 
                AU  - Duo, Wei 
                TI  - Sigma-1 receptor is involved in diminished ovarian reserve possibly by influencing endoplasmic reticulum stress-mediated granulosa cells apoptosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103166
                DO  - 10.18632/aging.103166
                SP  - 9041
                EP  - 9065
                PY  - 
                AB  - Sigma non-opioid intracellular receptor 1 (sigma-1 receptor), a non-opioid transmembrane protein, is located on cellular mitochondrial membranes and endoplasmic reticulum. Current research has demonstrated that sigma-1 receptor is related to human degenerative diseases. This study is focused on the effects of sigma-1 receptor on the pathophysiological process of diminished ovarian reserve (DOR) and granulosa cells (GCs) apoptosis. Sigma-1 receptor concentration in follicular fluid (FF) and serum were negatively correlated with basal follicle-stimulating hormone (FSH) and positively correlated with anti-mullerian hormone (AMH), antral follicle count (AFC). Sigma-1 receptor reduction in GCs was accompanied by endoplasmic reticulum stress (ERS)-mediated apoptosis in women with DOR. Plasmid transfection was used to establish SIGMAR1-overexpressed and SIGMAR1-knockdown human granulosa-like tumor (KGN) cell and thapsigargin (TG) was used to induce ERS KGN cells. We found that KGN cells treated with endogenous sigma-1 receptor ligand dehydroepiandrosterone (DHEA) and sigma-1 receptor agonist PRE-084 showed similar biological effects to SIGMAR1-overexpressed KGN cells and opposite effects to SIGMAR1-knockdown KGN cells. DHEA may improve DOR patients&apos; pregnancy outcomes by upregulating sigma-1 receptor and downregulating ERS-mediated apoptotic genes in GCs. Thus, sigma-1 receptor may be a potential ovarian reserve biomarker, and ligand-mediated sigma-1 receptor activation could be a future approach for DOR therapy.
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Overexpression of miR-142-5p inhibits the progression of nonalcoholic steatohepatitis by targeting TSLP and inhibiting JAK-STAT signaling pathway

Chao Zhou, Pu Wang, Lei Lei, Yi Huang, Yue Wu,

https://doi.org/10.18632/aging.103172 pp 9066—9084

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Zhou C, Wang P, Lei L, Huang Y, Wu Y, . Overexpression of miR-142-5p inhibits the progression of nonalcoholic steatohepatitis by targeting TSLP and inhibiting JAK-STAT signaling pathway. . 12:9066-9084. https://doi.org/10.18632/aging.103172

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                TY  - JOUR
                AU  - Zhou, Chao 
                AU  - Wang, Pu 
                AU  - Lei, Lei 
                AU  - Huang, Yi 
                AU  - Wu, Yue 
                TI  - Overexpression of miR-142-5p inhibits the progression of nonalcoholic steatohepatitis by targeting TSLP and inhibiting JAK-STAT signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103172
                DO  - 10.18632/aging.103172
                SP  - 9066
                EP  - 9084
                PY  - 
                AB  - This study aimed to figure out the underlying mechanism of miR-142-5p in the non-alcoholic steatohepatitis (NASH). Bioinformatics, luciferase assay and Western blot were performed. The NASH mouse model was established through feeding a high fat diet (HFD). Relative expressions of miR-142-5p, thymic stromal lymphopoietin (TSLP), inflammatory factors were detected by qRT-PCR. The injury level of liver was assessed via measurement of serum alanine aminotransferase (ALT) and serum aspartate aminotransferase (AST). H&amp;E staining and Masson&#x2019;s trichrome staining examine the liver fatty degeneration and fibrosis. MiR-142-5p and TSLP were differentially expressed and JAK-STAT signaling pathway was activated in the NASH group. Luciferase assay identified that TSLP was the downstream target of miR-142-5p. Through overexpression of miR-142-5p, ALT and AST in serum were inhibited, pro-inflammatory factors, liver fatty degeneration and fibrosis in liver tissues were decreased, while anti-inflammatory factors were increased. Overexpression of TSLP and JAK-STAT signaling pathway activation could reverse the effects of miR-142-5p on NASH. Taken together, overexpression of miR-142-5p could attenuate NASH progression via inhibiting TSLP and JAK-STAT pathway. MiR-142-5p might be a novel latent target for NASH therapy.
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lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150-5p/SLC38A1 axis

Yanni Yang, Wenlin Tai, Nihong Lu, Ting Li, Yongjun Liu, Wenjuan Wu, Zhengkun Li, Lin Pu, Xiaoyuan Zhao, Tao Zhang, Zhaoxing Dong,

https://doi.org/10.18632/aging.103176 pp 9085—9102

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Yang Y, Tai W, Lu N, Li T, Liu Y, Wu W, Li Z, Pu L, Zhao X, Zhang T, Dong Z, . lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150-5p/SLC38A1 axis. . 12:9085-9102. https://doi.org/10.18632/aging.103176

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                TY  - JOUR
                AU  - Yang, Yanni 
                AU  - Tai, Wenlin 
                AU  - Lu, Nihong 
                AU  - Li, Ting 
                AU  - Liu, Yongjun 
                AU  - Wu, Wenjuan 
                AU  - Li, Zhengkun 
                AU  - Pu, Lin 
                AU  - Zhao, Xiaoyuan 
                AU  - Zhang, Tao 
                AU  - Dong, Zhaoxing 
                TI  - lncRNA ZFAS1 promotes lung fibroblast-to-myofibroblast transition and ferroptosis via functioning as a ceRNA through miR-150-5p/SLC38A1 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103176
                DO  - 10.18632/aging.103176
                SP  - 9085
                EP  - 9102
                PY  - 
                AB  - Pulmonary fibrosis (PF) is a lethal fibrotic lung disease. The role of lncRNAs in multiple diseases has been confirmed, but the role and mechanism of lncRNA zinc finger antisense 1 (ZFAS1) in the progression of PF need to be elucidated further. Here, we found that lncRNA ZFAS1 was upregulated in bleomycin (BLM)-induced PF rats lung tissues and transforming growth factor-&#x3B2;1 (TGF-&#x3B2;1)-treated HFL1 cells, and positively correlated with the expression of solute carrier family 38 member 1 (SLC38A1), which is an important regulator of lipid peroxidation. Moreover, knockdown of lncRNA ZFAS1 significantly alleviated TGF-&#x3B2;1-induced fibroblast activation, inflammation and lipid peroxidation. In vivo experiments showed that inhibition of lncRNA ZFAS1 abolished BLM-induced lipid peroxidation and PF development. Mechanistically, silencing of lncRNA ZFAS1 attenuated ferroptosis and PF progression by lncRNA ZFAS1 acting as a competing endogenous RNA (ceRNA) and sponging miR-150-5p to downregulate SLC38A1 expression. Collectively, our studies demonstrated the role of the lncRNA ZFAS1/miR-150-5p/SLC38A1 axis in the progression of PF, and may provide a new biomarker for the treatment of PF patients.
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A novel 3’,5’-diprenylated chalcone induces concurrent apoptosis and GSDME-dependent pyroptosis through activating PKCδ/JNK signal in prostate cancer

Yongqiang Zhang, Jue Yang, Zhonghang Wen, Xiaoyue Chen, Jia Yu, Dongbo Yuan, Bixue Xu, Heng Luo, Jianguo Zhu,

https://doi.org/10.18632/aging.103178 pp 9103—9124

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Zhang Y, Yang J, Wen Z, Chen X, Yu J, Yuan D, Xu B, Luo H, Zhu J, . A novel 3’,5’-diprenylated chalcone induces concurrent apoptosis and GSDME-dependent pyroptosis through activating PKCδ/JNK signal in prostate cancer. . 12:9103-9124. https://doi.org/10.18632/aging.103178

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                TY  - JOUR
                AU  - Zhang, Yongqiang 
                AU  - Yang, Jue 
                AU  - Wen, Zhonghang 
                AU  - Chen, Xiaoyue 
                AU  - Yu, Jia 
                AU  - Yuan, Dongbo 
                AU  - Xu, Bixue 
                AU  - Luo, Heng 
                AU  - Zhu, Jianguo 
                TI  - A novel 3’,5’-diprenylated chalcone induces concurrent apoptosis and GSDME-dependent pyroptosis through activating PKCδ/JNK signal in prostate cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103178
                DO  - 10.18632/aging.103178
                SP  - 9103
                EP  - 9124
                PY  - 
                AB  - Although androgen deprivation therapy may initially be effective in prostate cancer, the disease can gradually progress to castration-resistant prostate cancer, at which point chemotherapy becomes the major clinical strategy. In this study, we demonstrated the anti-cancer potential of a novel 3&#x2019;,5&#x2019;-diprenylated chalcone (C10), which selectively inhibited the proliferation of PC3 cells in vitro and in vivo. C10 treatment elevated the proportion of PC3 cells in sub-G1 phase and induced programmed cell death. Interestingly, C10 elicited concurrent Caspase-dependent apoptotic and gasdermin E-dependent pyroptotic events. RNA-Seq and bioinformatics analyses revealed a strong correlation between protein kinase C delta (PKC&#x3B4;) and mitogen-activated protein kinase pathway activation in prostate cancer. PKC&#x3B4; silencing in PC3 cells suppressed the activation of the JNK pathway and the expression of its downstream genes, including Bax, interleukin-6 and interleukin-1&#x3B2;, which are involved in apoptotic and pyroptotic processes. Moreover, in PC3 cell xenograft tumor tissues, C10 treatment inhibited tumor growth and upregulated PKC&#x3B4;. These findings suggest that C10 treatment induces the PKC&#x3B4;/JNK pathway, thereby activating Caspase-3 and inducing the cleavage of PARP and gasdermin E to execute apoptosis and cell-lytic pyroptosis in prostate cancer cells.
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Cigarette smoke-induced lung inflammation in COPD mediated via CCR1/JAK/STAT /NF-κB pathway

Kaishun Zhao, Ran Dong, Yanfang Yu, Chunlin Tu, Ying Li, YuJuan Cui, Lei Bao, Chunhua Ling,

https://doi.org/10.18632/aging.103180 pp 9125—9138

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Zhao K, Dong R, Yu Y, Tu C, Li Y, Cui Y, Bao L, Ling C, . Cigarette smoke-induced lung inflammation in COPD mediated via CCR1/JAK/STAT /NF-κB pathway. . 12:9125-9138. https://doi.org/10.18632/aging.103180

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                TY  - JOUR
                AU  - Zhao, Kaishun 
                AU  - Dong, Ran 
                AU  - Yu, Yanfang 
                AU  - Tu, Chunlin 
                AU  - Li, Ying 
                AU  - Cui, YuJuan 
                AU  - Bao, Lei 
                AU  - Ling, Chunhua 
                TI  - Cigarette smoke-induced lung inflammation in COPD mediated via CCR1/JAK/STAT /NF-κB pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103180
                DO  - 10.18632/aging.103180
                SP  - 9125
                EP  - 9138
                PY  - 
                AB  - Inflammation is an important cause of chronic obstructive pulmonary disease (COPD) and its acute exacerbation. However, the critical role of C-C chemokine receptor (CCR)1 in progression of cigarette smoke-induced chronic inflammation remains unclear. We studied CCR1 expression using immunohistochemistry, immunofluorescence, and real-time polymerase chain reaction (RT-PCR) in COPD patients and controls. Cytokine levels in peripheral blood were measured by enzyme-linked immunosorbent assay (ELISA). In vitro, we investigated Janus kinase/signal transducers and activators of transcription (JAK/STAT)/nuclear factor-&#x3BA;B (NF-&#x3BA;B) signaling in cigarette smoke extract-induced or CCR1 deficiency/overexpressed mouse macrophage cell line MH-S by RT-PCR and western blot, and measured the cytokine levels in the supernatant with ELISA. We found that CCR1 expression was upregulated in COPD patients and there was a negative correlation between CCR1 mRNA levels and predicted % forced expiratory volume in 1 min. Inflammatory cytokine levels in the peripheral blood were higher in COPD patients than controls, and these were positively correlated with CCR1 levels. CCR1 was shown to play a critical role in regulating smoke-induced inflammation via JAK/STAT3/NF-&#x3BA;B signaling in vitro. CCR1 may play a critical role in airway inflammation in COPD. Additionally, understanding the molecular mechanism may help develop novel methods for the treatment of COPD.
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Klotho alleviates indoxyl sulfate-induced heart failure and kidney damage by promoting M2 macrophage polarization

Jing Lv, Jin Chen, Minjia Wang, Fei Yan,

https://doi.org/10.18632/aging.103183 pp 9139—9150

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Lv J, Chen J, Wang M, Yan F, . Klotho alleviates indoxyl sulfate-induced heart failure and kidney damage by promoting M2 macrophage polarization. . 12:9139-9150. https://doi.org/10.18632/aging.103183

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                TY  - JOUR
                AU  - Lv, Jing 
                AU  - Chen, Jin 
                AU  - Wang, Minjia 
                AU  - Yan, Fei 
                TI  - Klotho alleviates indoxyl sulfate-induced heart failure and kidney damage by promoting M2 macrophage polarization
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103183
                DO  - 10.18632/aging.103183
                SP  - 9139
                EP  - 9150
                PY  - 
                AB  - Indoxyl sulfate (IS) is a protein-bound uremic toxin that can accumulate in patients with chronic kidney disease (CKD) or acute kidney injury (AKI) and cause kidney and cardiac dysfunction. Klotho is an anti-aging protein that has reno- and cardio-protective effects. We investigated whether Klotho could alleviate IS-induced heart failure and kidney damage by regulating macrophages, which play a key role in the inflammatory response in CKD and AKI. Treatment of THP-1-derived macrophages with IS induced the production of the pro-inflammatory cytokines TNF&#x3B1;, IL-6, and IL-1&#x3B2;, and stimulated M1 polarization. Additionally, IS induced downregulation of Klotho expression in macrophages. Overexpression of Klotho suppressed the IS-induced inflammatory response in macrophages by stimulating M2 polarization. It also alleviated IS-induced cardiac hypertrophy and renal fibrosis in mice. A reduction in IS-induced phosphorylation of NF-kB p65 was observed in response to Klotho overexpression, suggesting that Klotho alleviates kidney and cardiac injury by inactivating NF-kB signaling and promoting macrophage M2 polarization.
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Downregulation of miRNA-146a-5p promotes malignant transformation of mesenchymal stromal/stem cells by glioma stem-like cells

Xingliang Dai, Yunfei Wang, Xuchen Dong, Minfeng Sheng, Haiyang Wang, Jia Shi, Yujing Sheng, Liang Liu, Qianqian Jiang, Yanming Chen, Bingshan Wu, Xuejun Yang, Hongwei Cheng, Chunsheng Kang, Jun Dong,

https://doi.org/10.18632/aging.103185 pp 9151—9172

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Dai X, Wang Y, Dong X, Sheng M, Wang H, Shi J, Sheng Y, Liu L, Jiang Q, Chen Y, Wu B, Yang X, Cheng H, et al, . Downregulation of miRNA-146a-5p promotes malignant transformation of mesenchymal stromal/stem cells by glioma stem-like cells. . 12:9151-9172. https://doi.org/10.18632/aging.103185

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                TY  - JOUR
                AU  - Dai, Xingliang 
                AU  - Wang, Yunfei 
                AU  - Dong, Xuchen 
                AU  - Sheng, Minfeng 
                AU  - Wang, Haiyang 
                AU  - Shi, Jia 
                AU  - Sheng, Yujing 
                AU  - Liu, Liang 
                AU  - Jiang, Qianqian 
                AU  - Chen, Yanming 
                AU  - Wu, Bingshan 
                AU  - Yang, Xuejun 
                AU  - Cheng, Hongwei 
                AU  - Kang, Chunsheng 
                AU  - Dong, Jun 
                TI  - Downregulation of miRNA-146a-5p promotes malignant transformation of mesenchymal stromal/stem cells by glioma stem-like cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103185
                DO  - 10.18632/aging.103185
                SP  - 9151
                EP  - 9172
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Dai, Xingliang 
                AU  - Wang, Yunfei 
                AU  - Dong, Xuchen 
                AU  - Sheng, Minfeng 
                AU  - Wang, Haiyang 
                AU  - Shi, Jia 
                AU  - Sheng, Yujing 
                AU  - Liu, Liang 
                AU  - Jiang, Qianqian 
                AU  - Chen, Yanming 
                AU  - Wu, Bingshan 
                AU  - Yang, Xuejun 
                AU  - Cheng, Hongwei 
                AU  - Kang, Chunsheng 
                AU  - Dong, Jun 
                TI  - Downregulation of miRNA-146a-5p promotes malignant transformation of mesenchymal stromal/stem cells by glioma stem-like cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103185
                DO  - 10.18632/aging.103185
                SP  - 9151
                EP  - 9172
                PY  - 
                AB  - Mesenchymal stromal/stem cells (MSCs) are promising carriers in cell-based therapies against central nervous system diseases, and have been evaluated in various clinical trials in recent years. However, bone marrow-derived MSCs (BMSCs) are reportedly involved in tumorigenesis initiated by glioma stem-like cells (GSCs). We therefore established three different orthotopic models of GSC-MSC interactions in vivo using dual-color fluorescence tracing. Cell sorting and micropipetting techniques were used to obtain highly proliferative MSC monoclones from each model, and these cells were identified as transformed MSC lines 1, 2 and 3. Nineteen miRNAs were upregulated and 24 miRNAs were downregulated in all three transformed MSC lines compared to normal BMSCs. Reduced miR-146a-5p expression in the transformed MSCs was associated with their proliferation, malignant transformation and overexpression of heterogeneous nuclear ribonucleoprotein D. These findings suggest that downregulation of miR-146a-5p leads to overexpression of its target gene, heterogeneous nuclear ribonucleoprotein D, thereby promoting malignant transformation of MSCs during interactions with GSCs. Given the risk that MSCs will undergo malignant transformation in the glioma microenvironment, targeted glioma therapies employing MSCs as therapeutic carriers should be considered cautiously.
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Dietary type 2 resistant starch improves systemic inflammation and intestinal permeability by modulating microbiota and metabolites in aged mice on high-fat diet

Yawen Zhang, Luyi Chen, Mengjia Hu, John J. Kim, Renbin Lin, Jilei Xu, Lina Fan, Yadong Qi, Lan Wang, Weili Liu, Yanyong Deng, Jianmin Si, Shujie Chen,

https://doi.org/10.18632/aging.103187 pp 9173—9187

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Zhang Y, Chen L, Hu M, Kim JJ, Lin R, Xu J, Fan L, Qi Y, Wang L, Liu W, Deng Y, Si J, Chen S, . Dietary type 2 resistant starch improves systemic inflammation and intestinal permeability by modulating microbiota and metabolites in aged mice on high-fat diet. . 12:9173-9187. https://doi.org/10.18632/aging.103187

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                TY  - JOUR
                AU  - Zhang, Yawen 
                AU  - Chen, Luyi 
                AU  - Hu, Mengjia 
                AU  - Kim, John J. 
                AU  - Lin, Renbin 
                AU  - Xu, Jilei 
                AU  - Fan, Lina 
                AU  - Qi, Yadong 
                AU  - Wang, Lan 
                AU  - Liu, Weili 
                AU  - Deng, Yanyong 
                AU  - Si, Jianmin 
                AU  - Chen, Shujie 
                TI  - Dietary type 2 resistant starch improves systemic inflammation and intestinal permeability by modulating microbiota and metabolites in aged mice on high-fat diet
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103187
                DO  - 10.18632/aging.103187
                SP  - 9173
                EP  - 9187
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Zhang, Yawen 
                AU  - Chen, Luyi 
                AU  - Hu, Mengjia 
                AU  - Kim, John J. 
                AU  - Lin, Renbin 
                AU  - Xu, Jilei 
                AU  - Fan, Lina 
                AU  - Qi, Yadong 
                AU  - Wang, Lan 
                AU  - Liu, Weili 
                AU  - Deng, Yanyong 
                AU  - Si, Jianmin 
                AU  - Chen, Shujie 
                TI  - Dietary type 2 resistant starch improves systemic inflammation and intestinal permeability by modulating microbiota and metabolites in aged mice on high-fat diet
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103187
                DO  - 10.18632/aging.103187
                SP  - 9173
                EP  - 9187
                PY  - 
                AB  - Type 2 resistant starch (RS2) is a fermentable dietary fiber conferring health benefits. We investigated the effects of RS2 on host, gut microbiota, and metabolites in aged mice on high-fat diet. In eighteen-month old mice randomly assigned to control, high-fat (HF), or high-fat+20% RS2 (HFRS) diet for 16 weeks, RS2 reversed the weight gain and hepatic steatosis induced by high-fat diet. Serum and fecal LPS, colonic IL-2 and hepatic IL-4 mRNA expressions decreased while colonic mucin 2 mRNA and protein expressions increased in the HFRS compared to the HF and the control group. 16s rRNA sequencing of fecal microbial DNA demonstrated that RS2 decreased the abundance of pathogen taxa associated with obesity, inflammation, and aging including Desulfovibrio (Proteobacteria phylum), Ruminiclostridium 9, Lachnoclostridium, Helicobacteria, Oscillibacter, Alistipes, Peptococcus, and Rikenella. Additionally, RS2 increased the colonic butyric acid by 2.6-fold while decreasing the isobutyric and isovaleric acid levels by half compared to the HF group. Functional analyses based on Clusters of Orthologous Groups showed that RS2 increased carbohydrate while decreasing amino acid metabolism. These findings demonstrate that RS2 can reverse weight gain, hepatic steatosis, inflammation, and increased intestinal permeability in aged mice on high-fat diet mediated by changes in gut microbiome and metabolites.
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A three-lncRNA signature predicts clinical outcomes in low-grade glioma patients after radiotherapy

Wanzun Lin, Zongwei Huang, Yanyan Xu, Xiaochuan Chen, Ting Chen, Yuling Ye, Jianming Ding, Zhangjie Chen, Long Chen, Xianxin Qiu, Sufang Qiu,

https://doi.org/10.18632/aging.103189 pp 9188—9204

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Lin W, Huang Z, Xu Y, Chen X, Chen T, Ye Y, Ding J, Chen Z, Chen L, Qiu X, Qiu S, . A three-lncRNA signature predicts clinical outcomes in low-grade glioma patients after radiotherapy. . 12:9188-9204. https://doi.org/10.18632/aging.103189

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                TY  - JOUR
                AU  - Lin, Wanzun 
                AU  - Huang, Zongwei 
                AU  - Xu, Yanyan 
                AU  - Chen, Xiaochuan 
                AU  - Chen, Ting 
                AU  - Ye, Yuling 
                AU  - Ding, Jianming 
                AU  - Chen, Zhangjie 
                AU  - Chen, Long 
                AU  - Qiu, Xianxin 
                AU  - Qiu, Sufang 
                TI  - A three-lncRNA signature predicts clinical outcomes in low-grade glioma patients after radiotherapy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103189
                DO  - 10.18632/aging.103189
                SP  - 9188
                EP  - 9204
                PY  - 
                AB  - Although radiation therapy (RT) plays a critical role in the treatment of low-grade glioma (LGG), many patients suffer from adverse effects without experiencing survival benefits. In various carcinomas, long non-coding RNAs (lncRNAs) contribute to pathogenic processes, including tumorigenesis, metastasis, chemoresistance, and radioresistance. Currently, the role of lncRNAs in the radiosensitivity of LGG is largely unknown. Here, we downloaded clinical data for 167 LGG patients from The Cancer Genome Atlas database and divided them between radiosensitive and radioresistant groups based on their clinical outcomes after receiving radiotherapy. We identified 37 lncRNAs that were differentially expressed (DElncRNAs) between the groups. Functional enrichment analysis revealed that their potential target mRNAs were mainly enriched in the PI3K-Akt and MAPK signaling pathways and in DNA damage response. Kaplan-Meier survival analysis revealed that increased expression of six lncRNAs was significantly associated with radiosensitivity. We then developed a risk signature based on three of the DElncRNAs that served as an independent biomarker for predicting LGG patient outcomes after radiotherapy. In vitro experiments further validated the biological function of these lncRNAs on low-grade glioma radiation response.
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Identification of potential novel differentially-expressed genes and their role in invasion and migration in renal cell carcinoma

Shen-Nan Shi, Xia Qin, Shuo Wang, Wen-Fu Wang, Yao-Feng Zhu, Yu Lin, Zun-Lin Zhou, Ben-Kang Shi, Xi-Gao Liu,

https://doi.org/10.18632/aging.103192 pp 9205—9223

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Shi S, Qin X, Wang S, Wang W, Zhu Y, Lin Y, Zhou Z, Shi B, Liu X, . Identification of potential novel differentially-expressed genes and their role in invasion and migration in renal cell carcinoma. . 12:9205-9223. https://doi.org/10.18632/aging.103192

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                TY  - JOUR
                AU  - Shi, Shen-Nan 
                AU  - Qin, Xia 
                AU  - Wang, Shuo 
                AU  - Wang, Wen-Fu 
                AU  - Zhu, Yao-Feng 
                AU  - Lin, Yu 
                AU  - Zhou, Zun-Lin 
                AU  - Shi, Ben-Kang 
                AU  - Liu, Xi-Gao 
                TI  - Identification of potential novel differentially-expressed genes and their role in invasion and migration in renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103192
                DO  - 10.18632/aging.103192
                SP  - 9205
                EP  - 9223
                PY  - 
                AB  - Clear cell renal cell carcinoma (ccRCC) remains one of the most common cancer types globally, and while it has been extensively studied, the molecular basis for its pathology remains incompletely understood. Herein, we profiled three previously published datasets (GSE66272, GSE100666, and GSE105261) in a single integrated analysis aimed at identifying disease-associated patterns of gene expression that may offer mechanistic insight into the drivers of this disease. We pooled expression data from 39 normal kidney samples and 39 kidney tumors, leading us to identify 310 differentially expressed genes (DEGs) that were linked to kidney cancer in all three analyzed datasets. Of these genes, 133 and 177 were up- and down-regulated, respectively, in cancer samples. We then incorporated these DEGs into a protein-protein interaction network with the STRING and Cytoscape tools, and we were able to identify signaling pathways significantly enriched for these DEGs. The relationship between DEG expression and ccRCC patient survival was further evaluated using a Kaplan-Meier approach, leading us to identify TIMP1 as an independent prognostic factor in ccRCC patients. When TIMP1 expression was disrupted in ccRCC cell lines, this impaired their migratory and invasive capabilities. In summary, we employed an integrative bioinformatics approach to identify ccRCC-related DEGs and associated signaling pathways. Together these findings offer novel insight into the mechanistic basis for ccRCC, potentially helping to identify novel therapeutic targets for the treatment of this deadly disease.
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Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways

Ting-Kuo Chang, Yu-Han Wang, Shu-Jui Kuo, Shih-Wei Wang, Chun-Hao Tsai, Yi-Chin Fong, Nan-Lin Wu, Shan-Chi Liu, Chih-Hsin Tang,

https://doi.org/10.18632/aging.103195 pp 9224—9239

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Chang T, Wang Y, Kuo S, Wang S, Tsai C, Fong Y, Wu N, Liu S, Tang C, . Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways. . 12:9224-9239. https://doi.org/10.18632/aging.103195

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                TY  - JOUR
                AU  - Chang, Ting-Kuo 
                AU  - Wang, Yu-Han 
                AU  - Kuo, Shu-Jui 
                AU  - Wang, Shih-Wei 
                AU  - Tsai, Chun-Hao 
                AU  - Fong, Yi-Chin 
                AU  - Wu, Nan-Lin 
                AU  - Liu, Shan-Chi 
                AU  - Tang, Chih-Hsin 
                TI  - Apelin enhances IL-1β expression in human synovial fibroblasts by inhibiting miR-144-3p through the PI3K and ERK pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103195
                DO  - 10.18632/aging.103195
                SP  - 9224
                EP  - 9239
                PY  - 
                AB  - Much data suggests intersecting activities between the adipokine apelin (APLN) and the pathologic processes of obesity and osteoarthritis (OA), with APLN modulating cartilage, synovium, bone, and various immune cell activities. The synovium plays an important role in the pathogenesis of OA. We investigated the crosstalk between APLN, a major OA-related adipokine, and interleukin 1 beta (IL-1&#x3B2;), a major proinflammatory cytokine, in human OA synovial fibroblasts (OASFs). We showed that APLN stimulated the synthesis of IL-1&#x3B2; in a concentration- and time-dependent manner, which was mitigated by blockade of the PI3K and ERK pathway. We also showed that APLN inhibited the expression of miRNA-144-3p, which blocks IL-1&#x3B2; transcription; this suppression activity was reversed via blockade of the PI3K and ERK pathway. Moreover, pathologic changes in OA cartilage were rescued when APLN was silenced by shAPLN transfection both in vitro and in vivo. Our evidence is the first to show that APLN stimulates the expression of IL-1&#x3B2; by activating the PI3K and ERK pathway and suppressing downstream expression of miRNA-144-3p in OASFs. We also demonstrate that knockdown of APLN expression by shAPLN transfection ameliorated changes in OA cartilage severity. These results shed light on OA pathogenesis and suggest a novel treatment pathway.
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BRD4 contributes to LPS-induced macrophage senescence and promotes progression of atherosclerosis-associated lipid uptake

Hui Wang, Haiping Fu, Ruigong Zhu, Xuan Wu, Xian Ji, Xuesong Li, Hong Jiang, Zhe Lin, Xin Tang, Shixiu Sun, Jiajing Chen, Xin Wang, Qingguo Li, Yong Ji, Hongshan Chen,

https://doi.org/10.18632/aging.103200 pp 9240—9259

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Wang H, Fu H, Zhu R, Wu X, Ji X, Li X, Jiang H, Lin Z, Tang X, Sun S, Chen J, Wang X, Li Q, et al, . BRD4 contributes to LPS-induced macrophage senescence and promotes progression of atherosclerosis-associated lipid uptake. . 12:9240-9259. https://doi.org/10.18632/aging.103200

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                TY  - JOUR
                AU  - Wang, Hui 
                AU  - Fu, Haiping 
                AU  - Zhu, Ruigong 
                AU  - Wu, Xuan 
                AU  - Ji, Xian 
                AU  - Li, Xuesong 
                AU  - Jiang, Hong 
                AU  - Lin, Zhe 
                AU  - Tang, Xin 
                AU  - Sun, Shixiu 
                AU  - Chen, Jiajing 
                AU  - Wang, Xin 
                AU  - Li, Qingguo 
                AU  - Ji, Yong 
                AU  - Chen, Hongshan 
                TI  - BRD4 contributes to LPS-induced macrophage senescence and promotes progression of atherosclerosis-associated lipid uptake
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103200
                DO  - 10.18632/aging.103200
                SP  - 9240
                EP  - 9259
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wang, Hui 
                AU  - Fu, Haiping 
                AU  - Zhu, Ruigong 
                AU  - Wu, Xuan 
                AU  - Ji, Xian 
                AU  - Li, Xuesong 
                AU  - Jiang, Hong 
                AU  - Lin, Zhe 
                AU  - Tang, Xin 
                AU  - Sun, Shixiu 
                AU  - Chen, Jiajing 
                AU  - Wang, Xin 
                AU  - Li, Qingguo 
                AU  - Ji, Yong 
                AU  - Chen, Hongshan 
                TI  - BRD4 contributes to LPS-induced macrophage senescence and promotes progression of atherosclerosis-associated lipid uptake
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103200
                DO  - 10.18632/aging.103200
                SP  - 9240
                EP  - 9259
                PY  - 
                AB  - Aging is closely associated with atherosclerosis. Macrophages accumulate in atherosclerotic lesions contributing to the development and progression of atherosclerosis. Although atherosclerotic lesions are known to contain senescent cells, the mechanism underlying the formation of senescent macrophages during atherosclerosis is still unclear. In this study, macrophages with different origins were collected, including THP-1 macrophages, telomerase reverse transcriptase knock out (Tert-/-) mouse peritoneal macrophages, and human peripheral blood mononuclear cells (PBMCs). We found Lipopolysaccharide (LPS) could induce the formation of senescent macrophages, which was typified by the morphological changes, senescence-associated secretory phenotype (SASP) secretory, and persistent DNA damage response. Mechanistically, bromodomain-containing protein 4 (BRD4), a chromosomal binding protein related to gene expression, was found to play a key role in the pathological process, which could offer new therapeutic perspectives. Inhibition of BRD4 by siBRD4 or inhibitors such as JQ-1 or I-BET762 prevented the aging of macrophages and lipid accumulation in the LPS-induced senescent macrophages by decreasing expression of SASP in autocrine and paracrine senescence. These findings have significant implications for the understanding of the pathobiology of age-associated diseases and may guide future studies on targeted clinical drug therapy.
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Integrative analysis of genomic and epigenetic regulation of endometrial cancer

Qihang Zhong, Junpeng Fan, Honglei Chu, Mujia Pang, Junsheng Li, Yong Fan, Ping Liu, Congying Wu, Jie Qiao, Rong Li, Jing Hang,

https://doi.org/10.18632/aging.103202 pp 9260—9274

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Zhong Q, Fan J, Chu H, Pang M, Li J, Fan Y, Liu P, Wu C, Qiao J, Li R, Hang J, . Integrative analysis of genomic and epigenetic regulation of endometrial cancer. . 12:9260-9274. https://doi.org/10.18632/aging.103202

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                TY  - JOUR
                AU  - Zhong, Qihang 
                AU  - Fan, Junpeng 
                AU  - Chu, Honglei 
                AU  - Pang, Mujia 
                AU  - Li, Junsheng 
                AU  - Fan, Yong 
                AU  - Liu, Ping 
                AU  - Wu, Congying 
                AU  - Qiao, Jie 
                AU  - Li, Rong 
                AU  - Hang, Jing 
                TI  - Integrative analysis of genomic and epigenetic regulation of endometrial cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103202
                DO  - 10.18632/aging.103202
                SP  - 9260
                EP  - 9274
                PY  - 
                AB  - Endometrial carcinomas (EC) are characterized by high DNA copy numbers and DNA methylation aberrations. In this study, we sought to comprehensively explore the effect of these two factors on development and progression of EC by analyzing integrated genomic and epigenetic analysis to. We found high DNA copy number and DNA methylation abnormalities in EC, with 6308 copy-number variation genes (CNV-G) and 4376 methylation genes (MET-G). We used these CNV-G and MET-G to subcategorize the samples for prognostic analysis, and identified three molecular subtypes (iC1, iC2, iC3). Moreover, the subtypes exhibited different tumor immune microenvironment characteristics. A further analysis of their molecular characteristics revealed three potential prognostic markers (KIAA1324, nonexpresser of pathogenesis-related genes1 (NPR1) and idiopathic hypogonadotropic hypogonadism (IHH)). Notably, all three markers showed distinct CNV, DNA methylation, and gene expression profiles. Analysis of mutations among the three subtypes revealed that iC2 had fewer mutations than the other subtypes. Conversely, iC2 showed significantly higher CNV levels than other subtypes. This comprehensive analysis of genomic and epigenetic profiles identified three prognostic markers, therefore, provides new insights into the multi-layered pathology of EC. These can be utilized for accurate treatment of EC patients.
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NAC1 attenuates BCL6 negative autoregulation and functions as a BCL6 coactivator of FOXQ1 transcription in cancer cells

Min Gao, Alice Laschuk Herlinger, Renchin Wu, Tian-Li Wang, Ie-Ming Shih, Beihua Kong, Leticia Batista Azevedo Rangel, Jin-Ming Yang,

https://doi.org/10.18632/aging.103203 pp 9275—9291

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Gao M, Herlinger AL, Wu R, Wang T, Shih I, Kong B, Rangel LBA, Yang J, . NAC1 attenuates BCL6 negative autoregulation and functions as a BCL6 coactivator of FOXQ1 transcription in cancer cells. . 12:9275-9291. https://doi.org/10.18632/aging.103203

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                TY  - JOUR
                AU  - Gao, Min 
                AU  - Herlinger, Alice Laschuk 
                AU  - Wu, Renchin 
                AU  - Wang, Tian-Li 
                AU  - Shih, Ie-Ming 
                AU  - Kong, Beihua 
                AU  - Rangel, Leticia Batista Azevedo 
                AU  - Yang, Jin-Ming 
                TI  - NAC1 attenuates BCL6 negative autoregulation and functions as a BCL6 coactivator of FOXQ1 transcription in cancer cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103203
                DO  - 10.18632/aging.103203
                SP  - 9275
                EP  - 9291
                PY  - 
                AB  - Background: Nucleus accumbens-associated protein 1 (NAC1) has multifaceted roles in cancer pathogenesis and progression, including the development of drug resistance, promotion of cytokinesis, and maintenance of &#x201C;stem cell-like&#x201D; phenotypes. NAC1 is a transcriptional co-regulator belonging to the bric-a-brac tramtrack broad (BTB) family of proteins, although it lacks the characteristic DNA binding motif of the BTB family. The formation of higher-order transcription complexes likely depends on its interaction with other DNA-binding co-factors.Results: NAC1 interacts with BCL6 via its C-terminal BEN domain and forms a complex that binds the promoter region and activates transcription of the NAC1 target gene, FOXQ1. NAC1 and BCL6 were coordinately upregulated. Our analysis also identified a novel function of NAC1 in attenuating BCL6 auto-downregulation in ovarian cancer. Lastly, we found a significant overlap among NAC1- and BCL6-regulated genes in tumor cells, suggesting that NAC1 and BCL6 coordinately control transcription in cancer.Conclusions: The results of this study provide a novel mechanistic insight into the oncogenic roles of NAC1 and underline the importance of developing the NAC1/BCL6-targeted cancer therapy.Methods: Using the Cistrome database and Chromatin Immunoprecipitation (ChIP) analyses, we identified BCL6 as a potential NAC1- interacting molecule. Co-immunoprecipitation (Co-IP), luciferase reporter assay, immunohistochemistry and microarray analysis were performed to analyze the interaction between NAC1 and BCL6 and the mechanisms by which they regulate the downstream genes including FOXQ1.
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PIWI-interacting RNAs piR-13643 and piR-21238 are promising diagnostic biomarkers of papillary thyroid carcinoma

Zhengyan Chang, Guo Ji, Runzhi Huang, Hong Chen, Yaohui Gao, Weifeng Wang, Xuechen Sun, Jie Zhang, Jiayi Zheng, Qing Wei,

https://doi.org/10.18632/aging.103206 pp 9292—9310

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Chang Z, Ji G, Huang R, Chen H, Gao Y, Wang W, Sun X, Zhang J, Zheng J, Wei Q, . PIWI-interacting RNAs piR-13643 and piR-21238 are promising diagnostic biomarkers of papillary thyroid carcinoma. . 12:9292-9310. https://doi.org/10.18632/aging.103206

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                TY  - JOUR
                AU  - Chang, Zhengyan 
                AU  - Ji, Guo 
                AU  - Huang, Runzhi 
                AU  - Chen, Hong 
                AU  - Gao, Yaohui 
                AU  - Wang, Weifeng 
                AU  - Sun, Xuechen 
                AU  - Zhang, Jie 
                AU  - Zheng, Jiayi 
                AU  - Wei, Qing 
                TI  - PIWI-interacting RNAs piR-13643 and piR-21238 are promising diagnostic biomarkers of papillary thyroid carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103206
                DO  - 10.18632/aging.103206
                SP  - 9292
                EP  - 9310
                PY  - 
                AB  - Emerging studies demonstrate that PIWI-interacting RNAs (piRNAs) participate in the development of cancers. 75 pairs of papillary thyroid carcinoma (PTC) samples and 31 benign thyroid nodule samples were included in this three-phase biomarker identifying study. First, piRNA expression profiles of five pairs of PTC samples were acquired piRNA sequencing. The expression of all upregulated piRNAs were further validated by RT-qPCR. Paired t and nonparametric test were used to evaluate the association between all upregulated piRNAs and clinic stage. The expression levels of key piRNAs were corrected by demographic data to construct a multivariate model to distinguish malignant nodules from benign. Additionally, the intersection between target genes of key piRNAs and differentially expressed genes in The Cancer Genome Atlas (TCGA) PTC samples were used to perform enrichment analysis. Only piR-13643 and piR-21238 were significantly upregulated in PTC and associated with clinic stage. Moreover, both piR-13643 (Area Under Curve (AUC): 0.821) and piR-21238 (AUC: 0.823) showed better performance in distinguishing malignant nodules from benign than currently used biomarkers HBME1 (AUC: 0.590). Based on our findings, piR-13643 and piR-21238 were observed to be significantly upregulated in human PTC. PIWI-interacting RNAs could serve as promising novel biomarkers for accurate detection of PTC.
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Single nucleotide polymorphisms within the Wnt pathway predict the risk of bone metastasis in patients with non-small cell lung cancer

Yiquan Xu, Hongru Li, Lihong Weng, Yanqin Qiu, Junqiong Zheng, Huaqiang He, Dongmei Zheng, Junfan Pan, Fan Wu, Yusheng Chen,

https://doi.org/10.18632/aging.103207 pp 9311—9327

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Xu Y, Li H, Weng L, Qiu Y, Zheng J, He H, Zheng D, Pan J, Wu F, Chen Y, . Single nucleotide polymorphisms within the Wnt pathway predict the risk of bone metastasis in patients with non-small cell lung cancer. . 12:9311-9327. https://doi.org/10.18632/aging.103207

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                TY  - JOUR
                AU  - Xu, Yiquan 
                AU  - Li, Hongru 
                AU  - Weng, Lihong 
                AU  - Qiu, Yanqin 
                AU  - Zheng, Junqiong 
                AU  - He, Huaqiang 
                AU  - Zheng, Dongmei 
                AU  - Pan, Junfan 
                AU  - Wu, Fan 
                AU  - Chen, Yusheng 
                TI  - Single nucleotide polymorphisms within the Wnt pathway predict the risk of bone metastasis in patients with non-small cell lung cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103207
                DO  - 10.18632/aging.103207
                SP  - 9311
                EP  - 9327
                PY  - 
                AB  - The Wingless-type (Wnt) signaling pathway plays an important role in the development and progression of cancer. This study aimed to evaluate the relationship between single nucleotide polymorphisms (SNPs) in the Wnt pathway and the risk of bone metastasis in patients with non-small cell lung cancer (NSCLC). We collected 500 blood samples from patients with NSCLC and genotyped eight SNPs from four core genes (WNT2, AXIN1, CTNNB1 and APC) present within the WNT pathway. Moreover, we assessed the potential relationship of these genes with bone metastasis development. Our results showed that the AC/AA genotype of CTNNB1: rs1880481 was associated with a decreased risk of bone metastasis. Polymorphisms with an HR of &lt; 1 had a cumulative protective impact on the risk of bone metastasis. Furthermore, patients with the AC/AA genotype of CTNNB1: rs1880481 was associated with Karnofsky performance status score, squamous cell carcinoma antigen and Ki-67 proliferation index. Lastly, patients with the AC/AA genotype of CTNNB1: rs1880481 had significantly longer median progression free survival time than those with the CC genotype. In conclusion, SNPs within the Wnt signaling pathway are associated with a decreased risk of bone metastasis, and may be valuable biomarkers for bone metastasis in patients with NSCLC.
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Establishing immune scoring model based on combination of the number, function, and phenotype of lymphocytes

Guoxing Tang, Xu Yuan, Ying Luo, Qun Lin, Zhishui Chen, Xue Xing, Huijuan Song, Shiji Wu, Hongyan Hou, Jing Yu, Liyan Mao, Weiyong Liu, Feng Wang, Ziyong Sun,

https://doi.org/10.18632/aging.103208 pp 9328—9343

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Tang G, Yuan X, Luo Y, Lin Q, Chen Z, Xing X, Song H, Wu S, Hou H, Yu J, Mao L, Liu W, Wang F, et al, . Establishing immune scoring model based on combination of the number, function, and phenotype of lymphocytes. . 12:9328-9343. https://doi.org/10.18632/aging.103208

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                TY  - JOUR
                AU  - Tang, Guoxing 
                AU  - Yuan, Xu 
                AU  - Luo, Ying 
                AU  - Lin, Qun 
                AU  - Chen, Zhishui 
                AU  - Xing, Xue 
                AU  - Song, Huijuan 
                AU  - Wu, Shiji 
                AU  - Hou, Hongyan 
                AU  - Yu, Jing 
                AU  - Mao, Liyan 
                AU  - Liu, Weiyong 
                AU  - Wang, Feng 
                AU  - Sun, Ziyong 
                TI  - Establishing immune scoring model based on combination of the number, function, and phenotype of lymphocytes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103208
                DO  - 10.18632/aging.103208
                SP  - 9328
                EP  - 9343
                PY  - 
                AB  - Background: Quantitatively assessing host immunity remains a challenge in clinical practice.Results: Most parameters in lymphocyte number, function and phenotype were correlated with age. The reference ranges of these parameters were established in four age groups (children, adolescents, adults, and elders). The numbers of CD4+ T cells, CD8+ T cells, B cells, but not NK cells, were negatively correlated with age. However, the function of CD4+ T cells, CD8+ T cells and NK cells was positively correlated with age. The expression of CD28 on T cells gradually decreased with increasing age and was negatively correlated with their function. An opposite phenomenon was observed in the expressions of HLA-DR and CD45RO on T cells. An immune scoring model was established by using 8 parameters (CD4+ T cell number &#xD7; function, CD28+CD4+ T cell number, HLA-DR+CD4+ T cell number, CD45RO+CD4+ T cell number, CD8+ T cell number &#xD7; function, CD28+CD8+ T cell number, HLA-DR+CD8+ T cell number, NK cell number &#xD7; function) from the results of lymphocyte number, function, and phenotype. This immune scoring model showed sensitivities of 70% and 71.4% in determining hyper-immune and hypo-immune status, respectively.Conclusions: An immune scoring model based on combination of lymphocyte number, function, and phenotype shows potential value in quantitatively assessing host immunity.Methods: 261 healthy individuals aged 1 to 82 years were recruited from Tongji Hospital. The number, function, and phenotype of CD4+ T cells, CD8+ T cells and NK cells were simultaneously determined.
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Body mass index across adult life and cognitive function in the American elderly

Yun Zhou, Tao Zhang, Daniel Lee, Lin Yang, Shengxu Li,

https://doi.org/10.18632/aging.103209 pp 9344—9353

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Zhou Y, Zhang T, Lee D, Yang L, Li S, . Body mass index across adult life and cognitive function in the American elderly. . 12:9344-9353. https://doi.org/10.18632/aging.103209

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                TY  - JOUR
                AU  - Zhou, Yun 
                AU  - Zhang, Tao 
                AU  - Lee, Daniel 
                AU  - Yang, Lin 
                AU  - Li, Shengxu 
                TI  - Body mass index across adult life and cognitive function in the American elderly
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103209
                DO  - 10.18632/aging.103209
                SP  - 9344
                EP  - 9353
                PY  - 
                AB  - This study aimed to examine the associations of body mass index (BMI) across adult life with cognitive function in 2,637 participants aged 60 years or over from NHANES 2011-2014. The primary outcome was a composite score based on test scores on word list learning, animal naming, and digit symbol substitution. Exposures of interest included BMI at age 25, BMI 10 years before the survey, BMI at the survey (current BMI), and BMI burden calculated from age 25 to age at survey. BMI at age 25 was inversely associated with the composite score (&#x3B2;=-0.0271&#xB1;0.0130 per kg/m2, P=0.038) and positively with low cognitive performance (odd ratio=1.04, 95% confidence interval: 1.01-1.07, P=0.010), defined as below 20 percentile of the composite score. Similar results were observed for BMI 10 years before the survey and BMI burden. Current BMI was positively associated with the composite score (&#x3B2;=0.0369&#xB1;0.0113, P=0.001) and inversely associated with low cognitive performance (odd ratio=0.96, 95% confidence interval: 0.94-0.99, P=0.004). In conclusion, high BMI in early adult life is associated with low cognitive function in late life, which underscores the importance of a healthy body weight across the life course. The association between BMI and cognitive function at late life requires further investigation.
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Efficacies of different ovarian hyperstimulation protocols in poor ovarian responders classified by the POSEIDON criteria

Fei Li, Tian Ye, Huijuan Kong, Jing Li, Linli Hu, HaiXia Jin, Yingchun Su, Gang Li,

https://doi.org/10.18632/aging.103210 pp 9354—9364

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Li F, Ye T, Kong H, Li J, Hu L, Jin H, Su Y, Li G, . Efficacies of different ovarian hyperstimulation protocols in poor ovarian responders classified by the POSEIDON criteria. . 12:9354-9364. https://doi.org/10.18632/aging.103210

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                TY  - JOUR
                AU  - Li, Fei 
                AU  - Ye, Tian 
                AU  - Kong, Huijuan 
                AU  - Li, Jing 
                AU  - Hu, Linli 
                AU  - Jin, HaiXia 
                AU  - Su, Yingchun 
                AU  - Li, Gang 
                TI  - Efficacies of different ovarian hyperstimulation protocols in poor ovarian responders classified by the POSEIDON criteria
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103210
                DO  - 10.18632/aging.103210
                SP  - 9354
                EP  - 9364
                PY  - 
                AB  - We retrospectively analyzed clinical data from 45,912 in vitro fertilization/intracytoplasmic sperm injection cycles in our reproductive medical center. We compared the clinical outcomes of three different ovarian hyperstimulation protocols in poor ovarian responders (classified by the POSEIDON criteria) to determine the most effective protocol for each POSEIDON group. In POSEIDON groups 1 and 3, the early-follicular-phase long-acting GnRH-agonist long (EFLL) protocol was associated with higher pregnancy rates per transfer and higher live birth rates than the mid-luteal-phase short-acting GnRH-agonist long (MLSL) and GnRH-antagonist protocols. We also examined the relationship between advanced age and reproductive outcomes, and observed a negative correlation between age and live birth rate for each protocol (EFLL: OR = 0.890, 95% CI: 0.870 - 0.911, P &lt; 0.001; MLSL: OR = 0.907, 95% CI: 0.885 - 0.926, P &lt; 0.001; GnRH-antagonist: OR = 0.891, 95% CI: 0.857 - 0.926, P &lt; 0.001). In terms of clinical outcomes, EFLL was the most effective protocol for young poor ovarian responders. However, there were no differences in the implantation rates, clinical pregnancy rates, or live birth rates among the protocols in older patients. Age is thus the most important determinant of oocyte quality, embryo ploidy, and delivery rate.
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Association of cerebrospinal fluid neurogranin levels with cognition and neurodegeneration in Alzheimer’s disease

Mei Xue, Fu-Rong Sun, Ya-Nan Ou, Xue-Ning Shen, Hong-Qi Li, Yu-Yuan Huang, Qiang Dong, Lan Tan, Jin-Tai Yu, Alzheimer’s Disease Neuroimaging Initiative,

https://doi.org/10.18632/aging.103211 pp 9365—9379

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Xue M, Sun F, Ou Y, Shen X, Li H, Huang Y, Dong Q, Tan L, Yu J, , . Association of cerebrospinal fluid neurogranin levels with cognition and neurodegeneration in Alzheimer’s disease. . 12:9365-9379. https://doi.org/10.18632/aging.103211

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                TY  - JOUR
                AU  - Xue, Mei 
                AU  - Sun, Fu-Rong 
                AU  - Ou, Ya-Nan 
                AU  - Shen, Xue-Ning 
                AU  - Li, Hong-Qi 
                AU  - Huang, Yu-Yuan 
                AU  - Dong, Qiang 
                AU  - Tan, Lan 
                AU  - Yu, Jin-Tai 
                AU  - ,  
                TI  - Association of cerebrospinal fluid neurogranin levels with cognition and neurodegeneration in Alzheimer’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103211
                DO  - 10.18632/aging.103211
                SP  - 9365
                EP  - 9379
                PY  - 
                AB  - Accumulating data suggest cerebrospinal fluid (CSF) neurogranin (Ng) as a potential biomarker for cognitive decline and neurodegeneration in Alzheimer disease (AD). To investigate whether the CSF Ng can be used for diagnosis, prognosis, and monitoring of AD, we examined 111 cognitively normal (CN) controls, 193 mild cognitive impairment (MCI) patients and 95 AD patients in the Alzheimer&#x2019;s Disease Neuroimaging Initiative (ADNI) cohort. Correlations were tested between baseline CSF Ng levels and baseline core AD biomarkers and longitudinal glucose metabolism, brain atrophy and cognitive decline. We detected that CSF Ng levels increased with disease severity, and correlated with phosphorylated tau and total tau levels within each diagnostic group. High baseline CSF Ng levels correlated with longitudinal reductions in cortical glucose metabolism within each diagnostic group and hippocampal volume within MCI group during follow-up. In addition, high baseline CSF Ng levels correlated with cognitive decline as reflected by decreased cognitive scale scores. The CSF Ng levels predicted future cognitive impairment (adjusted hazard ratio:3.66, 95%CI: 1.74-7.70, P = 0.001) in CN controls. These data demonstrate that CSF Ng offers diagnostic utility for AD and predicts future cognitive impairment in CN individuals and, therefore, may be a useful addition to the current AD biomarkers.
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Prognostic value of microRNAs in pancreatic cancer: a meta-analysis

Fei Zhao, Chao Wei, Meng-Ying Cui, Qiang-Qiang Xia, Shuai-Bin Wang, Yue Zhang,

https://doi.org/10.18632/aging.103214 pp 9380—9404

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Zhao F, Wei C, Cui M, Xia Q, Wang S, Zhang Y, . Prognostic value of microRNAs in pancreatic cancer: a meta-analysis. . 12:9380-9404. https://doi.org/10.18632/aging.103214

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                TY  - JOUR
                AU  - Zhao, Fei 
                AU  - Wei, Chao 
                AU  - Cui, Meng-Ying 
                AU  - Xia, Qiang-Qiang 
                AU  - Wang, Shuai-Bin 
                AU  - Zhang, Yue 
                TI  - Prognostic value of microRNAs in pancreatic cancer: a meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103214
                DO  - 10.18632/aging.103214
                SP  - 9380
                EP  - 9404
                PY  - 
                AB  - Background: The prognostic impact of microRNA (miRNA) expression levels in pancreatic cancer (PC) has been estimated for years, but the outcomes are controversial and heterogeneous. Therefore, we comprehensively reviewed the evidence collected on miRNA expression in PC to determine this effect.Results: PC patients with high miR-21 (HR=2.61, 95%CI=1.68-4.04), miR-451a (HR=2.23, 95%CI=1.23-4.04) or miR-1290 (HR=1.43, 95%CI=1.04-1.95) levels in blood had significantly poorer OS (P&lt;0.05). Furthermore, PC patients with high miR-10b (HR=1.73, 95%CI=1.09-2.76), miR-17-5p (HR=1.91, 95%CI=1.30-2.80), miR-21 (HR=1.90, 95%CI=1.61-2.25), miR-23a (HR=2.18, 95%CI=1.52-3.13), miR-155 (HR=2.22, 95%CI=1.27-3.88), miR-203 (HR=1.65, 95%CI=1.14-2.40), miR-221 (HR=1.72, 95%CI=1.08-2.74), miR-222 levels (HR=1.72, 95%CI=1.02-2.91) or low miR-29c (HR=1.39, 95%CI=1.08-1.79), miR-126 (HR=1.55, 95%CI=1.23-1.95), miR-218 (HR=2.62, 95%CI=1.41-4.88) levels in tissues had significantly shorter OS (P&lt;0.05).Conclusions: In summary, blood miR-21, miR-451a, miR-1290 and tissue miR-10b, miR-17-5p, miR-21, miR-23a, miR-29c, miR-126, miR-155, miR-203, miR-218, miR-221, miR-222 had significant prognostic value.Methods: We searched PubMed, EMBASE, Web of Science and Cochrane Database of Systematic Reviews to recognize eligible studies, and 57 studies comprising 5445 PC patients and 15 miRNAs were included to evaluate the associations between miRNA expression levels and overall survival (OS) up to June 1, 2019. Summary hazard ratios (HR) with 95% confidence intervals (CI) were calculated to assess the effect.
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Salidroside ameliorates Parkinson's disease by inhibiting NLRP3-dependent pyroptosis

Xue Zhang, Yiming Zhang, Rui Li, Lingpeng Zhu, Buqing Fu, Tianhua Yan,

https://doi.org/10.18632/aging.103215 pp 9405—9426

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Zhang X, Zhang Y, Li R, Zhu L, Fu B, Yan T, . Salidroside ameliorates Parkinson's disease by inhibiting NLRP3-dependent pyroptosis. . 12:9405-9426. https://doi.org/10.18632/aging.103215

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                TY  - JOUR
                AU  - Zhang, Xue 
                AU  - Zhang, Yiming 
                AU  - Li, Rui 
                AU  - Zhu, Lingpeng 
                AU  - Fu, Buqing 
                AU  - Yan, Tianhua 
                TI  - Salidroside ameliorates Parkinson's disease by inhibiting NLRP3-dependent pyroptosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103215
                DO  - 10.18632/aging.103215
                SP  - 9405
                EP  - 9426
                PY  - 
                AB  - Parkinson&apos;s disease (PD) is a common age-related neurodegenerative movement disorder, which is mainly due to the loss of dopaminergic neurons. Pyroptosis is a new programmed cell death characterized by NLR Family Pyrin Domain Containing 3 (NLRP3)-dependent, IL-1&#x3B2;, IL-18 and Gasdermin D. Salidroside (Sal) has been reported to have neuro-protective effect. However, the roles of pyroptosis and Sal on anti-pyroptosis in PD have not been elucidated. In this study, we tested underlying mechanisms of pyroptosis in PD and neuro-protective effects of Sal. We established 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced C57BL/6J mice and C57BL/10ScNJ (TLR4-deficient mice) in vivo, MPTP-induced PC-12 and LPS-induced BV2 in vitro. We found that Sal could ameliorate MPTP-induced PD symptoms and reduce the levels of IL-1&#x3B2;, IL-18 and Gasdermin D, which are main hallmarks of pyroptosis. Further study indicated that Sal alleviated PD through inhibiting NLRP3-dependent pyroptosis. In conclusion, pyroptosis plays a key role in PD and Sal protects dopaminergic neurons by inhibiting NLRP3-dependent pyroptosis through: (1) indirectly reducing the production of NLRP3, pro-IL-1&#x3B2; and pro-IL-18 by inhibiting TLR4/MyD88/NF-&#x3BA;B signaling pathways, (2) directly suppressing pyroptosis through inhibiting TXNIP/NLRP3/caspase-1 signaling pathways. These results indicated that inhibiting pyroptosis or administration of Sal could be a novel therapeutic strategy for PD.
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Development of a nomogram that predicts the risk for coronary atherosclerotic heart disease

Shuna Huang, Xiaoxu Xie, Yi Sun, Tingxing Zhang, Yingying Cai, Xingyan Xu, Huangyuan Li, Siying Wu,

https://doi.org/10.18632/aging.103216 pp 9427—9439

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Huang S, Xie X, Sun Y, Zhang T, Cai Y, Xu X, Li H, Wu S, . Development of a nomogram that predicts the risk for coronary atherosclerotic heart disease. . 12:9427-9439. https://doi.org/10.18632/aging.103216

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                TY  - JOUR
                AU  - Huang, Shuna 
                AU  - Xie, Xiaoxu 
                AU  - Sun, Yi 
                AU  - Zhang, Tingxing 
                AU  - Cai, Yingying 
                AU  - Xu, Xingyan 
                AU  - Li, Huangyuan 
                AU  - Wu, Siying 
                TI  - Development of a nomogram that predicts the risk for coronary atherosclerotic heart disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103216
                DO  - 10.18632/aging.103216
                SP  - 9427
                EP  - 9439
                PY  - 
                AB  - Studies seldom combine biological, behavioral and psychological factors to estimate coronary atherosclerotic heart disease (CHD) risk. Here, we evaluated the associations between these factors and CHD to develop a predictive nomogram to identify those at high risk of CHD. This case-control study included 4392 participants (1578 CHD cases and 2814 controls) in southeast China. Thirty-three biological, behavioral and psychological variables were evaluated. Following multivariate logistic regression analysis, which revealed eight risk factors associated with CHD, a predictive nomogram was developed based on a final model that included the three non-modifiable (sex, age and family history of CHD) and five modifiable (hypertension, hyperlipidemia, diabetes, recent experience of a major traumatic event, and anxiety) variables. The higher total nomogram score, the greater the CHD risk. Final model accuracy (as estimated from the area under the receiver operating characteristic curve) was 0.726 (95% confidence interval: 0.709-0.747). Validation analysis confirmed the high accuracy of the nomogram. High risk of CHD was associated with several biological, behavioral and psychological factors. We have thus developed an intuitive nomogram that could facilitate development of preliminary prevention strategies for CHD.
                ER  -

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Effects of passive smoking and its duration on the prevalence of prediabetes and type 2 diabetes mellitus in Chinese women

Juan Wu, Gui Pan, Yan-Ting Huang, Deng-Ke Liu, Hai-Xia Zeng, Xiao-Jun Zhou, Xiao-Yang Lai, Jian-Ping Liu,

https://doi.org/10.18632/aging.103217 pp 9440—9446

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Wu J, Pan G, Huang Y, Liu D, Zeng H, Zhou X, Lai X, Liu J, . Effects of passive smoking and its duration on the prevalence of prediabetes and type 2 diabetes mellitus in Chinese women. . 12:9440-9446. https://doi.org/10.18632/aging.103217

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                TY  - JOUR
                AU  - Wu, Juan 
                AU  - Pan, Gui 
                AU  - Huang, Yan-Ting 
                AU  - Liu, Deng-Ke 
                AU  - Zeng, Hai-Xia 
                AU  - Zhou, Xiao-Jun 
                AU  - Lai, Xiao-Yang 
                AU  - Liu, Jian-Ping 
                TI  - Effects of passive smoking and its duration on the prevalence of prediabetes and type 2 diabetes mellitus in Chinese women
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103217
                DO  - 10.18632/aging.103217
                SP  - 9440
                EP  - 9446
                PY  - 
                AB  - Several studies have shown that active smoking is a risk factor for type 2 diabetes mellitus (T2DM). However, the effects of passive smoking on T2DM remains unknown. In this study, we investigated the effects of passive smoking and its duration on the prevalence of prediabetes and T2DM. According to passive smoking status, participants were divided into Group A (passive smokers) and Group B (controls). Furthermore, Group A was divided into three subgroups according to the duration of passive smoking: Group A1 (&#x2264;10 years), Group A2 (10&#x2013;20 years), and Group A3 (&gt;20 years). We found that the prevalence of impaired glucose tolerance (IGT) in Group A (26.6%), Group A2 (28%), and Group A3 (37.8%) was significantly higher than that in Group B (19.6%), and the prevalence gradually increased with an increase in the duration of passive smoking. Multiple logistic regression analysis showed that passive smoking for &gt;10 years was a risk factor for impaired fasting glucose (IFG), IGT, and T2DM. Therefore, passive smoking not only increases the prevalence of IGT in a time-dependent manner, but also a risk factor for IFG, IGT, and T2DM when its duration is over 10 years.
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Resistance training increases muscle NAD⁺ and NADH concentrations as well as NAMPT protein levels and global sirtuin activity in middle-aged, overweight, untrained individuals

Donald A. Lamb, Johnathon H. Moore, Paulo Henrique Caldeira Mesquita, Morgan A. Smith, Christopher G. Vann, Shelby C. Osburn, Carlton D. Fox, Hector L. Lopez, Tim N. Ziegenfuss, Kevin W. Huggins, Michael D. Goodlett, Andrew D. Fruge, Andreas N. Kavazis, Kaelin C. Young, Michael D. Roberts,

https://doi.org/10.18632/aging.103218 pp 9447—9460

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Lamb DA, Moore JH, Mesquita PHC, Smith MA, Vann CG, Osburn SC, Fox CD, Lopez HL, Ziegenfuss TN, Huggins KW, Goodlett MD, Fruge AD, Kavazis AN, et al, . Resistance training increases muscle NAD⁺ and NADH concentrations as well as NAMPT protein levels and global sirtuin activity in middle-aged, overweight, untrained individuals. . 12:9447-9460. https://doi.org/10.18632/aging.103218

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Provider: 
 TY - JOUR
 AU - Lamb, Donald A. 
 AU - Moore, Johnathon H. 
 AU - Mesquita, Paulo Henrique Caldeira 
 AU - Smith, Morgan A. 
 AU - Vann, Christopher G. 
 AU - Osburn, Shelby C. 
 AU - Fox, Carlton D. 
 AU - Lopez, Hector L. 
 AU - Ziegenfuss, Tim N. 
 AU - Huggins, Kevin W. 
 AU - Goodlett, Michael D. 
 AU - Fruge, Andrew D. 
 AU - Kavazis, Andreas N. 
 AU - Young, Kaelin C. 
 AU - Roberts, Michael D. 
 TI - Resistance training increases muscle NAD+ and NADH concentrations as well as NAMPT protein levels and global sirtuin activity in middle-aged, overweight, untrained individuals
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103218
 DO - 10.18632/aging.103218
 SP - 9447
 EP - 9460
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Lamb, Donald A. 
 AU - Moore, Johnathon H. 
 AU - Mesquita, Paulo Henrique Caldeira 
 AU - Smith, Morgan A. 
 AU - Vann, Christopher G. 
 AU - Osburn, Shelby C. 
 AU - Fox, Carlton D. 
 AU - Lopez, Hector L. 
 AU - Ziegenfuss, Tim N. 
 AU - Huggins, Kevin W. 
 AU - Goodlett, Michael D. 
 AU - Fruge, Andrew D. 
 AU - Kavazis, Andreas N. 
 AU - Young, Kaelin C. 
 AU - Roberts, Michael D. 
 TI - Resistance training increases muscle NAD+ and NADH concentrations as well as NAMPT protein levels and global sirtuin activity in middle-aged, overweight, untrained individuals
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103218
 DO - 10.18632/aging.103218
 SP - 9447
 EP - 9460
 PY - 
 AB - We examined if resistance training affected muscle NAD+ and NADH concentrations as well as nicotinamide phosphoribosyltransferase (NAMPT) protein levels and sirtuin (SIRT) activity markers in middle-aged, untrained (MA) individuals. MA participants (59&#xB1;4 years old; n=16) completed 10 weeks of full-body resistance training (2 d/wk). Body composition, knee extensor strength, and vastus lateralis muscle biopsies were obtained prior to training (Pre) and 72 hours following the last training bout (Post). Data from trained college-aged men (22&#xB1;3 years old, training age: 6&#xB1;2 years old; n=15) were also obtained for comparative purposes. Muscle NAD+ (+127%, p&lt;0.001), NADH (+99%, p=0.002), global SIRT activity (+13%, p=0.036), and NAMPT protein (+15%, p=0.014) increased from Pre to Post in MA participants. Additionally, Pre muscle NAD+ and NADH in MA participants were lower than college-aged participants (p&lt;0.05), whereas Post values were similar between cohorts (p&gt;0.10). Interestingly, muscle citrate synthase activity levels (i.e., mitochondrial density) increased in MA participants from Pre to Post (+183%, p&lt;0.001), and this increase was significantly associated with increases in muscle NAD+ (r2=0.592, p=0.001). In summary, muscle NAD+, NADH, and global SIRT activity are positively affected by resistance training in middle-aged, untrained individuals. Whether these adaptations facilitated mitochondrial biogenesis remains to be determined.
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Regulation of PGC-1α mediated by acetylation and phosphorylation in MPP+ induced cell model of Parkinson’s disease

Fei Fan, Songlin Li, Zhipeng Wen, Qiaoyue Ye, Xiaochun Chen, Qinyong Ye,

https://doi.org/10.18632/aging.103219 pp 9461—9474

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Fan F, Li S, Wen Z, Ye Q, Chen X, Ye Q, . Regulation of PGC-1α mediated by acetylation and phosphorylation in MPP+ induced cell model of Parkinson’s disease. . 12:9461-9474. https://doi.org/10.18632/aging.103219

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                TY  - JOUR
                AU  - Fan, Fei 
                AU  - Li, Songlin 
                AU  - Wen, Zhipeng 
                AU  - Ye, Qiaoyue 
                AU  - Chen, Xiaochun 
                AU  - Ye, Qinyong 
                TI  - Regulation of PGC-1α mediated by acetylation and phosphorylation in MPP+ induced cell model of Parkinson’s disease
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103219
                DO  - 10.18632/aging.103219
                SP  - 9461
                EP  - 9474
                PY  - 
                AB  - Background: Parkinson&#x2019;s disease (PD) is one of the most common neurodegenerative diseases with complex etiology in sporadic cases. Accumulating evidence suggests that oxidative stress and defects in mitochondrial dynamics are associated with the pathogenesis of PD. The oxidative stress and mitochondrial dynamics are regulated strictly by peroxisome proliferator-activated receptor &#x3B3; coactivator-1&#x3B1; (PGC-1&#x3B1;). We investigated whether acetylation and phosphorylation of PGC-1&#x3B1; contribute to protecting neuronal cell against oxidative stress.Results: We found that acetylation and phosphorylation mediated the nuclear translocation of PGC-1&#x3B1; protects against oxidative damage. In contrast to the increased nuclear PGC-1&#x3B1;, the cytosolic PGC-1&#x3B1; was decreased upon inhibition of GCN5 acetyltransferase. Similarly to the inhibition of GCN5 acetyltransferase, the increased nuclear PGC-1&#x3B1; and the decreased cytosolic PGC-1&#x3B1; were observed upon p38MAPK and AMPK activation. Briefly, the significantly increased nuclear PGC-1&#x3B1; is regulated either by inhibiting the acetylation of PGC-1&#x3B1; or by the phosphorylating PGC-1&#x3B1;, which results in a reduction in ROS.Conclusion: PGC-1&#x3B1; protects neuronal cells against MPP+-induced toxicity partially through the acetylation of PGC-1&#x3B1; mediated by GCN5, and mostly through the phosphorylation PGC-1&#x3B1; mediated by p38MAPK or AMPK. Therapeutic reagents activating PGC-1&#x3B1; may be valuable for preventing mitochondrial dysfunction in PD by against oxidative damage.Methods: With established the 1-methyl-4-phenylpyridinium (MPP+)-induced cell model of PD, the effects of MPP+ and experimental reagents on the cell viability was investigated. The expression of PGC-1&#x3B1;, general control of nucleotide synthesis 5 (GCN5), p38 mitogen-activated protein kinase (p38MAPK) and adenosine monophosphate activated protein kinase (AMPK) were detected by Western blotting and quantitative real-time PCR. The level of reactive oxygen species (ROS) was measured by flow cytometry. All statistical analyses were carried out using one-way ANOVA.
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Amphiregulin promotes cisplatin chemoresistance by upregulating ABCB1 expression in human chondrosarcoma

Yu-Wen Huang, Chih-Yang Lin, Hsiao-Chi Tsai, Yi-Chin Fong, Chien-Kuo Han, Yuan-Li Huang, Wen-Tung Wu, Shih-Ping Cheng, Hao-Chiun Chang, Kuang-Wen Liao, Shih-Wei Wang, Chih-Hsin Tang,

https://doi.org/10.18632/aging.103220 pp 9475—9488

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Huang Y, Lin C, Tsai H, Fong Y, Han C, Huang Y, Wu W, Cheng S, Chang H, Liao K, Wang S, Tang C, . Amphiregulin promotes cisplatin chemoresistance by upregulating ABCB1 expression in human chondrosarcoma. . 12:9475-9488. https://doi.org/10.18632/aging.103220

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                TY  - JOUR
                AU  - Huang, Yu-Wen 
                AU  - Lin, Chih-Yang 
                AU  - Tsai, Hsiao-Chi 
                AU  - Fong, Yi-Chin 
                AU  - Han, Chien-Kuo 
                AU  - Huang, Yuan-Li 
                AU  - Wu, Wen-Tung 
                AU  - Cheng, Shih-Ping 
                AU  - Chang, Hao-Chiun 
                AU  - Liao, Kuang-Wen 
                AU  - Wang, Shih-Wei 
                AU  - Tang, Chih-Hsin 
                TI  - Amphiregulin promotes cisplatin chemoresistance by upregulating ABCB1 expression in human chondrosarcoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103220
                DO  - 10.18632/aging.103220
                SP  - 9475
                EP  - 9488
                PY  - 
                AB  - Chondrosarcomas are well known for their resistance to chemotherapeutic agents, including cisplatin, which is commonly used in chondrosarcomas. Amphiregulin (AR), a ligand of epidermal growth factor receptor (EGFR), plays an important role in drug resistance. We therefore sought to determine the role of AR in cisplatin chemoresistance. We found that AR inhibits cisplatin-induced cell apoptosis and promotes ATP-binding cassette subfamily B member 1 (ABCB1) expression, while knockdown of ABCB1 by small interfering RNA (siRNA) reverses these effects. High phosphoinositide 3-kinase (PI3K), Akt and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-&#x3BA;B) phosphorylation levels were observed in cisplatin-resistant cells. Pretreating chondrosarcoma cells with PI3K, Akt and NF-&#x3BA;B inhibitors or transfecting the cells with p85, Akt and p65 siRNAs potentiated cisplatin-induced cytotoxicity. In a mouse xenograft model, knockdown of AR expression in chondrosarcoma cells increased the cytotoxic effects of cisplatin and also decreased tumor volume and weight. These results indicate that AR upregulates ABCB1 expression through the PI3K/Akt/NF-&#x3BA;B signaling pathway and thus contributes to cisplatin resistance in chondrosarcoma.
                ER  -

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PI3K-Akt-mTOR inhibition by GNE-477 inhibits renal cell carcinoma cell growth in vitro and in vivo

Xueting Ye, Jian-Wei Ruan, Hang Huang, Wei-Ping Huang, Yan Zhang, Fangyi Zhang,

https://doi.org/10.18632/aging.103221 pp 9489—9499

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Ye X, Ruan J, Huang H, Huang W, Zhang Y, Zhang F, . PI3K-Akt-mTOR inhibition by GNE-477 inhibits renal cell carcinoma cell growth in vitro and in vivo. . 12:9489-9499. https://doi.org/10.18632/aging.103221

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Provider: 
 TY - JOUR
 AU - Ye, Xueting 
 AU - Ruan, Jian-Wei 
 AU - Huang, Hang 
 AU - Huang, Wei-Ping 
 AU - Zhang, Yan 
 AU - Zhang, Fangyi 
 TI - PI3K-Akt-mTOR inhibition by GNE-477 inhibits renal cell carcinoma cell growth in vitro and in vivo
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103221
 DO - 10.18632/aging.103221
 SP - 9489
 EP - 9499
 PY - 
 AB - Sustained activation of PI3K-Akt-mTOR cascade is important for renal cell carcinoma (RCC) cell progression. GNE-477 is a novel and efficacious PI3K-mTOR dual inhibitor. The current study tested its anti-RCC cell activity. In the primary cultured human RCC cells, GNE-477 potently inhibited cell growth, viability and proliferation, as well as cell cycle progression, migration and invasion. Furthermore, it induced robust apoptosis activation in primary RCC cells, but being non-cytotoxic to HK-2 epithelial cells and primary human renal epithelial cells. In the primary RCC cells GNE-477 inactivated PI3K-Akt-mTOR cascade by blocking phosphorylation of p85, Akt1, p70S6K1 and S6. Restoring Akt-mTOR activation by a constitutively-active Akt1 reversed GNE-477-induced anti-RCC cell activity. In nude mice intraperitoneal injection of GNE-477 potently suppressed RCC xenograft tumor growth. Collectively, targeting PI3K-Akt-mTOR cascade by GNE-477 inhibits RCC cell growth in vitro and in vivo.
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MiR-16-5p regulates postmenopausal osteoporosis by directly targeting VEGFA

Tao Yu, Xiaomeng You, Haichao Zhou, Wenbao He, Zihua Li, Bing Li, Jiang Xia, Hui Zhu, Youguang Zhao, Guangrong Yu, Yuan Xiong, Yunfeng Yang,

https://doi.org/10.18632/aging.103223 pp 9500—9514

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Yu T, You X, Zhou H, He W, Li Z, Li B, Xia J, Zhu H, Zhao Y, Yu G, Xiong Y, Yang Y, . MiR-16-5p regulates postmenopausal osteoporosis by directly targeting VEGFA. . 12:9500-9514. https://doi.org/10.18632/aging.103223

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                TY  - JOUR
                AU  - Yu, Tao 
                AU  - You, Xiaomeng 
                AU  - Zhou, Haichao 
                AU  - He, Wenbao 
                AU  - Li, Zihua 
                AU  - Li, Bing 
                AU  - Xia, Jiang 
                AU  - Zhu, Hui 
                AU  - Zhao, Youguang 
                AU  - Yu, Guangrong 
                AU  - Xiong, Yuan 
                AU  - Yang, Yunfeng 
                TI  - MiR-16-5p regulates postmenopausal osteoporosis by directly targeting VEGFA
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103223
                DO  - 10.18632/aging.103223
                SP  - 9500
                EP  - 9514
                PY  - 
                AB  - In this study, we used bioinformatics tools, and experiments with patient tissues and human mesenchymal stem cells (hMSCs) to identify differentially regulated genes (DEGs) and microRNAs (miRNAs) that promote postmenopausal osteoporosis. By analyzing the GSE56815 dataset from the NCBI GEO database, we identified 638 DEGs, including 371 upregulated and 267 downregulated genes, in postmenopausal women with low bone density. Enrichment and protein-protein interaction network analyses showed that TP53, RPS27A, and VEGFA were the top three hub genes with the highest degree of betweenness and closeness centrality. TargetScanHuman and DIANA software analyses and dual luciferase reporter assays confirmed that miR-16a-5p directly targets the 3&#x2019;UTR of VEGFA. Postmenopausal patients with osteoporosis showed higher miR-16-5p and lower VEGFA levels than those without osteoporosis (n=10 each). VEGFA levels were higher in miR-16-5p knockdown hMSCs and were reduced in miR-16-5p-overexpressing hMSCs. mRNA expression of osteogenic markers, ALP, OCN, and RUNX2, as well as calcium deposition based on Alizarin red staining, correlated inversely with miR-16-5p levels and correlated positively with VEGFA levels. These findings suggest that miR-16-5p suppresses osteogenesis by inhibiting VEGFA expression and is a promising target for postmenopausal osteoporosis therapy.
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Clioquinol improves motor and non-motor deficits in MPTP-induced monkey model of Parkinson’s disease through AKT/mTOR pathway

Liangqin Shi, Chao Huang, Qihui Luo, Yu Xia, Wentao Liu, Wen Zeng, Anchun Cheng, Riyi Shi, Chen Zhengli,

https://doi.org/10.18632/aging.103225 pp 9515—9533

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Shi L, Huang C, Luo Q, Xia Y, Liu W, Zeng W, Cheng A, Shi R, Zhengli C, . Clioquinol improves motor and non-motor deficits in MPTP-induced monkey model of Parkinson’s disease through AKT/mTOR pathway. . 12:9515-9533. https://doi.org/10.18632/aging.103225

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                TY  - JOUR
                AU  - Shi, Liangqin 
                AU  - Huang, Chao 
                AU  - Luo, Qihui 
                AU  - Xia, Yu 
                AU  - Liu, Wentao 
                AU  - Zeng, Wen 
                AU  - Cheng, Anchun 
                AU  - Shi, Riyi 
                AU  - Zhengli, Chen 
                TI  - Clioquinol improves motor and non-motor deficits in MPTP-induced monkey model of Parkinson’s disease through AKT/mTOR pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103225
                DO  - 10.18632/aging.103225
                SP  - 9515
                EP  - 9533
                PY  - 
                AB  - Despite decades of research into the pathology mechanisms of Parkinson&#x2019;s disease (PD), disease-modifying therapy of PD is scarce. Thus, searching for new drugs or more effective neurosurgical treatments has elicited much interest. Clioquinol (CQ) has been shown to have therapeutic benefits in rodent models of neurodegenerative disorders. However, it&#x2019;s neuroprotective role and mechanisms in PD primate models and PD patients, especially in the advanced stages, are not fully understood. Furthermore, issues such as spontaneous recovery of motor function and high symptom variability in different monkeys after the same toxic protocol, has not been resolved before the present study. In this study, we designed a chronic and long-term progressive protocol to generate a stabilized PD monkey model showed with classic motor and non-motor deficits, followed by treatment analysis of CQ. We found that CQ could remarkably improve the motor and non-motor deficits, which were based on the reduction of iron content and ROS level in the SN and further improvement in pathology. Meanwhile, we also showed that ferroptosis was probably involved in the pathogenesis of PD. In addition, the study shows a positive effect of CQ on AKT/mTOR survival pathway and a blocking effect on p53 medicated cell death in vivo and in vitro.
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Dexmedetomidine inhibits LPS-induced proinflammatory responses via suppressing HIF1α-dependent glycolysis in macrophages

Qingyuan Meng, Pinhao Guo, Zhengyu Jiang, Lulong Bo, Jinjun Bian,

https://doi.org/10.18632/aging.103226 pp 9534—9548

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Meng Q, Guo P, Jiang Z, Bo L, Bian J, . Dexmedetomidine inhibits LPS-induced proinflammatory responses via suppressing HIF1α-dependent glycolysis in macrophages. . 12:9534-9548. https://doi.org/10.18632/aging.103226

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                TY  - JOUR
                AU  - Meng, Qingyuan 
                AU  - Guo, Pinhao 
                AU  - Jiang, Zhengyu 
                AU  - Bo, Lulong 
                AU  - Bian, Jinjun 
                TI  - Dexmedetomidine inhibits LPS-induced proinflammatory responses via suppressing HIF1α-dependent glycolysis in macrophages
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103226
                DO  - 10.18632/aging.103226
                SP  - 9534
                EP  - 9548
                PY  - 
                AB  - Dexmedetomidine, a highly selective &#x3B1;2-adrenoceptor agonist, has been reported to exert an anti-inflammatory effect in several animal models, but the mechanism remains unclear. Previous studies have shown that hypoxia inducible factor 1&#x3B1;-induced glycolysis is essential for the activation of inflammatory macrophages. However, whether dexmedetomidine influences hypoxia inducible factor 1&#x3B1;-induced glycolysis and thus exerts an anti-inflammatory effect has been poorly investigated. This study aims to elucidate the anti-inflammatory mechanism of dexmedetomidine involving the hypoxia inducible factor 1&#x3B1;-dependent glycolytic pathway. We showed that dexmedetomidine could suppress lipopolysaccharide-induced inflammatory cytokine production; inhibit the extracellular acidification rate, glucose consumption and lactate production; and decrease the expression of glycolytic genes in macrophages. The enhancement of glycolysis by the granulocyte-macrophage colony-stimulating factor or higher concentration of glucose could reverse the anti-inflammatory effect of dexmedetomidine on lipopolysaccharide-treated macrophages. Moreover, dexmedetomidine significantly inhibited the upregulation of hypoxia inducible factor 1&#x3B1; at the mRNA and protein levels. Genetic inhibition of hypoxia inducible factor 1&#x3B1; expression could reverse the anti-inflammatory effect of dexmedetomidine. Taken together, our results indicate that dexmedetomidine attenuates lipopolysaccharide-induced proinflammatory responses partially by suppressing hypoxia inducible factor 1&#x3B1;-dependent glycolysis in macrophages.
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MiR-1908/EXO1 and MiR-203a/FOS, regulated by scd1, are associated with fracture risk and bone health in postmenopausal diabetic women

Yi-sheng Chen, Xue-ran Kang, Zi-hui Zhou, Jiang Yang, Qi Xin, Chen-ting Ying, Yun-peng Zhang, Jie Tao,

https://doi.org/10.18632/aging.103227 pp 9549—9584

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Chen Y, Kang X, Zhou Z, Yang J, Xin Q, Ying C, Zhang Y, Tao J, . MiR-1908/EXO1 and MiR-203a/FOS, regulated by scd1, are associated with fracture risk and bone health in postmenopausal diabetic women. . 12:9549-9584. https://doi.org/10.18632/aging.103227

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                TY  - JOUR
                AU  - Chen, Yi-sheng 
                AU  - Kang, Xue-ran 
                AU  - Zhou, Zi-hui 
                AU  - Yang, Jiang 
                AU  - Xin, Qi 
                AU  - Ying, Chen-ting 
                AU  - Zhang, Yun-peng 
                AU  - Tao, Jie 
                TI  - MiR-1908/EXO1 and MiR-203a/FOS, regulated by scd1, are associated with fracture risk and bone health in postmenopausal diabetic women
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103227
                DO  - 10.18632/aging.103227
                SP  - 9549
                EP  - 9584
                PY  - 
                AB  - Background: Stearoyl&#x2013;coenzyme A desaturase-1 (SCD1) can inhibit the development of diabetic bone disease by promoting osteogenesis. In this study, we examined whether this regulation by SCD1 is achieved by regulating the expression of related miRNAs.Methods: SCD1 expression levels were observed in human bone-marrow mesenchymal stem cells (BM-MSCs) of patients with type 2 diabetes mellitus (T2DM), and the effect of SCD1 on osteogenesis was observed in human adipose-derived MSCs transfected with the SCD1 lentiviral system. We designed a bioinformatics prediction model to select important differentially expressed miRNAs, and established protein&#x2013;protein interaction and miRNA&#x2013;mRNA networks. miRNAs and mRNAs were extracted and their differential expression was detected. The SCD1&#x2013;miRNA&#x2013;mRNA network was validated.Findings: SCD1 expression in bone marrow was downregulated in patients with T2DM and low-energy fracture, and SCD1 expression promotes BM-MSC osteogenic differentiation. The predictors in the nomogram were seven microRNAs, including hsa-miR-1908 and hsa-miR-203a. SCD1 inhibited the expression of CDKN1A and FOS, but promoted the expression of EXO1 and PLS1. miR-1908 was a regulator of EXO1 expression, and miR-203a was a regulator of FOS expression.Interpretation: The regulation of BM-MSCs by SCD1 is a necessary condition for osteogenesis through the miR-203a/FOS and miR-1908/EXO1 regulatory pathways.
                ER  -

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Attenuation of doxorubicin-induced cardiotoxicity by cryptotanshinone detected through association analysis of transcriptomic profiling and KEGG pathway

Le Li, Bin Wu, Qiangqiang Zhao, Jian Li, Yunfeng Han, Xiaohang Fan, Junli Dong, Pengcheng Li,

https://doi.org/10.18632/aging.103228 pp 9585—9603

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Li L, Wu B, Zhao Q, Li J, Han Y, Fan X, Dong J, Li P, . Attenuation of doxorubicin-induced cardiotoxicity by cryptotanshinone detected through association analysis of transcriptomic profiling and KEGG pathway. . 12:9585-9603. https://doi.org/10.18632/aging.103228

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Provider: 
 TY - JOUR
 AU - Li, Le 
 AU - Wu, Bin 
 AU - Zhao, Qiangqiang 
 AU - Li, Jian 
 AU - Han, Yunfeng 
 AU - Fan, Xiaohang 
 AU - Dong, Junli 
 AU - Li, Pengcheng 
 TI - Attenuation of doxorubicin-induced cardiotoxicity by cryptotanshinone detected through association analysis of transcriptomic profiling and KEGG pathway
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103228
 DO - 10.18632/aging.103228
 SP - 9585
 EP - 9603
 PY - 
 AB - Objective: The cardiotoxicity of doxorubicin (DOX) reduces the quality of life and prognosis of cancer patients, and therefore its clinical application has been largely restricted. This study aimed to assess the effects of cryptotanshione (CPT) on DOX-induced rat cardiac insufficiency.Results: CPT treatment significantly suppressed apoptosis in vitro. The oral administration of CPT significantly improved cardiac function in the rat model, reduced collagen production and suppressed apoptosis and the production of reactive oxygen species in the heart tissue. Transcriptomic profiling and its relevant bioinformatics analysis showed that CPT suppressed doxorubicin-induced cardiotoxicity by inhibiting p53 signaling pathway.Conclusion: Transcriptomic profiling and bioinformatics analysis can be used to evaluate the cardio-protective effect of CPT through inactivating p53 signaling pathway in the doxorubicin-mediated myocardial damage model.Methods: F-actin staining and flow cytometry were used to assess the effects of CPT on cardiomyocytes. In vivo, echocardiography and hemodynamic evaluation were used to assess the effects of CPT on the cardiac dysfunction in rats. Furthermore, transcriptomic profiling and bioinformatics analysis, as well as western blot analysis, were used to determine that CPT induced changes in the signaling pathways in the model.
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KMT2A regulates cervical cancer cell growth through targeting VDAC1

Changlin Zhang, Yijun Hua, Huijuan Qiu, Tianze Liu, Qian Long, Wei Liao, Jiehong Qiu, Nang Wang, Miao Chen, Dingbo Shi, Yue Yan, Chuanbo Xie, Wuguo Deng, Tian Li, Yizhuo Li,

https://doi.org/10.18632/aging.103229 pp 9604—9620

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Zhang C, Hua Y, Qiu H, Liu T, Long Q, Liao W, Qiu J, Wang N, Chen M, Shi D, Yan Y, Xie C, Deng W, et al, . KMT2A regulates cervical cancer cell growth through targeting VDAC1. . 12:9604-9620. https://doi.org/10.18632/aging.103229

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                TY  - JOUR
                AU  - Zhang, Changlin 
                AU  - Hua, Yijun 
                AU  - Qiu, Huijuan 
                AU  - Liu, Tianze 
                AU  - Long, Qian 
                AU  - Liao, Wei 
                AU  - Qiu, Jiehong 
                AU  - Wang, Nang 
                AU  - Chen, Miao 
                AU  - Shi, Dingbo 
                AU  - Yan, Yue 
                AU  - Xie, Chuanbo 
                AU  - Deng, Wuguo 
                AU  - Li, Tian 
                AU  - Li, Yizhuo 
                TI  - KMT2A regulates cervical cancer cell growth through targeting VDAC1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103229
                DO  - 10.18632/aging.103229
                SP  - 9604
                EP  - 9620
                PY  - 
                AB  - Cervical cancer is an aggressive cutaneous malignancy, illuminating the molecular mechanisms of tumorigenesis and discovering novel therapeutic targets are urgently needed. KMT2A is a transcriptional co-activator regulating gene expression during early development and hematopoiesis, but the role of KMT2A in cervical cancer remains unknown. Here, we demonstrated that KMT2A regulated cervical cancer growth via targeting VADC1. Knockdown of KMT2A significantly suppressed cell proliferation and migration and induced apoptosis in cervical cancer cells, accompanying with activation of PARP/caspase pathway and inhibition of VADC1. Overexpression of VDAC1 reversed the KMT2A knockdown-mediated regulation of cell proliferation, migration and apoptosis. The in vivo results from a cervical cancer xenograft mouse model also validated that KMT2A knockdown suppressed tumor growth by inhibiting VDAC1, whereas KMT2A overexpression promoted cervical cancer growth. Moreover, analyses of Biewenga cervix database and clinical samples showed that both KMT2A and VDAC1 were upregulated in cervix squamous cell carcinoma compared with cervix uteri tissues, and their expression was negatively correlated with the differentiation grade of cervical cancer. Our results therefore indicated that the KMT2A/VDAC1 signaling axis may be a potential new mechanism of cervical carcinogenesis.
                ER  -

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Pyrrolo [3,4-b]-quinolin-9-amine compound FZU-0038-056 suppresses triple-negative breast cancer partially through inhibiting the expression of Bcl-2

Danping Wang, Zhi Nie, Xiaoyan Jiang, Jinxiang Ye, Zhimin Wei, Dating Cheng, Chenyang Wang, Yingying Wu, Rong Liu, Haijun Chen, Ceshi Chen, Chunyan Wang,

https://doi.org/10.18632/aging.103232 pp 9621—9632

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Wang D, Nie Z, Jiang X, Ye J, Wei Z, Cheng D, Wang C, Wu Y, Liu R, Chen H, Chen C, Wang C, . Pyrrolo [3,4-b]-quinolin-9-amine compound FZU-0038-056 suppresses triple-negative breast cancer partially through inhibiting the expression of Bcl-2. . 12:9621-9632. https://doi.org/10.18632/aging.103232

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Provider: 
 TY - JOUR
 AU - Wang, Danping 
 AU - Nie, Zhi 
 AU - Jiang, Xiaoyan 
 AU - Ye, Jinxiang 
 AU - Wei, Zhimin 
 AU - Cheng, Dating 
 AU - Wang, Chenyang 
 AU - Wu, Yingying 
 AU - Liu, Rong 
 AU - Chen, Haijun 
 AU - Chen, Ceshi 
 AU - Wang, Chunyan 
 TI - Pyrrolo [3,4-b]-quinolin-9-amine compound FZU-0038-056 suppresses triple-negative breast cancer partially through inhibiting the expression of Bcl-2
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103232
 DO - 10.18632/aging.103232
 SP - 9621
 EP - 9632
 PY - 
 AB - Triple-negative breast cancer (TNBC) has a poorer prognosis than other subtypes of breast cancer; however, it lacks effective targeted therapies clinically. In this study, we found FZU-0038-056, a novel compound derived from last-stage functionalization of tetrahydro-&#x3B2;-carboline scaffold, showed the most potent anti-cancer activity against TNBC cells among the 42 synthesized derivatives. We found FZU-0038-056 significantly induces apoptosis in HCC1806 and HCC1937 TNBC cells. FZU-0038-056 reduces the expression levels of several anti-apoptosis proteins, including Bcl-2, Mcl-1 and XIAP. Furthermore, we found FZU-0038-056 induces apoptosis partially through inhibiting the expression of Bcl-2. Finally, we found FZU-0038-056 significantly suppresses HCC1806 xenograft tumor growth in nude mice without affecting their body weight. Therefore, FZU-0038-056 has the potential to be a new anticancer agent for treating human TNBC.
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MicroRNA-214-3p targets the PLAGL2-MYH9 axis to suppress tumor proliferation and metastasis in human colorectal cancer

Zili Zhou, Liang Wu, Zhengyi Liu, Xudan Zhang, Shengbo Han, Ning Zhao, Haijun Bao, Wenzheng Yuan, Jinhuang Chen, Jintong Ji, Xiaogang Shu,

https://doi.org/10.18632/aging.103233 pp 9633—9657

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Zhou Z, Wu L, Liu Z, Zhang X, Han S, Zhao N, Bao H, Yuan W, Chen J, Ji J, Shu X, . MicroRNA-214-3p targets the PLAGL2-MYH9 axis to suppress tumor proliferation and metastasis in human colorectal cancer. . 12:9633-9657. https://doi.org/10.18632/aging.103233

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                TY  - JOUR
                AU  - Zhou, Zili 
                AU  - Wu, Liang 
                AU  - Liu, Zhengyi 
                AU  - Zhang, Xudan 
                AU  - Han, Shengbo 
                AU  - Zhao, Ning 
                AU  - Bao, Haijun 
                AU  - Yuan, Wenzheng 
                AU  - Chen, Jinhuang 
                AU  - Ji, Jintong 
                AU  - Shu, Xiaogang 
                TI  - MicroRNA-214-3p targets the PLAGL2-MYH9 axis to suppress tumor proliferation and metastasis in human colorectal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103233
                DO  - 10.18632/aging.103233
                SP  - 9633
                EP  - 9657
                PY  - 
                AB  - Evidence has shown that microRNAs (miRNAs) participate in the progression of CRC. Previous studies have indicated that miR-214-3p is abnormally expressed in various malignant tumors. However, the biological function it plays in CRC and the potential mechanism are unclear. Here, we demonstrated that miR-214-3p was obviously downregulated in CRC. Moreover, we found a strong correlation between the miR-214-3p level and tumor size and lymphatic metastasis. Furthermore, when miR-214-3p was decreased by an Lv-miR-214-3p inhibitor, the proliferation and migration of SW480 and HCT116 cells were significantly increased. As expected, the ability of proliferation and migration was significantly suppressed when miR-214-3p was overexpressed in DLD1 cells. According to the dual-luciferase reporter results, PLAGL2 was found to be a direct downstream molecule of miR-214-3p. Chromatin immunoprecipitation (CHIP) confirmed that MYH9, a well-known cytoskeleton molecule in CRC, was a direct targeting gene of PLAGL2. Silencing PLAGL2 or MYH9 could reverse the effect of a miR-214-3p inhibitor on CRC cells. In summary, our studies proved that low expression of miR-214-3p and overexpression of downstream PLAGL2 in CRC indicated a poor prognosis. MiR-214-3p suppressed the malignant behaviors of colorectal cancer by regulating the PLAGL2/MYH9 axis. MiR-214-3p might be a novel therapeutic target or prognostic marker for CRC.
                ER  -

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Prognostic value of prostaglandin I2 synthase and its correlation with tumor-infiltrating immune cells in lung cancer, ovarian cancer, and gastric cancer

Danian Dai, Bo Chen, Yanling Feng, Weizhong Wang, Yanhui Jiang, He Huang, Jihong Liu,

https://doi.org/10.18632/aging.103235 pp 9658—9685

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Dai D, Chen B, Feng Y, Wang W, Jiang Y, Huang H, Liu J, . Prognostic value of prostaglandin I2 synthase and its correlation with tumor-infiltrating immune cells in lung cancer, ovarian cancer, and gastric cancer. . 12:9658-9685. https://doi.org/10.18632/aging.103235

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                TY  - JOUR
                AU  - Dai, Danian 
                AU  - Chen, Bo 
                AU  - Feng, Yanling 
                AU  - Wang, Weizhong 
                AU  - Jiang, Yanhui 
                AU  - Huang, He 
                AU  - Liu, Jihong 
                TI  - Prognostic value of prostaglandin I2 synthase and its correlation with tumor-infiltrating immune cells in lung cancer, ovarian cancer, and gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103235
                DO  - 10.18632/aging.103235
                SP  - 9658
                EP  - 9685
                PY  - 
                AB  - Background: Prostaglandin I2 synthase (PTGIS) is a crucial gene for the synthesis of prostaglandin I2, which has multiple roles in inflammation and immune modulation. However, studies on the prognostic value of PTGIS and its correlation with tumor-infiltrating immune cells in multiple cancers are still rare.Results: Multiple datasets of the Oncomine database showed that PTGIS was expressed at low levels in lung cancer and ovarian cancer compared to the levels in normal tissues. Kaplan-Meier plotter showed that high PTGIS was associated with poor overall survival and progression-free survival in lung, ovarian, and gastric cancers. Moreover, PTGIS expression was significantly positively correlated with infiltrating levels of macrophages and was strongly associated with a variety of immune markers, especially tumor-associated macrophages (TAMs) and T-regulatory cells (Tregs).Conclusions: High expression of PTGIS could promote the infiltration of TAMs and Tregs in the tumor microenvironment and deteriorate outcomes of patients with lung, ovarian, and gastric cancers. These findings suggest that PTGIS could be taken as a potential biomarker of prognosis and tumor-infiltrating immune cells.Methods: PTGIS expression was investigated in different datasets of the Oncomine database, and its expression levels in various tumors and corresponding normal tissues were analyzed by the Tumor Immune Estimation Resource (TIMER). Then, the clinical prognostic value of PTGIS was assessed with online public databases. In addition, we initially explored the correlation between PTGIS and tumor-infiltrating immune cells by TIMER and Gene Expression Profiling Interactive Analysis (GEPIA).
                ER  -

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Ovulation and ovarian wound healing are impaired with advanced reproductive age

Jamie N. Mara, Luhan T. Zhou, Megan Larmore, Brian Johnson, Rebecca Ayiku, Farners Amargant, Michele T. Pritchard, Francesca E. Duncan,

https://doi.org/10.18632/aging.103237 pp 9686—9713

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Mara JN, Zhou LT, Larmore M, Johnson B, Ayiku R, Amargant F, Pritchard MT, Duncan FE, . Ovulation and ovarian wound healing are impaired with advanced reproductive age. . 12:9686-9713. https://doi.org/10.18632/aging.103237

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                TY  - JOUR
                AU  - Mara, Jamie N. 
                AU  - Zhou, Luhan T. 
                AU  - Larmore, Megan 
                AU  - Johnson, Brian 
                AU  - Ayiku, Rebecca 
                AU  - Amargant, Farners 
                AU  - Pritchard, Michele T. 
                AU  - Duncan, Francesca E. 
                TI  - Ovulation and ovarian wound healing are impaired with advanced reproductive age
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103237
                DO  - 10.18632/aging.103237
                SP  - 9686
                EP  - 9713
                PY  - 
                AB  - Aging is associated with reduced tissue remodeling efficiency and increased fibrosis, characterized by excess collagen accumulation and altered matrix degradation. Ovulation, the process by which an egg is released from the ovary, is one of the most dynamic cycles of tissue wounding and repair. Because the ovary is one of the first organs to age, ovulation and ovarian wound healing is impaired with advanced reproductive age. To test this hypothesis, we induced superovulation in reproductively young and old mice and determined the numbers of eggs ovulated and corpora lutea (CLs), the progesterone producing glands formed post-ovulation. Reproductively old mice ovulated fewer eggs and had fewer CLs relative to young controls. Moreover, reproductively old mice exhibited a greater number of oocytes trapped within CLs and expanded cumulus oocyte complexes within unruptured antral follicles, indicative of failed ovulation. In addition, post-ovulatory tissue remodeling was compromised with age as evidenced by reduced CL vasculature, increased collagen, decreased hyaluronan, decreased cell proliferation and apoptosis, impaired wound healing capacity, and aberrant morphology of the ovarian surface epithelium (OSE). These findings demonstrate that ovulatory dysfunction is an additional mechanism underlying the age-related loss of fertility beyond the reduction of egg quantity and quality.
                ER  -

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Qigesan inhibits esophageal cancer cell invasion and migration by inhibiting Gas6/Axl-induced epithelial-mesenchymal transition

Lingyu Kong, Xin Lu, Xuanyu Chen, Yunyan Wu, Yushuang Zhang, Huijuan Shi, Jing Li,

https://doi.org/10.18632/aging.103238 pp 9714—9725

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Kong L, Lu X, Chen X, Wu Y, Zhang Y, Shi H, Li J, . Qigesan inhibits esophageal cancer cell invasion and migration by inhibiting Gas6/Axl-induced epithelial-mesenchymal transition. . 12:9714-9725. https://doi.org/10.18632/aging.103238

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                TY  - JOUR
                AU  - Kong, Lingyu 
                AU  - Lu, Xin 
                AU  - Chen, Xuanyu 
                AU  - Wu, Yunyan 
                AU  - Zhang, Yushuang 
                AU  - Shi, Huijuan 
                AU  - Li, Jing 
                TI  - Qigesan inhibits esophageal cancer cell invasion and migration by inhibiting Gas6/Axl-induced epithelial-mesenchymal transition
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103238
                DO  - 10.18632/aging.103238
                SP  - 9714
                EP  - 9725
                PY  - 
                AB  - Qigesan (QGS) has been used to effectively treat esophageal cancer (EC) for decades in China, but the mechanism by which it suppresses EC metastasis remains unknown. In this study, we examined the effects of QGS on EC cell mobility. Using immunohistochemistry and immunofluorescence, expression of Gas6 and Axl, which promote tumor cell migration and invasion, was examined in carcinoma tissues and adjacent normal tissues from EC patients. Levels of Gas6, Axl, and the Gas6/Axl complex were also examined in ECA109 and TE13 EC cells treated with QGS. In addition, immunofluorescent staining and quantitative protein analysis were used to examine E-cadherin, N-cadherin, and Snail levels in ECA109 and TE13 EC cells after QSG administration, and cell mobility was assessed. The results demonstrated that levels of Gas6 and Axl expression are higher in EC tissues than in adjacent normal tissues. Moreover, QGS decreased Gas6/Axl levels, increased E-cadherin expression, decreased Snail and N-cadherin expression, and inhibited epithelial-mesenchymal transition (EMT) in EC cells. QGS thus suppresses EMT in EC by inhibiting Gas6/Axl binding.
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NF2 deficiency accelerates neointima hyperplasia following vascular injury via promoting YAP-TEAD1 interaction in vascular smooth muscle cells

Xiongshan Sun, Shuang Li, Xueqing Gan, Ken Chen, Dachun Yang, Yongjian Yang,

https://doi.org/10.18632/aging.103240 pp 9726—9744

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Sun X, Li S, Gan X, Chen K, Yang D, Yang Y, . NF2 deficiency accelerates neointima hyperplasia following vascular injury via promoting YAP-TEAD1 interaction in vascular smooth muscle cells. . 12:9726-9744. https://doi.org/10.18632/aging.103240

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                TY  - JOUR
                AU  - Sun, Xiongshan 
                AU  - Li, Shuang 
                AU  - Gan, Xueqing 
                AU  - Chen, Ken 
                AU  - Yang, Dachun 
                AU  - Yang, Yongjian 
                TI  - NF2 deficiency accelerates neointima hyperplasia following vascular injury via promoting YAP-TEAD1 interaction in vascular smooth muscle cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103240
                DO  - 10.18632/aging.103240
                SP  - 9726
                EP  - 9744
                PY  - 
                AB  - Neurofibromin 2 (NF2), a potent tumor suppressor, is reported to inhibit proliferation in several cell types. The role of NF2 in neointima hyperplasia after vascular injury is unknown. We explored the role of NF2 in proliferation, migration of vascular smooth muscle cell (VSMC) and neointima hyperplasia after vascular injury. NF2 phosphorylation was elevated in VSMC subjected to platelet-derived growth factor (PDGF)-BB and in artery subjected to vascular injury. Mice deficient for Nf2 in VSMC showed enhanced neointima hyperplasia after injury, increased proliferation and migration of VSMC after PDGF-BB treatment. Mechanistically, we observed increased nuclear p-NF2, declined p-Yes-Associated Protein (YAP), nuclear translocation of YAP after PDGF-BB treatment or injury. NF2 knockdown or YAP overexpression showed similar phenotype in VSMC proliferation, migration and neointima hyperplasia. YAP inhibition abolished the above effects mediated by NF2 knockdown. Finally, NF2 knockdown further promoted YAP-TEA Domain Transcription Factor 1 (TEAD1) interaction after PDGF-BB treatment. Inhibition of TEAD1 blocked PDGF-BB-induced VSMC proliferation and migration, which were not reversed by either NF2 knockdown or YAP overexpression. In conclusion, NF2 knockdown promotes VSMC proliferation, migration and neointima hyperplasia after vascular injury via inducing YAP-TEAD1 interaction.
                ER  -

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Loss of macroH2A1 decreases mitochondrial metabolism and reduces the aggressiveness of uveal melanoma cells

Sebastiano Giallongo, Michelino Di Rosa, Rosario Caltabiano, Lucia Longhitano, Michele Reibaldi, Alfio Distefano, Oriana Lo Re, Angela Maria Amorini, Lidia Puzzo, Lucia Salvatorelli, Stefano Palmucci, Daniele Tibullo, Andrea Russo, Antonio Longo, Giacomo Lazzarino, Giovanni Li Volti, Manlio Vinciguerra,

https://doi.org/10.18632/aging.103241 pp 9745—9760

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Giallongo S, Di Rosa M, Caltabiano R, Longhitano L, Reibaldi M, Distefano A, Lo Re O, Amorini AM, Puzzo L, Salvatorelli L, Palmucci S, Tibullo D, Russo A, et al, . Loss of macroH2A1 decreases mitochondrial metabolism and reduces the aggressiveness of uveal melanoma cells. . 12:9745-9760. https://doi.org/10.18632/aging.103241

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                TY  - JOUR
                AU  - Giallongo, Sebastiano 
                AU  - Di Rosa, Michelino 
                AU  - Caltabiano, Rosario 
                AU  - Longhitano, Lucia 
                AU  - Reibaldi, Michele 
                AU  - Distefano, Alfio 
                AU  - Lo Re, Oriana 
                AU  - Amorini, Angela Maria 
                AU  - Puzzo, Lidia 
                AU  - Salvatorelli, Lucia 
                AU  - Palmucci, Stefano 
                AU  - Tibullo, Daniele 
                AU  - Russo, Andrea 
                AU  - Longo, Antonio 
                AU  - Lazzarino, Giacomo 
                AU  - Li Volti, Giovanni 
                AU  - Vinciguerra, Manlio 
                TI  - Loss of macroH2A1 decreases mitochondrial metabolism and reduces the aggressiveness of uveal melanoma cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103241
                DO  - 10.18632/aging.103241
                SP  - 9745
                EP  - 9760
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Giallongo, Sebastiano 
                AU  - Di Rosa, Michelino 
                AU  - Caltabiano, Rosario 
                AU  - Longhitano, Lucia 
                AU  - Reibaldi, Michele 
                AU  - Distefano, Alfio 
                AU  - Lo Re, Oriana 
                AU  - Amorini, Angela Maria 
                AU  - Puzzo, Lidia 
                AU  - Salvatorelli, Lucia 
                AU  - Palmucci, Stefano 
                AU  - Tibullo, Daniele 
                AU  - Russo, Andrea 
                AU  - Longo, Antonio 
                AU  - Lazzarino, Giacomo 
                AU  - Li Volti, Giovanni 
                AU  - Vinciguerra, Manlio 
                TI  - Loss of macroH2A1 decreases mitochondrial metabolism and reduces the aggressiveness of uveal melanoma cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103241
                DO  - 10.18632/aging.103241
                SP  - 9745
                EP  - 9760
                PY  - 
                AB  - Uveal melanoma (UM) is the most common primary intraocular tumour in adults. The most accurate prognostic factor of UM is classification by gene expression profiling. Currently, the role of epigenetics is much less defined compared to genetic mechanisms. We recently showed a strong prognostic role of the expression levels of histone variant macroH2A1 in UM patients. Here, we assessed the mechanistic effects of macroH2A1 on UM progression.UM cell lines were stably knocked down (KD) for macroH2A1, and proliferation and colony formation capacity were evaluated. Mitochondrial function was assayed through qPCR and HPLC analyses. Correlation between mitochondrial gene expression and cancer aggressiveness was studied using a bioinformatics approach.MacroH2A1 loss significantly attenuated UM cells proliferation and aggressiveness. Furthermore, genes involved in oxidative phosphorylation displayed a decreased expression in KD cells. Consistently, macroH2A1 loss resulted also in a significant decrease of mitochondrial transcription factor A (TFAM) expression, suggesting impaired mitochondrial replication. Bioinformatics analyses uncovered that the expression of genes involved in mitochondrial metabolism correlates with macroH2A1 and with cancer aggressiveness in UM patients. Altogether, our results suggest that macroH2A1 controls UM cells progression and it may represent a molecular target to develop new pharmacological strategies for UM treatment.
                ER  -

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Physiological and metabolic features of mice with CRISPR/Cas9-mediated loss-of-function in growth hormone-releasing hormone

Mert Icyuz, Michael Fitch, Fang Zhang, Anil Challa, Liou Y. Sun,

https://doi.org/10.18632/aging.103242 pp 9761—9780

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Icyuz M, Fitch M, Zhang F, Challa A, Sun LY, . Physiological and metabolic features of mice with CRISPR/Cas9-mediated loss-of-function in growth hormone-releasing hormone. . 12:9761-9780. https://doi.org/10.18632/aging.103242

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                TY  - JOUR
                AU  - Icyuz, Mert 
                AU  - Fitch, Michael 
                AU  - Zhang, Fang 
                AU  - Challa, Anil 
                AU  - Sun, Liou Y. 
                TI  - Physiological and metabolic features of mice with CRISPR/Cas9-mediated loss-of-function in growth hormone-releasing hormone
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103242
                DO  - 10.18632/aging.103242
                SP  - 9761
                EP  - 9780
                PY  - 
                AB  - Our previous study demonstrated that the loss of growth hormone releasing hormone (GHRH) results in increased lifespan and improved metabolic homeostasis in the mouse model generated by classical embryonic stem cell-based gene-targeting method. In this study, we targeted the GHRH gene using the CRISPR/Cas9 technology to avoid passenger alleles/mutations and performed in-depth physiological and metabolic characterization. In agreement with our previous observations, male and female GHRH-/- mice have significantly reduced body weight and enhanced insulin sensitivity when compared to wild type littermates. Dual-energy X-ray absorptiometry showed that there were significant decreases in lean mass, bone mineral content and density, and a dramatic increase in fat mass of GHRH-/- mice when compared to wild type littermates. Indirect calorimetry measurements showed dramatic reductions in oxygen consumption, carbon dioxide production and energy expenditure in GHRH-/- mice compared to wild type mice in both light and dark cycles. Respiratory exchange ratio was significantly lower in GHRH-/- mice during the light cycle, but not during the dark cycle, indicating a circadian related metabolic shift towards fat utilization in the growth hormone deficient mice. The novel CRISPR/Cas9 GHRH-/- mice are exhibiting the consistent and unique physiological and metabolic characteristics, which might mediate the longevity effects of growth hormone deficiency in mice.
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LncRNA DSCAM-AS1 promotes colorectal cancer progression by acting as a molecular sponge of miR-384 to modulate AKT3 expression

Bo Li, Hai Sun, Jiayu Zhang,

https://doi.org/10.18632/aging.103243 pp 9781—9792

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Li B, Sun H, Zhang J, . LncRNA DSCAM-AS1 promotes colorectal cancer progression by acting as a molecular sponge of miR-384 to modulate AKT3 expression. . 12:9781-9792. https://doi.org/10.18632/aging.103243

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                TY  - JOUR
                AU  - Li, Bo 
                AU  - Sun, Hai 
                AU  - Zhang, Jiayu 
                TI  - LncRNA DSCAM-AS1 promotes colorectal cancer progression by acting as a molecular sponge of miR-384 to modulate AKT3 expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103243
                DO  - 10.18632/aging.103243
                SP  - 9781
                EP  - 9792
                PY  - 
                AB  - Down Syndrome Cell Adhesion Molecule antisense1 (DSCAM-AS1), a novel long non-coding RNA (lncRNA), reportedly contributes to the development and progression of several cancers. There is a lack of information on its biological role and regulatory mechanism with respect to colorectal cancer (CRC). Here, we discovered that the expression of DSCAM-AS1 exhibited a significant upregulation in CRC tissues and cell lines in comparison with the corresponding control. Increased DSCAM-AS1 expression was associated with poor prognosis for those diagnosed with CRC. Loss-of function assay illustrated that knockdown of DSCAM-AS1 resulted in significant inhibition of cell proliferation, invasion and migration in vitro, and impaired tumor growth in vivo. MicroRNA-384(miR-384) was directly targeted by DSCAM-AS1 in CRC cells, and repression of DSCAM-AS1 inhibited the expression of AKT3, a known target of miR-384 in CRC. In addition, repression of miR-384 or overexpression of AKT3 could partially rescue the inhibitory effect of DSCAM-AS1 knockdown on CRC progression. In summary, DSCAM-AS1 exerted an oncogenic role in CRC by functioning as a competing endogenous RNA of miR-384 to bring about regulation of AKT3 expression. These results implied that DSCAM-AS1 might be a novel therapeutic target for patients suffering from CRC.
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Circular RNA hsa_circ_0003141 promotes tumorigenesis of hepatocellular carcinoma via a miR-1827/UBAP2 axis

Yong Wang, Rongfen Gao, Jinpeng Li, Shaotao Tang, Shuai Li, Qiangsong Tong, Yongzhong Mao,

https://doi.org/10.18632/aging.103244 pp 9793—9806

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Wang Y, Gao R, Li J, Tang S, Li S, Tong Q, Mao Y, . Circular RNA hsa_circ_0003141 promotes tumorigenesis of hepatocellular carcinoma via a miR-1827/UBAP2 axis. . 12:9793-9806. https://doi.org/10.18632/aging.103244

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                TY  - JOUR
                AU  - Wang, Yong 
                AU  - Gao, Rongfen 
                AU  - Li, Jinpeng 
                AU  - Tang, Shaotao 
                AU  - Li, Shuai 
                AU  - Tong, Qiangsong 
                AU  - Mao, Yongzhong 
                TI  - Circular RNA hsa_circ_0003141 promotes tumorigenesis of hepatocellular carcinoma via a miR-1827/UBAP2 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103244
                DO  - 10.18632/aging.103244
                SP  - 9793
                EP  - 9806
                PY  - 
                AB  - Circular RNAs (circRNAs) play an important role in the tumorigenesis of hepatocellular carcinoma (HCC), but their specific functions in HCC remain largely unknown. Using bioinformatics analysis, we have found that the expression of circRNA hsa_circ_0003141 is significantly increased in HCC tissues. Ubiquitin-associated protein 2 (UBAP2) is the parent gene for hsa_circ_0003141, and its high expression correlates with poor overall survival rates in HCC patients. In addition, our results show that miR-1827 is a binding target of hsa_circ_0003141, and indicate that hsa_circ_0003141 regulates UBAP2 expression by sponging miR-1827 in HCC cells. Downregulation of hsa_circ_0003141 suppresses UBAP2 expression, induces apoptosis, and inhibits proliferation and invasion by HCC Huh-7 cells. Importantly, downregulation of hsa_circ_0003141 inhibits tumorigenesis in a xenograft mouse model of HCC. Together, our results indicate that hsa_circ_0003141 functions as an oncogene in HCC cells, and suggest that the hsa_circ_0003141/miR-1827/UBAP2 axis might represent a novel therapeutic option for the treatment of HCC.
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Identification and validation of hub microRNAs dysregulated in esophageal squamous cell carcinoma

Chen Sang, Ce Chao, Min Wang, Youpu Zhang, Guanghua Luo, Xiaoying Zhang,

https://doi.org/10.18632/aging.103245 pp 9807—9824

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Sang C, Chao C, Wang M, Zhang Y, Luo G, Zhang X, . Identification and validation of hub microRNAs dysregulated in esophageal squamous cell carcinoma. . 12:9807-9824. https://doi.org/10.18632/aging.103245

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                TY  - JOUR
                AU  - Sang, Chen 
                AU  - Chao, Ce 
                AU  - Wang, Min 
                AU  - Zhang, Youpu 
                AU  - Luo, Guanghua 
                AU  - Zhang, Xiaoying 
                TI  - Identification and validation of hub microRNAs dysregulated in esophageal squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103245
                DO  - 10.18632/aging.103245
                SP  - 9807
                EP  - 9824
                PY  - 
                AB  - Esophageal squamous cell carcinoma (ESCC) is one of the deadliest cancers worldwide, and its morbidity is exacerbated by the lack of early symptoms. Bioinformatics analyses enable discovery of differentially expressed genes and non-protein-coding RNAs of potential prognostic and/or therapeutic relevance in ESCC and other cancers. Using bioinformatics tools, we searched for dysregulated miRNAs in two ESCC microarray datasets from the Gene Expression Omnibus (GEO) database. After identification of three upregulated and five downregulated miRNAs shared between databases, protein-protein interaction (PPI) network analysis was used to identify the top 10 hub-gene targets. Thereafter, a miRNA-gene interaction network predicted that most hub genes are regulated by miR-196a-5p and miR-1-3p, which are respectively upregulated and downregulated in ESCC. Functional enrichment analyses in the GO and KEGG databases indicated the potential involvement of these miRNAs in tumorigenesis-related processes and pathways, while both differential expression and correlation with T stage were demonstrated for each miRNA in a cohort of ESCC patients. Overexpression showed that miR-196a-5p increased, whereas miR-1-3p attenuated, proliferation and invasion in human ESCC cell lines grown in vitro. These findings suggest miR-196a-5p and miR-1-3p jointly contribute to ESCC tumorigenesis and are potential targets for diagnosis and treatment.
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Association between metabolic syndrome and endometrial cancer risk: a systematic review and meta-analysis of observational studies

Lan Wang, Zhen-Hua Du, Jia-Ming Qiao, Song Gao,

https://doi.org/10.18632/aging.103247 pp 9825—9839

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Wang L, Du Z, Qiao J, Gao S, . Association between metabolic syndrome and endometrial cancer risk: a systematic review and meta-analysis of observational studies. . 12:9825-9839. https://doi.org/10.18632/aging.103247

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                TY  - JOUR
                AU  - Wang, Lan 
                AU  - Du, Zhen-Hua 
                AU  - Qiao, Jia-Ming 
                AU  - Gao, Song 
                TI  - Association between metabolic syndrome and endometrial cancer risk: a systematic review and meta-analysis of observational studies
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103247
                DO  - 10.18632/aging.103247
                SP  - 9825
                EP  - 9839
                PY  - 
                AB  - Existing evidence has revealed inconsistent results on the association between metabolic syndrome (MetS) and endometrial cancer (EC) risk. Herein, we aim to better understand this association. Systematic searches of PubMed, EMBASE, and Web of Science through 12 December 2019 were conducted. Observational studies that provided risk estimates of MetS and EC risk were eligible. The quality of the included studies was judged based on the Newcastle&#x2013;Ottawa scale. Summary odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a random-effects model. Six studies, comprising 17,772 EC cases and 150,371 participants were included. MetS, diagnosed according to the criteria of the National Cholesterol Education Program&#x2014;Third Adult Treatment Panel, was associated with an increased risk of EC (OR: 1.62; 95% CI = 1.26&#x2013;2.07) with substantial heterogeneity (I2 = 78.3%). Furthermore, we found that women with MetS, diagnosed according to the criteria of the International Diabetes Federation, had a significantly higher risk of EC compared to healthy controls (OR: 1.45; 95% CI = 1.16&#x2013;1.81; I2 = 64.6%). Our findings were generally consistent with the main results in the majority of prespecified subgroups, as well as in sensitivity analyses. In conclusion, MetS is associated with EC risk.
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Development of a machine learning-based multimode diagnosis system for lung cancer

Shuyin Duan, Huimin Cao, Hong Liu, Lijun Miao, Jing Wang, Xiaolei Zhou, Wei Wang, Pingzhao Hu, Lingbo Qu, Yongjun Wu,

https://doi.org/10.18632/aging.103249 pp 9840—9854

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Duan S, Cao H, Liu H, Miao L, Wang J, Zhou X, Wang W, Hu P, Qu L, Wu Y, . Development of a machine learning-based multimode diagnosis system for lung cancer. . 12:9840-9854. https://doi.org/10.18632/aging.103249

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                TY  - JOUR
                AU  - Duan, Shuyin 
                AU  - Cao, Huimin 
                AU  - Liu, Hong 
                AU  - Miao, Lijun 
                AU  - Wang, Jing 
                AU  - Zhou, Xiaolei 
                AU  - Wang, Wei 
                AU  - Hu, Pingzhao 
                AU  - Qu, Lingbo 
                AU  - Wu, Yongjun 
                TI  - Development of a machine learning-based multimode diagnosis system for lung cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103249
                DO  - 10.18632/aging.103249
                SP  - 9840
                EP  - 9854
                PY  - 
                AB  - As an emerging technology, artificial intelligence has been applied to identify various physical disorders. Here, we developed a three-layer diagnosis system for lung cancer, in which three machine learning approaches including decision tree C5.0, artificial neural network (ANN) and support vector machine (SVM) were involved. The area under the curve (AUC) was employed to evaluate their decision powers. In the first layer, the AUCs of C5.0, ANN and SVM were 0.676, 0.736 and 0.640, ANN was better than C5.0 and SVM. In the second layer, ANN was similar with SVM but superior to C5.0 supported by the AUCs of 0.804, 0.889 and 0.825. Much higher AUCs of 0.908, 0.910 and 0.849 were identified in the third layer, where the highest sensitivity of 94.12% was found in C5.0. These data proposed a three-layer diagnosis system for lung cancer: ANN was used as a broad-spectrum screening subsystem basing on 14 epidemiological data and clinical symptoms, which was firstly adopted to screen high-risk groups; then, combining with additional 5 tumor biomarkers, ANN was used as an auxiliary diagnosis subsystem to determine the suspected lung cancer patients; C5.0 was finally employed to confirm lung cancer patients basing on 22 CT nodule-based radiomic features.
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Red blood cell distribution width is associated with neuronal damage in acute ischemic stroke

Rong-Hua Hong, Jian Zhu, Ze-Zhi Li, Jian Yuan, Pei Zhao, Jie Ding, Qing-Lei Fan, Jin Yang, Bao-Guo Liu, Jian Cai, De-Sheng Zhu, Yang-tai Guan,

https://doi.org/10.18632/aging.103250 pp 9855—9867

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Hong R, Zhu J, Li Z, Yuan J, Zhao P, Ding J, Fan Q, Yang J, Liu B, Cai J, Zhu D, Guan Y, . Red blood cell distribution width is associated with neuronal damage in acute ischemic stroke. . 12:9855-9867. https://doi.org/10.18632/aging.103250

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                TY  - JOUR
                AU  - Hong, Rong-Hua 
                AU  - Zhu, Jian 
                AU  - Li, Ze-Zhi 
                AU  - Yuan, Jian 
                AU  - Zhao, Pei 
                AU  - Ding, Jie 
                AU  - Fan, Qing-Lei 
                AU  - Yang, Jin 
                AU  - Liu, Bao-Guo 
                AU  - Cai, Jian 
                AU  - Zhu, De-Sheng 
                AU  - Guan, Yang-tai 
                TI  - Red blood cell distribution width is associated with neuronal damage in acute ischemic stroke
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103250
                DO  - 10.18632/aging.103250
                SP  - 9855
                EP  - 9867
                PY  - 
                AB  - Elevated red blood cell distribution width (RDW) has been found to be associated with the occurrence of ischemic stroke. However, there is no defined relationship between RDW and neuronal damage in acute ischemic stroke (AIS). This study was designed to determine the relationship between RDW and neuronal damage in AIS patients. A total of 442 consecutive AIS patients from January 2018 to June 2019 were evaluated for neuronal damage, which was estimated by serum neuron-specific enolase (NSE) levels. Red blood cell distribution width-standard deviation (RDW-SD), a parameter that reflects the heterogeneity of red blood cell volume, was also assessed. We evaluated the association between the RDW-SD and serum NSE level through multivariate-adjusted linear regression analysis. Both the serum NSE level and the incidence of high NSE increased according to the increased RDW-SD tertile in AIS patients (p&lt;0.01). There was a positive correlation between RDW-SD and serum NSE levels (r=0.275, 95% CI: 0.187-0.359, p&lt;0.001). The beta coefficients (95% CI) between RDW-SD and serum NSE levels were 0.32 (0.21-0.42, p&lt;0.001) and 0.26 (0.15-0.38, p&lt;0.001), respectively, in AIS patients before and after adjusting for potential confounders. In conclusion, we found a significant positive association between RDW-SD and neuronal damage in AIS patients.
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Construction of immune-related and prognostic lncRNA clusters and identification of their immune and genomic alterations characteristics in lung adenocarcinoma samples

Jia Li, Chenyue Zhang, Chenxing Zhang, Haiyong Wang,

https://doi.org/10.18632/aging.103251 pp 9868—9881

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Li J, Zhang C, Zhang C, Wang H, . Construction of immune-related and prognostic lncRNA clusters and identification of their immune and genomic alterations characteristics in lung adenocarcinoma samples. . 12:9868-9881. https://doi.org/10.18632/aging.103251

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                TY  - JOUR
                AU  - Li, Jia 
                AU  - Zhang, Chenyue 
                AU  - Zhang, Chenxing 
                AU  - Wang, Haiyong 
                TI  - Construction of immune-related and prognostic lncRNA clusters and identification of their immune and genomic alterations characteristics in lung adenocarcinoma samples
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103251
                DO  - 10.18632/aging.103251
                SP  - 9868
                EP  - 9881
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) play an important role in various biological processes of lung adenocarcinoma (LUAD), such as immune response regulation, tumor microenvironment remodeling and genomic alteration. Nevertheless, immune-related lncRNAs and their immune and genomic alterations characteristics in LUAD samples still remain unreported. Here, using various public databases, statistic and software tools, we constructed two immune-related lncRNA clusters with different immune and genomic alterations characteristics. Notably, cluster 1 had a stronger immunosuppressive tumor microenvironment (TME) and a higher mutation frequency than cluster 2, especially the mutant genes, such as Kelch-like ECH-associated protein 1 (KEAP1) and toll like receptor 4 (TLR4). In cluster 1, both the amplified and deleted portions of copy number variation (CNV) segments were enriched and cyclin dependent kinase inhibitor 2A (CDKN2A) was significantly deleted. GSVA analysis revealed that these immune-related lncRNAs may be involved in stem cell and EMT functions. Furthermore, cluster 1 was related to worse prognosis of LUAD patients. Therefore, we constructed two immune-related and prognostic lncRNA clusters and identified their immune and genomic alterations characteristics in LUAD samples, which could well divide LUAD patients into different immune phenotypes and help to understand immune molecular mechanisms of LUAD.
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Systematic metabolic analysis of potential target, therapeutic drug, diagnostic method and animal model applicability in three neurodegenerative diseases

Wen-Xing Li, Gong-Hua Li, Xin Tong, Peng-Peng Yang, Jing-Fei Huang, Lin Xu, Shao-Xing Dai,

https://doi.org/10.18632/aging.103253 pp 9882—9914

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Li W, Li G, Tong X, Yang P, Huang J, Xu L, Dai S, . Systematic metabolic analysis of potential target, therapeutic drug, diagnostic method and animal model applicability in three neurodegenerative diseases. . 12:9882-9914. https://doi.org/10.18632/aging.103253

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                TY  - JOUR
                AU  - Li, Wen-Xing 
                AU  - Li, Gong-Hua 
                AU  - Tong, Xin 
                AU  - Yang, Peng-Peng 
                AU  - Huang, Jing-Fei 
                AU  - Xu, Lin 
                AU  - Dai, Shao-Xing 
                TI  - Systematic metabolic analysis of potential target, therapeutic drug, diagnostic method and animal model applicability in three neurodegenerative diseases
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103253
                DO  - 10.18632/aging.103253
                SP  - 9882
                EP  - 9914
                PY  - 
                AB  - Considerable evidence suggests that metabolic abnormalities are associated with neurodegenerative diseases. This study aimed to conduct a systematic metabolic analysis of Alzheimer&#x2019;s disease (AD), Parkinson&#x2019;s disease (PD) and Huntington&#x2019;s disease (HD). Human and mouse model microarray datasets were downloaded from the Gene Expression Omnibus database. The metabolic genes and pathways were collected from the Recon 3D human metabolic model. Drug and target information was obtained from the DrugBank database. This study identified ATP1A1, ATP6V1G2, GOT1, HPRT1, MAP2K1, PCMT1 and PLK2 as key metabolic genes that were downregulated in AD, PD and HD. We screened 57 drugs that target these genes, such as digoxin, ouabain and diazoxide. This study constructed multigene diagnostic models for AD, PD and HD by using metabolic gene expression profiles in blood, all models showed high accuracy (AUC &gt; 0.8) both in the experimental and validation sets. Furthermore, analysis of animal models showed that there was almost no consistency among the metabolic changes between mouse models and human diseases. This study systematically revealed the metabolic damage among AD, PD, and HD and uncovered the differences between animal models and human diseases. This information may be helpful for understanding the metabolic mechanisms and drug development for neurodegenerative diseases.
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ZNF139/circZNF139 promotes cell proliferation, migration and invasion via activation of PI3K/AKT pathway in bladder cancer

Jie Yao, Kaiyu Qian, Chen Chen, Xiaoping Liu, Donghu Yu, Xin Yan, Tongzu Liu, Sheng Li,

https://doi.org/10.18632/aging.103256 pp 9915—9934

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Yao J, Qian K, Chen C, Liu X, Yu D, Yan X, Liu T, Li S, . ZNF139/circZNF139 promotes cell proliferation, migration and invasion via activation of PI3K/AKT pathway in bladder cancer. . 12:9915-9934. https://doi.org/10.18632/aging.103256

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 TY - JOUR
 AU - Yao, Jie 
 AU - Qian, Kaiyu 
 AU - Chen, Chen 
 AU - Liu, Xiaoping 
 AU - Yu, Donghu 
 AU - Yan, Xin 
 AU - Liu, Tongzu 
 AU - Li, Sheng 
 TI - ZNF139/circZNF139 promotes cell proliferation, migration and invasion via activation of PI3K/AKT pathway in bladder cancer
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103256
 DO - 10.18632/aging.103256
 SP - 9915
 EP - 9934
 PY - 
 AB - Existing reports identify the involved roles of ZNF139 and its one circular RNA (circRNA), circZNF139, in the progression of various tumors. However, their relevance and function role in bladder cancer (BC) remain largely unexplored. Herein, we aimed to reconnoiter the role and potential mechanism of ZNF139 and circZNF139 in the progression of BC. Firstly, bioinformatics analyses indicated ZNF139 was upregulated in BC tissues and correlated with disease-free survival of BC patients. The subcellular localization and structural analyses of ZNF139 conveyed the possibility of ZNF139 functioning as a transcription factor. Secondly, circZNF139 was validated by bioinformatics analyses and RNase R tests. ZNF139 and circZNF139 were both significantly upregulated in BC cell lines. Functionally, ZNF139/circZNF139 had facilitated effects on the proliferative, clonal, migratory, and invasive potential of BC cells. Mechanistically, GO, KEGG pathway analyses and western blot assays altogether unveiled ZNF139/circZNF139 activated PI3K/AKT pathway in BC cells, supported by the alteration of AKT at phosphorylation level and PI3K at the protein level. Collectively, this work reveals ZNF139 and circZNF139 cooperate closely with each other to promote cell proliferation, migration and invasion via activation of PI3K/AKT pathway in BC.
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Gorlin syndrome-induced pluripotent stem cells form medulloblastoma with loss of heterozygosity in PTCH1

Yu Ikemoto, Toshiyuki Miyashita, Michiyo Nasu, Hiromi Hatsuse, Kazuhiro Kajiwara, Katsunori Fujii, Toshino Motojima, Ibuki Kokido, Masashi Toyoda, Akihiro Umezawa,

https://doi.org/10.18632/aging.103258 pp 9935—9947

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Ikemoto Y, Miyashita T, Nasu M, Hatsuse H, Kajiwara K, Fujii K, Motojima T, Kokido I, Toyoda M, Umezawa A, . Gorlin syndrome-induced pluripotent stem cells form medulloblastoma with loss of heterozygosity in PTCH1. . 12:9935-9947. https://doi.org/10.18632/aging.103258

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 TY - JOUR
 AU - Ikemoto, Yu 
 AU - Miyashita, Toshiyuki 
 AU - Nasu, Michiyo 
 AU - Hatsuse, Hiromi 
 AU - Kajiwara, Kazuhiro 
 AU - Fujii, Katsunori 
 AU - Motojima, Toshino 
 AU - Kokido, Ibuki 
 AU - Toyoda, Masashi 
 AU - Umezawa, Akihiro 
 TI - Gorlin syndrome-induced pluripotent stem cells form medulloblastoma with loss of heterozygosity in PTCH1
 JO - 
 JA - 
 VL - 12
 IS - 10
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103258
 DO - 10.18632/aging.103258
 SP - 9935
 EP - 9947
 PY - 
 AB - Gorlin syndrome is a rare autosomal dominant hereditary disease with a high incidence of tumors such as basal cell carcinoma and medulloblastoma. Disease-specific induced pluripotent stem cells (iPSCs) and an animal model have been used to analyze disease pathogenesis. In this study, we generated iPSCs derived from fibroblasts of four patients with Gorlin syndrome (Gln-iPSCs) with heterozygous mutations of the PTCH1 gene. Gln-iPSCs from the four patients developed into medulloblastoma, a manifestation of Gorlin syndrome, in 100% (four out of four), of teratomas after implantation into immunodeficient mice, but none (0/584) of the other iPSC-teratomas did so. One of the medulloblastomas showed loss of heterozygosity in the PTCH1 gene while the benign teratoma, i.e. the non-medulloblastoma portion, did not, indicating a close clinical correlation between tumorigenesis in Gorlin syndrome patients and Gln-iPSCs.
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Topoisomerase II-binding protein 1 promotes the progression of prostate cancer via ATR-CHK1 signaling pathway

Kaiwen Li, Shirong Peng, Zean Li, Yiming Lai, Qiong Wang, Yiran Tao, Wanhua Wu, Qianghua Zhou, Ze Gao, Junxiu Chen, Hui Li, Wenli Cai, Zhenghui Guo, Hai Huang,

https://doi.org/10.18632/aging.103260 pp 9948—9958

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Li K, Peng S, Li Z, Lai Y, Wang Q, Tao Y, Wu W, Zhou Q, Gao Z, Chen J, Li H, Cai W, Guo Z, et al, . Topoisomerase II-binding protein 1 promotes the progression of prostate cancer via ATR-CHK1 signaling pathway. . 12:9948-9958. https://doi.org/10.18632/aging.103260

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                TY  - JOUR
                AU  - Li, Kaiwen 
                AU  - Peng, Shirong 
                AU  - Li, Zean 
                AU  - Lai, Yiming 
                AU  - Wang, Qiong 
                AU  - Tao, Yiran 
                AU  - Wu, Wanhua 
                AU  - Zhou, Qianghua 
                AU  - Gao, Ze 
                AU  - Chen, Junxiu 
                AU  - Li, Hui 
                AU  - Cai, Wenli 
                AU  - Guo, Zhenghui 
                AU  - Huang, Hai 
                TI  - Topoisomerase II-binding protein 1 promotes the progression of prostate cancer via ATR-CHK1 signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103260
                DO  - 10.18632/aging.103260
                SP  - 9948
                EP  - 9958
                PY  - 
                AB  - DNA damage response (DDR) plays an important role in the progression of cancers, including prostate cancer (PCa). Topoisomerase II-binding protein 1 (TopBP1) is an essential promotor of ATR-mediated DDR. Herein, we investigated the association between TopBP1 and PCa and determined its effect on the progression of PCa. The expression and clinical features of TopBP1 were analyzed using large-scale cohort of tissue microarray analyses and The Cancer Genome Atlas database, which indicated that TopBP1 was positively correlated with high Gleason Score, advanced clinical and pathological stages, the metastasis status. Multivariate analysis revealed that the upregulation of TopBP1 was an independent predictor for a worse biochemical recurrence-free survival (BCR-free survival). Furthermore, we discovered that downregulation of TopBP1 significantly suppressed the growth and migration ability of PCa lines by loss-of-function assays in vitro. Further mechanistic investigations clarified that TopBP1 promoted proliferation and migration by activating ATR-Chk1 signaling pathway.
                ER  -

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COVID-19
Why does COVID-19 disproportionately affect older people?

Amber L. Mueller, Maeve S. McNamara, David A. Sinclair,

https://doi.org/10.18632/aging.103344 pp 9959—9981

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Mueller AL, McNamara MS, Sinclair DA, . Why does COVID-19 disproportionately affect older people?. . 12:9959-9981. https://doi.org/10.18632/aging.103344

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                TY  - JOUR
                AU  - Mueller, Amber L. 
                AU  - McNamara, Maeve S. 
                AU  - Sinclair, David A. 
                TI  - Why does COVID-19 disproportionately affect older people?
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103344
                DO  - 10.18632/aging.103344
                SP  - 9959
                EP  - 9981
                PY  - 
                AB  - The severity and outcome of coronavirus disease 2019 (COVID-19) largely depends on a patient&#x2019;s age. Adults over 65 years of age represent 80% of hospitalizations and have a 23-fold greater risk of death than those under 65. In the clinic, COVID-19 patients most commonly present with fever, cough and dyspnea, and from there the disease can progress to acute respiratory distress syndrome, lung consolidation, cytokine release syndrome, endotheliitis, coagulopathy, multiple organ failure and death. Comorbidities such as cardiovascular disease, diabetes and obesity increase the chances of fatal disease, but they alone do not explain why age is an independent risk factor. Here, we present the molecular differences between young, middle-aged and older people that may explain why COVID-19 is a mild illness in some but life-threatening in others. We also discuss several biological age clocks that could be used in conjunction with genetic tests to identify both the mechanisms of the disease and individuals most at risk. Finally, based on these mechanisms, we discuss treatments that could increase the survival of older people, not simply by inhibiting the virus, but by restoring patients&#x2019; ability to clear the infection and effectively regulate immune responses.
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Relevance of oxidative stress and inflammation in frailty based on human studies and mouse models

María Álvarez-Satta, Alejandro Berna-Erro, Estefania Carrasco-Garcia, Ainhoa Alberro, Ander Saenz-Antoñanzas, Itziar Vergara, David Otaegui, Ander Matheu,

https://doi.org/10.18632/aging.103295 pp 9982—9999

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Álvarez-Satta M, Berna-Erro A, Carrasco-Garcia E, Alberro A, Saenz-Antoñanzas A, Vergara I, Otaegui D, Matheu A, . Relevance of oxidative stress and inflammation in frailty based on human studies and mouse models. . 12:9982-9999. https://doi.org/10.18632/aging.103295

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                TY  - JOUR
                AU  - Álvarez-Satta, María 
                AU  - Berna-Erro, Alejandro 
                AU  - Carrasco-Garcia, Estefania 
                AU  - Alberro, Ainhoa 
                AU  - Saenz-Antoñanzas, Ander 
                AU  - Vergara, Itziar 
                AU  - Otaegui, David 
                AU  - Matheu, Ander 
                TI  - Relevance of oxidative stress and inflammation in frailty based on human studies and mouse models
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103295
                DO  - 10.18632/aging.103295
                SP  - 9982
                EP  - 9999
                PY  - 
                AB  - Frailty represents a state of vulnerability and increases the risk of negative health outcomes, which is becoming an important public health problem. Over recent years, multiple independent studies have attempted to identify biomarkers that can predict, diagnose, and monitor frailty at the biological level. Among them, several promising candidates have been associated with frailty status including antioxidants and free radicals, and also inflammatory response biomarkers. In this review, we will summarize the more recent advances in this field. Moreover, the identification of scales and measurements to detect and quantify frailty in aged mice, as well as the generation of mouse models, have started to unravel the underlying biological and molecular mechanisms of frailty. We will discuss them here with an emphasis on murine models with overexpression of glucose-6-phosphate dehydrogenase and loss of function of superoxide dismutase and interleukin 10, which reveal that altered oxidative stress and inflammation pathways are involved in the physiopathology of frailty. In summary, we provide the current available evidence, from both human cohorts and experimental animal models, that highlights oxidative damage and inflammation as relevant biomarkers and drivers of frailty.
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Correction for: Hypothalamic S1P/S1PR1 axis controls energy homeostasis in Middle-Aged Rodents: the reversal effects of physical exercise

Vagner Ramon Rodrigues Silva, Carlos Kiyoshi Katashima, Carla G. Bueno Silva, Luciene Lenhare, Thayana Oliveira Micheletti, Rafael Ludemann Camargo, Ana Carolina Ghezzi, Juliana Alves Camargo, Alexandre Moura Assis, Natalia Tobar, Joseane Morari, Daniela S. Razolli, Leandro Pereira Moura, José Rodrigo Pauli, Dennys Esper Cintra, Lício Augusto Velloso, Mario J.A. Saad, Eduardo Rochete Ropelle,

https://doi.org/10.18632/aging.103194 pp 10000

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Rodrigues Silva VR, Katashima CK, Silva CGB, Lenhare L, Micheletti TO, Camargo RL, Ghezzi AC, Camargo JA, Assis AM, Tobar N, Morari J, Razolli DS, Moura LP, et al, . Correction for: Hypothalamic S1P/S1PR1 axis controls energy homeostasis in Middle-Aged Rodents: the reversal effects of physical exercise. . 12:10000-10000. https://doi.org/10.18632/aging.103194

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                TY  - JOUR
                AU  - Rodrigues Silva, Vagner Ramon 
                AU  - Katashima, Carlos Kiyoshi 
                AU  - Silva, Carla G. Bueno 
                AU  - Lenhare, Luciene 
                AU  - Micheletti, Thayana Oliveira 
                AU  - Camargo, Rafael Ludemann 
                AU  - Ghezzi, Ana Carolina 
                AU  - Camargo, Juliana Alves 
                AU  - Assis, Alexandre Moura 
                AU  - Tobar, Natalia 
                AU  - Morari, Joseane 
                AU  - Razolli, Daniela S. 
                AU  - Moura, Leandro Pereira 
                AU  - Pauli, José Rodrigo 
                AU  - Cintra, Dennys Esper 
                AU  - Velloso, Lício Augusto 
                AU  - Saad, Mario J.A. 
                AU  - Ropelle, Eduardo Rochete 
                TI  - Correction for: Hypothalamic S1P/S1PR1 axis controls energy homeostasis in Middle-Aged Rodents: the reversal effects of physical exercise
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103194
                DO  - 10.18632/aging.103194
                SP  - 10000
                EP  - 10000
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Rodrigues Silva, Vagner Ramon 
                AU  - Katashima, Carlos Kiyoshi 
                AU  - Silva, Carla G. Bueno 
                AU  - Lenhare, Luciene 
                AU  - Micheletti, Thayana Oliveira 
                AU  - Camargo, Rafael Ludemann 
                AU  - Ghezzi, Ana Carolina 
                AU  - Camargo, Juliana Alves 
                AU  - Assis, Alexandre Moura 
                AU  - Tobar, Natalia 
                AU  - Morari, Joseane 
                AU  - Razolli, Daniela S. 
                AU  - Moura, Leandro Pereira 
                AU  - Pauli, José Rodrigo 
                AU  - Cintra, Dennys Esper 
                AU  - Velloso, Lício Augusto 
                AU  - Saad, Mario J.A. 
                AU  - Ropelle, Eduardo Rochete 
                TI  - Correction for: Hypothalamic S1P/S1PR1 axis controls energy homeostasis in Middle-Aged Rodents: the reversal effects of physical exercise
                JO  - 
                JA  - 
                VL  - 12
                IS  - 10
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103194
                DO  - 10.18632/aging.103194
                SP  - 10000
                EP  - 10000
                PY  - 
                AB  - 
                ER  -

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Volume 12, Issue 10

About the Cover

Research Perspective

COVID-19 Metformin and SARS-CoV-2: mechanistic lessons on air pollution to weather the cytokine/thrombotic storm in COVID-19

Javier A. Menendez,

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Xinna Li, Jacquelyn A. Frazier, Edward Spahiu, Madaline McPherson, Richard A. Miller,

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Melod Mehdipour, Colin Skinner, Nathan Wong, Michael Lieb, Chao Liu, Jessy Etienne, Cameron Kato, Dobri Kiprov, Michael J. Conboy, Irina M. Conboy,

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Research Papers

Jingjing Jiang, Xuanyu Piao, Siying Hu, Jingbo Gao, Min Bao,

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Xueru Li, Yu Leng, Xiangji Li, Yawei Wang, Peng Luo, Chi Zhang, Ziwen Wang, Xiaofeng Yue, Chongxing Shen, Long Chen, Zujuan Liu, Chunmeng Shi, Lin Xie,

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Yuhao Chen, Dian Fu, Hai Zhao, Wen Cheng, Feng Xu,

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Keqiang Yan, Lifang Hou, Tiantian Liu, Wei Jiao, Qian Ma, Zhiqing Fang, Shimin Zhang, Daoqing Song, Jikai Liu, Xinghua Gao, Yidong Fan,

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Ruinian Zheng, Jun Jia, Ling Guan, Huiling Yuan, Kejun Liu, Chun Liu, Weibiao Ye, Yuting Liao, Shunhuan Lin, Ou Huang,

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Xiaofeng Shi, Shuang Pan, Li Li, Yongqi Li, Wei Ma, Han Wang, Caiming Xu, Lei Li, Dong Wang,

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Nan Zhang, Yuan Xing, Yongzhou Yu, Chao Liu, Baohua Jin, Lifang Huo, Dezhi Kong, Zuxiao Yang, Xiangjian Zhang, Ruimao Zheng, Zhanfeng Jia, Lin Kang, Wei Zhang,

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Jiaying Tan, Jun Shen, Huigeng Zhu, Ye Gong, Hechen Zhu, Junping Li, Shan Lin, Gang Wu, Tao Sun,

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Dimin Wang, Kai Wang, Zhenlei Liu, Zonglin Wang, Hao Wu,

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Yuan Xiong, Lang Chen, Tao Yu, Chenchen Yan, Wu Zhou, Faqi Cao, Xiaomeng You, Yingqi Zhang, Yun Sun, Jing Liu, Hang Xue, Yiqiang Hu, Dong Chen, Bobin Mi, Guohui Liu,

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Imran Tarique, Yonghong Shi, Noor Samad Gandahi, Baitao Ding, Ping Yang, Chang Chen, Waseem Ali Vistro, Quisheng Chen,

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Yang Lu, Li Zhou, Lijun Wang, Shan He, Honglei Ren, Nian Zhou, Zhenming Hu,

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Li Luo, Lusheng Xiao, Guili Lian, Huajun Wang, Liangdi Xie,

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Sonali Nashine, M. Cristina Kenney,

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Lile Jiang, Jinquan Cui, Cuilian Zhang, Juanke Xie, Shaodi Zhang, Dongjun Fu, Wei Duo,

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Chao Zhou, Pu Wang, Lei Lei, Yi Huang, Yue Wu,

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COVID-19
Metformin and SARS-CoV-2: mechanistic lessons on air pollution to weather the cytokine/thrombotic storm in COVID-19