Volume 11, Issue 22

Bakula D, Ablasser A, Aguzzi A, Antebi A, Barzilai N, Bittner M, Jensen MB, Calkhoven CF, Chen D, Grey ADd, Feige JN, Georgievskaya A, Gladyshev VN, et al, . Latest advances in aging research and drug discovery. . 11:9971-9981. https://doi.org/10.18632/aging.102487

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                TY  - JOUR
                AU  - Bakula, Daniela 
                AU  - Ablasser, Andrea 
                AU  - Aguzzi, Adriano 
                AU  - Antebi, Adam 
                AU  - Barzilai, Nir 
                AU  - Bittner, Martin-Immanuel 
                AU  - Jensen, Martin Borch 
                AU  - Calkhoven, Cornelis F. 
                AU  - Chen, Danica 
                AU  - Grey, Aubrey D.N.J. de 
                AU  - Feige, Jerome N. 
                AU  - Georgievskaya, Anastasia 
                AU  - Gladyshev, Vadim N. 
                AU  - Golato, Tyler 
                AU  - Gudkov, Andrei V. 
                AU  - Hoppe, Thorsten 
                AU  - Kaeberlein, Matt 
                AU  - Katajisto, Pekka 
                AU  - Kennedy, Brian K. 
                AU  - Lal, Unmesh 
                AU  - Martin-Villalba, Ana 
                AU  - Moskalev, Alexey A. 
                AU  - Ozerov, Ivan 
                AU  - Petr, Michael A. 
                AU  - Reason,  
                AU  - Rubinsztein, David C. 
                AU  - Tyshkovskiy, Alexander 
                AU  - Vanhaelen, Quentin 
                AU  - Zhavoronkov, Alex 
                AU  - Scheibye-Knudsen, Morten 
                TI  - Latest advances in aging research and drug discovery
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102487
                DO  - 10.18632/aging.102487
                SP  - 9971
                EP  - 9981
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Bakula, Daniela 
                AU  - Ablasser, Andrea 
                AU  - Aguzzi, Adriano 
                AU  - Antebi, Adam 
                AU  - Barzilai, Nir 
                AU  - Bittner, Martin-Immanuel 
                AU  - Jensen, Martin Borch 
                AU  - Calkhoven, Cornelis F. 
                AU  - Chen, Danica 
                AU  - Grey, Aubrey D.N.J. de 
                AU  - Feige, Jerome N. 
                AU  - Georgievskaya, Anastasia 
                AU  - Gladyshev, Vadim N. 
                AU  - Golato, Tyler 
                AU  - Gudkov, Andrei V. 
                AU  - Hoppe, Thorsten 
                AU  - Kaeberlein, Matt 
                AU  - Katajisto, Pekka 
                AU  - Kennedy, Brian K. 
                AU  - Lal, Unmesh 
                AU  - Martin-Villalba, Ana 
                AU  - Moskalev, Alexey A. 
                AU  - Ozerov, Ivan 
                AU  - Petr, Michael A. 
                AU  - Reason,  
                AU  - Rubinsztein, David C. 
                AU  - Tyshkovskiy, Alexander 
                AU  - Vanhaelen, Quentin 
                AU  - Zhavoronkov, Alex 
                AU  - Scheibye-Knudsen, Morten 
                TI  - Latest advances in aging research and drug discovery
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102487
                DO  - 10.18632/aging.102487
                SP  - 9971
                EP  - 9981
                PY  - 
                AB  - An increasing aging population poses a significant challenge to societies worldwide. A better understanding of the molecular, cellular, organ, tissue, physiological, psychological, and even sociological changes that occur with aging is needed in order to treat age-associated diseases. The field of aging research is rapidly expanding with multiple advances transpiring in many previously disconnected areas. Several major pharmaceutical, biotechnology, and consumer companies made aging research a priority and are building internal expertise, integrating aging research into traditional business models and exploring new go-to-market strategies. Many of these efforts are spearheaded by the latest advances in artificial intelligence, namely deep learning, including generative and reinforcement learning. To facilitate these trends, the Center for Healthy Aging at the University of Copenhagen and Insilico Medicine are building a community of Key Opinion Leaders (KOLs) in these areas and launched the annual conference series titled &#x201C;Aging Research and Drug Discovery (ARDD)&#x201D; held in the capital of the pharmaceutical industry, Basel, Switzerland (www.agingpharma.org). This ARDD collection contains summaries from the 6th annual meeting that explored aging mechanisms and new interventions in age-associated diseases. The 7th annual ARDD exhibition will transpire 2nd-4th of September, 2020, in Basel.
                ER  -

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Circular RNA hsa_circ_0000515 acts as a miR-326 sponge to promote cervical cancer progression through up-regulation of ELK1

Qiu Tang, Zhigang Chen, Liangping Zhao, Hai Xu,

https://doi.org/10.18632/aging.102356 pp 9982—9999

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Tang Q, Chen Z, Zhao L, Xu H, . Circular RNA hsa_circ_0000515 acts as a miR-326 sponge to promote cervical cancer progression through up-regulation of ELK1. . 11:9982-9999. https://doi.org/10.18632/aging.102356

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                TY  - JOUR
                AU  - Tang, Qiu 
                AU  - Chen, Zhigang 
                AU  - Zhao, Liangping 
                AU  - Xu, Hai 
                TI  - Circular RNA hsa_circ_0000515 acts as a miR-326 sponge to promote cervical cancer progression through up-regulation of ELK1
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102356
                DO  - 10.18632/aging.102356
                SP  - 9982
                EP  - 9999
                PY  - 
                AB  - This study investigates the role of circular RNA (circRNA) hsa_circ_0000515 in cervical cancer and the underlying mechanism associated with microRNA-326 (miR-326). hsa_circ_0000515 and ETS transcription factor ELK1 (ELK1) were initially over-expressed and miR-326 was down-regulated in cervical cancer tissues and cells. Low hsa_circ_0000515 expression was found to be associated with favorable prognosis of patients with cervical cancer. A series of mimics, inhibitors, over-expression plasmids or siRNAs were introduced into cervical cancer cells to alter the expression of hsa_circ_0000515, miR-326 and ELK1. In vitro experiments exhibited that silencing of hsa_circ_0000515 or upregulation of miR-326 resulted in suppressed proliferation and invasion, along with induced apoptosis and autophagy of cervical cancer cells. Dual-luciferase reporter assay, RNA pull-down and RIP assays highlighted that hsa_circ_0000515 was able to act as a ceRNA of miR-326 to increase ELK1. Furthermore, enhancement of ELK1 expression resulted in enhanced proliferation and invasion but repressed apoptosis and autophagy of cervical cancer cells. In vivo experiments further confirmed the suppressed tumor growth by hsa_circ_0000515 silencing. Our findings demonstrated that hsa_circ_0000515 acts as a tumor promoter in cervical cancer. The study provides evidence for targeting hsa_circ_0000515 for therapeutic purposes in treating cervical cancer.
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Mapping the patterns of cortical thickness in single- and multiple-domain amnestic mild cognitive impairment patients: a pilot study

Pan Sun, Wutao Lou, Jianghong Liu, Lin Shi, Kuncheng Li, Defeng Wang, Vincent CT Mok, Peipeng Liang,

https://doi.org/10.18632/aging.102362 pp 10000—10015

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Sun P, Lou W, Liu J, Shi L, Li K, Wang D, Mok VC, Liang P, . Mapping the patterns of cortical thickness in single- and multiple-domain amnestic mild cognitive impairment patients: a pilot study. . 11:10000-10015. https://doi.org/10.18632/aging.102362

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                TY  - JOUR
                AU  - Sun, Pan 
                AU  - Lou, Wutao 
                AU  - Liu, Jianghong 
                AU  - Shi, Lin 
                AU  - Li, Kuncheng 
                AU  - Wang, Defeng 
                AU  - Mok, Vincent CT 
                AU  - Liang, Peipeng 
                TI  - Mapping the patterns of cortical thickness in single- and multiple-domain amnestic mild cognitive impairment patients: a pilot study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102362
                DO  - 10.18632/aging.102362
                SP  - 10000
                EP  - 10015
                PY  - 
                AB  - Amnestic mild cognitive impairment (aMCI) is considered as a transitional stage between the expected cognitive decline of normal aging and Alzheimer&#x2019;s disease (AD). Structural brain difference has shown the potential in cognitive related diagnosis, however cortical thickness patterns transferred from aMCI to AD, especially in the subtypes of aMCI, is still unclear. In this study, we investigated the cortical thickness discrepancies among AD, aMCI and normal control (NC) entities, especially for two subtypes of aMCI - multiple-domain aMCI (aMCI-m) and single-domain aMCI (aMCI-s). Both region of interest (ROI)-based and vertex-based statistical strategies were performed for group-level cortical thickness comparison. Spearman correlation was utilized to identify the correlation between cortical thickness and clinical neuropsychological scores. The result demonstrated that there was a significant cortical thickness decreasing tendency in fusiform gyrus from NC to aMCI-s to aMCI-m to finally AD in both left and right hemispheres. Meanwhile, the two subtypes of aMCI showed cortical thickness difference in middle temporal gyrus in left hemisphere. Spearman correlation indicated that neuropsychological scores had significant correlations with entorhinal, inferior temporal and middle temporal gyrus. The findings suggested that cortical thickness might serve as a potential imaging biomarker for the differential diagnosis of cognitive impairment.
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Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice

Yongyao Yang, Feng Tang, Fang Wei, Long Yang, Chunyan Kuang, Hongming Zhang, Jiusheng Deng, Qiang Wu,

https://doi.org/10.18632/aging.102388 pp 10016—10030

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Yang Y, Tang F, Wei F, Yang L, Kuang C, Zhang H, Deng J, Wu Q, . Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice. . 11:10016-10030. https://doi.org/10.18632/aging.102388

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                TY  - JOUR
                AU  - Yang, Yongyao 
                AU  - Tang, Feng 
                AU  - Wei, Fang 
                AU  - Yang, Long 
                AU  - Kuang, Chunyan 
                AU  - Zhang, Hongming 
                AU  - Deng, Jiusheng 
                AU  - Wu, Qiang 
                TI  - Silencing of long non-coding RNA H19 downregulates CTCF to protect against atherosclerosis by upregulating PKD1 expression in ApoE knockout mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102388
                DO  - 10.18632/aging.102388
                SP  - 10016
                EP  - 10030
                PY  - 
                AB  - This study aimed to explore the interactions among long non-coding RNA H19, transcriptional factor CCCTC-binding factor (CTCF) and polycystic kidney disease 1 (PKD1), and to investigate its potentially regulatory effect on vulnerable plaque formation and angiogenesis of atherosclerosis. We established an atherosclerosis mouse model in ApoE knockout mice, followed by gain- and loss-of-function approaches. H19 was upregulated in aortic tissues of atherosclerosis mice, but silencing of H19 significantly inhibited atherosclerotic vulnerable plaque formation and intraplaque angiogenesis, accompanied by a downregulated expression of MMP-2, VEGF, and p53 and an upregulated expression of TIMP-1. Moreover, opposite results were found in the aortic tissues of atherosclerosis mice treated with H19 or CTCF overexpression. H19 was capable of recruiting CTCF to suppress PKD1, thus promoting atherosclerotic vulnerable plaque formation and intraplaque angiogenesis in atherosclerosis mice. The present study provides evidence that H19 recruits CTCF to downregulate the expression of PKD1, thereby promoting vulnerable plaque formation and intraplaque angiogenesis in mice with atherosclerosis.
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DNA methylation profile is a quantitative measure of biological aging in children

Xiaohui Wu, Weidan Chen, Fangqin Lin, Qingsheng Huang, Jiayong Zhong, Huan Gao, Yanyan Song, Huiying Liang,

https://doi.org/10.18632/aging.102399 pp 10031—10051

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Wu X, Chen W, Lin F, Huang Q, Zhong J, Gao H, Song Y, Liang H, . DNA methylation profile is a quantitative measure of biological aging in children. . 11:10031-10051. https://doi.org/10.18632/aging.102399

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                TY  - JOUR
                AU  - Wu, Xiaohui 
                AU  - Chen, Weidan 
                AU  - Lin, Fangqin 
                AU  - Huang, Qingsheng 
                AU  - Zhong, Jiayong 
                AU  - Gao, Huan 
                AU  - Song, Yanyan 
                AU  - Liang, Huiying 
                TI  - DNA methylation profile is a quantitative measure of biological aging in children
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102399
                DO  - 10.18632/aging.102399
                SP  - 10031
                EP  - 10051
                PY  - 
                AB  - DNA methylation changes within the genome can be used to predict human age. However, the existing biological age prediction models based on DNA methylation are predominantly adult-oriented. We established a methylation-based age prediction model for children (9-212 months old) using data from 716 blood samples in 11 DNA methylation datasets. Our elastic net model includes 111 CpG sites, mostly in genes associated with development and aging. The model performed well and exhibited high precision, yielding a 98% correlation between the DNA methylation age and the chronological age, with an error of only 6.7 months. When we used the model to assess age acceleration in children based on their methylation data, we observed the following: first, the aging rate appears to be fastest in mid-childhood, and this acceleration is more pronounced in autistic children; second, lead exposure early in life increases the aging rate in boys, but not in girls; third, short-term recombinant human growth hormone treatment has little effect on the aging rate of children. Our child-specific methylation-based age prediction model can effectively detect epigenetic changes and health imbalances early in life. This may thus be a useful model for future studies of epigenetic interventions for age-related diseases.
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Late stage gastric cancer patients with extra gained HER2 positivity by dual block assessment may not show compromised efficacy to trastuzumab treatment

Chen Xu, Yalan Liu, Dongxian Jiang, Xiaowen Ge, Jie Huang, Jieakesu Su, Xue Zhang, Shaohua Lu, Yuan Ji, Jun Hou, Tianshu Liu, Yingyong Hou,

https://doi.org/10.18632/aging.102415 pp 10052—10060

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Xu C, Liu Y, Jiang D, Ge X, Huang J, Su J, Zhang X, Lu S, Ji Y, Hou J, Liu T, Hou Y, . Late stage gastric cancer patients with extra gained HER2 positivity by dual block assessment may not show compromised efficacy to trastuzumab treatment. . 11:10052-10060. https://doi.org/10.18632/aging.102415

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                TY  - JOUR
                AU  - Xu, Chen 
                AU  - Liu, Yalan 
                AU  - Jiang, Dongxian 
                AU  - Ge, Xiaowen 
                AU  - Huang, Jie 
                AU  - Su, Jieakesu 
                AU  - Zhang, Xue 
                AU  - Lu, Shaohua 
                AU  - Ji, Yuan 
                AU  - Hou, Jun 
                AU  - Liu, Tianshu 
                AU  - Hou, Yingyong 
                TI  - Late stage gastric cancer patients with extra gained HER2 positivity by dual block assessment may not show compromised efficacy to trastuzumab treatment
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102415
                DO  - 10.18632/aging.102415
                SP  - 10052
                EP  - 10060
                PY  - 
                AB  - Dual block HER2 assessment can effectively increase the HER2 positive rate in resected specimens of gastric cancer (GC). The aim of this study is to explore whether GC patients with extra gained HER2 positivity by dual block assessment can benefit from trastuzumab therapy. Twenty-eight GC patients receiving gastrectomy prior to trastuzumab treatment were retrospectively analyzed. All the cases routinely accepted dual block HER2 assessment. The cases were divided into 2 cohorts based on HER2 status: cohort A with concordant HER2 results and cohort B with discordant HER2 results between the two blocks (cases with extra gained HER2 positivity). Response rate (RR), progress free survival (PFS) and overall survival (OS) were compared between the two cohorts. The results showed that no significant differences were found between the two cohorts in main clinicopathologic characteristics. No statistical difference was found in response rate (47.6% vs 57.1%) (P=1.0), either. The two cohorts did not demonstrate statistical differences in the PFS (10.5 months (95%CI 6.4-14.6) vs 8.0 months (95%CI 3.2-12.8), P=0.686) and the OS (23.3 months (95%CI 12.1-34.5) vs 20.0 months (95%CI 10.1-29.9), P=0.776). In conclusion, our study suggests that patients with extra gained HER2 positivity may not show compromised efficacy to trastuzumab treatment.
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PGC1α activation by pterostilbene ameliorates acute doxorubicin cardiotoxicity by reducing oxidative stress via enhancing AMPK and SIRT1 cascades

Dong Liu, Zhiqiang Ma, Liqun Xu, Xiaoyan Zhang, Shubin Qiao, Jiansong Yuan,

https://doi.org/10.18632/aging.102418 pp 10061—10073

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Liu D, Ma Z, Xu L, Zhang X, Qiao S, Yuan J, . PGC1α activation by pterostilbene ameliorates acute doxorubicin cardiotoxicity by reducing oxidative stress via enhancing AMPK and SIRT1 cascades. . 11:10061-10073. https://doi.org/10.18632/aging.102418

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                TY  - JOUR
                AU  - Liu, Dong 
                AU  - Ma, Zhiqiang 
                AU  - Xu, Liqun 
                AU  - Zhang, Xiaoyan 
                AU  - Qiao, Shubin 
                AU  - Yuan, Jiansong 
                TI  - PGC1α activation by pterostilbene ameliorates acute doxorubicin cardiotoxicity by reducing oxidative stress via enhancing AMPK and SIRT1 cascades
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102418
                DO  - 10.18632/aging.102418
                SP  - 10061
                EP  - 10073
                PY  - 
                AB  - Doxorubicin (DOX) is a widely used and potent anticancer agent, but DOX dose-dependently induced cardiotoxicity greatly limits its use in clinic. Pterostilbene, a natural analog of resveratrol, is a known antioxidant and exerts myocardial protection. The present study explored the action and detailed mechanism of pterostilbene on DOX-treated cardiomyocytes. We investigated the effects of pterostilbene on established acute DOX-induced cardiotoxicity models in both H9c2 cells treated with 1 &#x3BC;M DOX and C57BL/6 mice with DOX (20 mg/kg cumulative dose) exposure. Pterostilbene markedly alleviated the DOX exposure-induced acute myocardial injury. Both in vitro and in vivo studies revealed that pterostilbene inhibited the acute DOX exposure-caused oxidative stress and mitochondrial morphological disorder via the PGC1&#x3B1; upregulation through activating AMPK and via PGC1&#x3B1; deacetylation through enhancing SIRT1. However, these effects were partially reversed by knockdown of AMPK or SIRT1 in vitro and treatment of Compound C (AMPK inhibitor) or EX527 (SIRT1 inhibitor) in vivo. Our results indicate that pterostilbene protects cardiomyocytes from acute DOX exposure-induced oxidative stress and mitochondrial damage via PGC1&#x3B1; upregulation and deacetylation through activating AMPK and SIRT1 cascades.
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Characterization of long non-coding RNA and messenger RNA profiles in laryngeal cancer by weighted gene co-expression network analysis

Huanhuan Liu, Yi Sun, Huan Tian, Xiaolian Xiao, Jiaqi Zhang, Yongzhen Wang, Fengyan Yu,

https://doi.org/10.18632/aging.102419 pp 10074—10099

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Liu H, Sun Y, Tian H, Xiao X, Zhang J, Wang Y, Yu F, . Characterization of long non-coding RNA and messenger RNA profiles in laryngeal cancer by weighted gene co-expression network analysis. . 11:10074-10099. https://doi.org/10.18632/aging.102419

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                TY  - JOUR
                AU  - Liu, Huanhuan 
                AU  - Sun, Yi 
                AU  - Tian, Huan 
                AU  - Xiao, Xiaolian 
                AU  - Zhang, Jiaqi 
                AU  - Wang, Yongzhen 
                AU  - Yu, Fengyan 
                TI  - Characterization of long non-coding RNA and messenger RNA profiles in laryngeal cancer by weighted gene co-expression network analysis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102419
                DO  - 10.18632/aging.102419
                SP  - 10074
                EP  - 10099
                PY  - 
                AB  - Laryngeal cancer (LC) is a malignant tumor in the head and neck region. It was recently elucidated that long non-coding RNAs (lncRNAs) participate in the pathogenesis of LC. However, the detailed mechanism of lncRNA in LC and whether long non-coding RNAs serve as effective biomarkers remains unclear. Ribonucleic acid (RNA) sequence data of LC and 11 patient clinical traits were extracted from The Cancer Genome Atlas (TCGA) database and analyzed by weighted gene co-expression network analysis (WGCNA). A total of 9 co-expression modules were identified. The co-expression Pink module significantly correlated with four clinical traits, including history of smoking, lymph node count, tumor status, and the success of follow-up treatment. Based on the co-expression Pink module, lncRNA-microRNA (miRNA)-messenger RNA (mRNA) and lncRNA-RNA binding protein-mRNA networks were constructed. We found that 8 lncRNAs significantly impacted overall survival (OS) in LC patients. These identified lncRNA and hub gene biomarkers were also validated in multiple LC cells in vitro via qPCR. Taken together, this study provided the framework of co-expression gene modules of LC and identified some important biomarkers in LC development and disease progression.
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Decreased inter-hemispheric interactions but increased intra-hemispheric integration during typical aging

Qunlin Chen, Yunman Xia, Kaixiang Zhuang, Xinran Wu, Guangyuan Liu, Jiang Qiu,

https://doi.org/10.18632/aging.102421 pp 10100—10115

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Chen Q, Xia Y, Zhuang K, Wu X, Liu G, Qiu J, . Decreased inter-hemispheric interactions but increased intra-hemispheric integration during typical aging. . 11:10100-10115. https://doi.org/10.18632/aging.102421

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                TY  - JOUR
                AU  - Chen, Qunlin 
                AU  - Xia, Yunman 
                AU  - Zhuang, Kaixiang 
                AU  - Wu, Xinran 
                AU  - Liu, Guangyuan 
                AU  - Qiu, Jiang 
                TI  - Decreased inter-hemispheric interactions but increased intra-hemispheric integration during typical aging
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102421
                DO  - 10.18632/aging.102421
                SP  - 10100
                EP  - 10115
                PY  - 
                AB  - Normal aging is known to be accompanied by decreased segregation across the whole-brain functional network, which is associated with cognitive decline. Although compelling evidence supports reduced segregation and increased integration in whole-brain functional connectivity with aging, the age effect on the reorganization of large-scale functional networks at the hemispheric level remains unclear. Here, we aimed to examine age-related differences in inter-hemispheric interactions and intra-hemispheric integration by using resting-state functional MRI data of a healthy adult lifespan sample. The results showed that age-related decreases in inter-hemispheric integration were found in entire functional networks in both hemispheres, except for the sensorimotor network (SMN) and posterior default mode network (DMN). Specifically, aging was accompanied by increasing inter-hemispheric segregation in the left frontoparietal network (FPN) and left ventral attention network (VAN), as well as right-brain networks located in the auditory network (AN), visual network (VN), and temporal parts of the DMN. Moreover, aging was associated with increasing intra-hemispheric integration within the bilateral VN and posterior DMN while decreasing intra-hemispheric integration within the right VAN. These remarkable changes with aging confirm that there are dynamic interactions between functional networks across the lifespan and provide a means of investigating the mechanisms of cognitive aging.
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The construction and analysis of tumor-infiltrating immune cell and ceRNA networks in recurrent soft tissue sarcoma

Runzhi Huang, Tong Meng, Rui Chen, Penghui Yan, Jie Zhang, Peng Hu, Xiaolong Zhu, Huabin Yin, Dianwen Song, Zongqiang Huang,

https://doi.org/10.18632/aging.102424 pp 10116—10143

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Huang R, Meng T, Chen R, Yan P, Zhang J, Hu P, Zhu X, Yin H, Song D, Huang Z, . The construction and analysis of tumor-infiltrating immune cell and ceRNA networks in recurrent soft tissue sarcoma. . 11:10116-10143. https://doi.org/10.18632/aging.102424

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                TY  - JOUR
                AU  - Huang, Runzhi 
                AU  - Meng, Tong 
                AU  - Chen, Rui 
                AU  - Yan, Penghui 
                AU  - Zhang, Jie 
                AU  - Hu, Peng 
                AU  - Zhu, Xiaolong 
                AU  - Yin, Huabin 
                AU  - Song, Dianwen 
                AU  - Huang, Zongqiang 
                TI  - The construction and analysis of tumor-infiltrating immune cell and ceRNA networks in recurrent soft tissue sarcoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102424
                DO  - 10.18632/aging.102424
                SP  - 10116
                EP  - 10143
                PY  - 
                AB  - Soft tissue sarcoma (STS) is one of the most challenging tumors for medical oncologists, with a high rate of recurrence after initial resection. In this study, a recurrent STS-specific competitive endogenous RNA (ceRNA) network including seven recurrence and overall survival (OS)-associated genes (LPP-AS2, MUC1, GAB2, hsa-let-7i-5p, hsa-let-7f-5p, hsa-miR-101-3p and hsa-miR-1226-3p) was established based on the gene expression profiling of 259 primary sarcomas and 3 local recurrence samples from the TCGA database. The algorithm &#x201C;cell type identification by estimating relative subsets of RNA transcripts (CIBERSORT)&#x201D; was applied to estimate the fraction of immune cells in sarcomas. Based on 5 recurrence and OS-associated immune cells (NK cells activated, dendritic cells resting, mast cells resting, mast cells activated and macrophages M1), we constructed a recurrent STS-specific immune cells network. Both nomograms were identified to have good reliabilities (Area Under Curve (AUC) of 5-year survival is 0.724 and 0.773, respectively). Then the co-expression analysis was performed to identify the potential regulation network among recurrent STS-specific immune cells and ceRNAs. Hsa-miR-1226-3p and MUC1 were significantly correlated and dendritic cells resting was related to hsa-miR-1226-3p. Additionally, the expression of MUC1 and dendritic cell marker CD11c were also verified by immunohistochemistry (IHC) assay and multidimensional databases. In conclusion, this study illustrated the potential mechanism of hsa-miR-1226-3p regulating MUC1 and dendritic cells resting might play an important role in STS recurrence. These findings might provide potential prognostic biomarkers and therapeutic targets for recurrent STS.
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Long noncoding RNA LINC00899 suppresses breast cancer progression by inhibiting miR-425

Wenying Zhou, Jiao Gong, Yaqiong Chen, Jiahao Chen, Qi Zhuang, Jing Cao, Zhixiong Mei, Bo Hu,

https://doi.org/10.18632/aging.102426 pp 10144—10153

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Zhou W, Gong J, Chen Y, Chen J, Zhuang Q, Cao J, Mei Z, Hu B, . Long noncoding RNA LINC00899 suppresses breast cancer progression by inhibiting miR-425. . 11:10144-10153. https://doi.org/10.18632/aging.102426

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                TY  - JOUR
                AU  - Zhou, Wenying 
                AU  - Gong, Jiao 
                AU  - Chen, Yaqiong 
                AU  - Chen, Jiahao 
                AU  - Zhuang, Qi 
                AU  - Cao, Jing 
                AU  - Mei, Zhixiong 
                AU  - Hu, Bo 
                TI  - Long noncoding RNA LINC00899 suppresses breast cancer progression by inhibiting miR-425
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102426
                DO  - 10.18632/aging.102426
                SP  - 10144
                EP  - 10153
                PY  - 
                AB  - Long non-coding RNAs (lncRNAs) have emerged as important regulators in cancer, including breast cancer. The precise expression pattern of long noncoding RNA 00899 (LINC00899) in breast cancer and its mechanisms of action have not been reported. Here, we found that LINC00899 is downregulated in breast cancer tissues and cell lines. Kaplan-Meier analysis showed that elevated LINC00899 expression is closely associated with better relapse-free survival (RFS) in breast cancer, including the basal, luminal A or luminal B breast cancer subtypes. Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes pathway analysis suggested that LINC00899 is closely related to several cancer associated processes, including tight junction- and metabolism-associated pathways. Functional assays indicated that LINC00899 overexpression suppresses proliferation, migration and invasion of breast cancer cells in vitro. Moreover, LINC00899 was found to competitively bind miR-425, thereby functioning as a tumor suppressor by enhancing DICER1. Overexpression of miR-425 attenuated the LINC00899-induced inhibition of breast cancer cell proliferation and invasion. These findings highlight the important role of the LINC00899-miR-425-DICER1 axis in breast cancer cell proliferation and invasion, and could potentially lead to new lncRNA-based diagnostics or therapeutics for breast cancer.
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Prognostic genes in the tumor microenvironment in cervical squamous cell carcinoma

Xin-Bin Pan, Yan Lu, Jian-Li Huang, Ying Long, De-Sheng Yao,

https://doi.org/10.18632/aging.102429 pp 10154—10166

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Pan X, Lu Y, Huang J, Long Y, Yao D, . Prognostic genes in the tumor microenvironment in cervical squamous cell carcinoma. . 11:10154-10166. https://doi.org/10.18632/aging.102429

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                TY  - JOUR
                AU  - Pan, Xin-Bin 
                AU  - Lu, Yan 
                AU  - Huang, Jian-Li 
                AU  - Long, Ying 
                AU  - Yao, De-Sheng 
                TI  - Prognostic genes in the tumor microenvironment in cervical squamous cell carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102429
                DO  - 10.18632/aging.102429
                SP  - 10154
                EP  - 10166
                PY  - 
                AB  - Cervical squamous cell carcinoma (CSCC) is one of the most commonly occurring gynecological malignancies. Because CSCC is a biologically heterogeneous disease, its prognosis varies. Therefore, identifying prognostic biomarkers that reflect its biological heterogeneity could lead to better interventions for patients with a poor prognosis. This study used the ESTIMATE algorithm to identify immune related prognostic genes within the tumor microenvironment of CSCC. The results revealed that high immune scores were associated with better overall survival (P = 0.029). Differential expression analysis revealed 384 intersection genes influencing both the immune and stromal scores. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses showed the 384 intersection genes to be mainly enriched for T cell activation, the region of the membrane, carbohydrate binding, and cytokine-cytokine receptor interaction. Among them, 149 immune genes were predictive of overall survival in CSCC. These findings provide a more comprehensive understanding of immune genes within the tumor microenvironment as well as a list of immune genes prognostic in CSCC.
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Tissue plasminogen activator disrupts the blood-brain barrier through increasing the inflammatory response mediated by pericytes after cerebral ischemia

Eryan Yang, Ying Cai, Xiuhua Yao, Ji Liu, Qixue Wang, Weili Jin, Qiaoli Wu, Weijia Fan, Lina Qiu, Chunsheng Kang, Jialing Wu,

https://doi.org/10.18632/aging.102431 pp 10167—10182

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Yang E, Cai Y, Yao X, Liu J, Wang Q, Jin W, Wu Q, Fan W, Qiu L, Kang C, Wu J, . Tissue plasminogen activator disrupts the blood-brain barrier through increasing the inflammatory response mediated by pericytes after cerebral ischemia. . 11:10167-10182. https://doi.org/10.18632/aging.102431

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                TY  - JOUR
                AU  - Yang, Eryan 
                AU  - Cai, Ying 
                AU  - Yao, Xiuhua 
                AU  - Liu, Ji 
                AU  - Wang, Qixue 
                AU  - Jin, Weili 
                AU  - Wu, Qiaoli 
                AU  - Fan, Weijia 
                AU  - Qiu, Lina 
                AU  - Kang, Chunsheng 
                AU  - Wu, Jialing 
                TI  - Tissue plasminogen activator disrupts the blood-brain barrier through increasing the inflammatory response mediated by pericytes after cerebral ischemia
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102431
                DO  - 10.18632/aging.102431
                SP  - 10167
                EP  - 10182
                PY  - 
                AB  - Pericytes, important elements of the blood-brain barrier (BBB), play critical roles in maintaining BBB integrity and modulating hemostasis, angiogenesis, inflammation and phagocytic function. We investigated whether pericytes are involved in the recombinant tissue plasminogen activator (rt-PA)-induced inflammatory response, which disrupts the BBB, and investigated the potential mechanisms. Middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation (OGD) were employed to mimic hypoxic-ischemic conditions. Rt-PA was intravenously injected into mice 1 h after 1 h MCAO, and Rt-PA was added to the culture medium after 4 h OGD. Rt-PA treatment aggravated the disruption of the BBB compared with hypoxia treatment, and etanercept (TNF-&#x3B1; inhibitor) combined with rt-PA alleviated the rt-PA-induced BBB disruption in vivo and in vitro. Rt-PA treatment increased the TNF-&#x3B1; and MCP-1 levels and decreased the TGF-&#x3B2;, p-Smad2/3 and PDGFR-&#x3B2; levels compared with hypoxia treatment in vivo and vitro. TGF-&#x3B2; combined with rt-PA decreased TNF-&#x3B1; and MCP-1 secretion and alleviated BBB disruption compared with rt-PA; these changes were abrogated by TPO427736 HCL (a TGF-&#x3B2;/p-Smad2/3 pathway inhibitor) cotreatment in vitro. Rt-PA did not decrease TGF-&#x3B2; and p-Smad2/3 expression in PDGFR-&#x3B2;-overexpressing pericytes after OGD. These findings identify PDGFR-&#x3B2;/TGF-&#x3B2;/p-Smad2/3 signaling in pericytes as a new therapeutic target for the treatment of rt-PA-induced BBB damage.
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Development and validation of a metastasis-associated prognostic signature based on single-cell RNA-seq in clear cell renal cell carcinoma

Chuanjie Zhang, Hongchao He, Xin Hu, Ao Liu, Da Huang, Yang Xu, Lu Chen, Danfeng Xu,

https://doi.org/10.18632/aging.102434 pp 10183—10202

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Zhang C, He H, Hu X, Liu A, Huang D, Xu Y, Chen L, Xu D, . Development and validation of a metastasis-associated prognostic signature based on single-cell RNA-seq in clear cell renal cell carcinoma. . 11:10183-10202. https://doi.org/10.18632/aging.102434

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                TY  - JOUR
                AU  - Zhang, Chuanjie 
                AU  - He, Hongchao 
                AU  - Hu, Xin 
                AU  - Liu, Ao 
                AU  - Huang, Da 
                AU  - Xu, Yang 
                AU  - Chen, Lu 
                AU  - Xu, Danfeng 
                TI  - Development and validation of a metastasis-associated prognostic signature based on single-cell RNA-seq in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102434
                DO  - 10.18632/aging.102434
                SP  - 10183
                EP  - 10202
                PY  - 
                AB  - Single-cell RNA sequencing (scRNA-seq) was recently adopted for deciphering intratumoral heterogeneity across cell sub-populations, including clear cell renal cell carcinoma (ccRCC). Here, we characterized the single-cell expression profiling of 121 cell samples and found 44 metastasis-associated marker genes. Accordingly, we trained and validated 17 pivotal metastasis-associated genes (MAGs) in 626 patients incorporating internal and external cohorts to evaluate the model for predicting overall survival (OS) and progression-free survival (PFS). Correlation analysis revealed that the MAGs correlated significantly with several risk clinical characteristics. Moreover, we conducted Cox regression analysis integrating these independent clinical variables into a MAGs nomogram with superior accuracy in predicting progression events. We further revealed the differential landscape of somatic tumor mutation burden (TMB) between two nomogram-score groups and observed that TMB was also a prognostic biomarker; patients with high MAGs-nomogram scores suffered from a higher TMB, potentially leading to worse prognosis. Last, higher MAGs-nomogram scores correlated with the upregulation of oxidative phosphorylation, the Wnt signaling pathway, and MAPK signaling crosstalk in ccRCC. Overall, we constructed the robust MAGs through scRNA-seq and validated the model in a large patient population, which was valuable for prognostic stratification and providing potential targets against metastatic ccRCC.
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Mitochondrial fission regulator 2 (MTFR2) promotes growth, migration, invasion and tumour progression in breast cancer cells

Guanming Lu, Yuanhui Lai, Tiantian Wang, Weihao Lin, Jinlan Lu, Yanfei Ma, Yongcheng Chen, Haiqing Ma, Ruilei Liu, Jie Li,

https://doi.org/10.18632/aging.102442 pp 10203—10219

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Lu G, Lai Y, Wang T, Lin W, Lu J, Ma Y, Chen Y, Ma H, Liu R, Li J, . Mitochondrial fission regulator 2 (MTFR2) promotes growth, migration, invasion and tumour progression in breast cancer cells. . 11:10203-10219. https://doi.org/10.18632/aging.102442

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                TY  - JOUR
                AU  - Lu, Guanming 
                AU  - Lai, Yuanhui 
                AU  - Wang, Tiantian 
                AU  - Lin, Weihao 
                AU  - Lu, Jinlan 
                AU  - Ma, Yanfei 
                AU  - Chen, Yongcheng 
                AU  - Ma, Haiqing 
                AU  - Liu, Ruilei 
                AU  - Li, Jie 
                TI  - Mitochondrial fission regulator 2 (MTFR2) promotes growth, migration, invasion and tumour progression in breast cancer cells
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102442
                DO  - 10.18632/aging.102442
                SP  - 10203
                EP  - 10219
                PY  - 
                AB  - Introduction: Mitochondrial fission regulator 2 (MTFR2) belongs to the MTFR family, and 2 isoforms of MTFR2 are produced by alternative splicing. The role of MTFR2 in breast cancer (BC) remains unknown.Results: MTFR2 was upregulated in BC tissues and was strongly associated with tumor characteristics. Moreover, Kaplan-Meier and Cox proportional hazards analyses indicated that high MTFR2 expression was related to poor overall survival. In addition, the capacity for migration and invasion decreased in two BC cell lines after knockdown of MTFR2. The epithelial-mesenchymal transition pathway was inhibited in MTFR2-silenced cells. MTFR2 can switch glucose metabolism from OXPHS to glycolysis in a HIF1&#x3B1;- and HIF2&#x3B1;-dependent manner.Conclusion: Taken together, our results indicate that increased expression of MTFR2 is associated with tumour progression in breast cancer cells through switching glucose metabolism from OXPHS to glycolysis in a HIF1&#x3B1;- and HIF2&#x3B1;-dependent manner.Materials and methods: We obtained data from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) to analyse MTFR2 expression in BC. The prognostic value of MTFR2 expression was assessed using the Kaplan-Meier method. The biological influence of MTFR2 on BC cell lines was studied using proliferation, Transwell migration, invasion and mitochondrial function assays.
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Circular RNA CircCCNB1 sponges micro RNA-449a to inhibit cellular senescence by targeting CCNE2

Ai Qing Yu, Zhi Xiao Wang, Wu Wu, Ke Yu Chen, Shi Rong Yan, Ze Bin Mao,

https://doi.org/10.18632/aging.102449 pp 10220—10241

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Yu AQ, Wang ZX, Wu W, Chen KY, Yan SR, Mao ZB, . Circular RNA CircCCNB1 sponges micro RNA-449a to inhibit cellular senescence by targeting CCNE2. . 11:10220-10241. https://doi.org/10.18632/aging.102449

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                TY  - JOUR
                AU  - Yu, Ai Qing 
                AU  - Wang, Zhi Xiao 
                AU  - Wu, Wu 
                AU  - Chen, Ke Yu 
                AU  - Yan, Shi Rong 
                AU  - Mao, Ze Bin 
                TI  - Circular RNA CircCCNB1 sponges micro RNA-449a to inhibit cellular senescence by targeting CCNE2
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102449
                DO  - 10.18632/aging.102449
                SP  - 10220
                EP  - 10241
                PY  - 
                AB  - Circular RNAs (CircRNAs) are a novel subset of non-coding RNA widely present in eukaryotes that play a central role in physiological and pathological conditions. Accumulating evidence has indicated that CircRNAs participated in modulating tumorigenesis by acting as a competing endogenous RNA (CeRNA). However, the roles and functions of CircRNAs in cellular senescence and aging of organisms remain largely obscure. We performed whole transcriptome sequencing to compare the expression patterns of circular RNAs in young and prematurely senescent human diploid fibroblast 2BS cells, and identified senescence-associated circRNAs (SAC-RNAs). Among these SAC-RNAs, we observed the significantly downregulated expression of CircRNAs originating from exons 6 and 7 circularization of the cyclin B1 gene (CCNB1), termed CircCCNB1. Reduced CircCCNB1 expression triggered senescence in young 2BS cells, as measured by increased senescence associated-beta-galactosidase (SA-&#x3B2;-gal) activity, enhanced expression of cyclin-dependent kinase inhibitor 1A (CDKN1A)/P21 and tumor protein 53 (TP53) expression, and reduced cell proliferation. Mechanistically, reduced CircCCNB1 level inhibited cyclin E2 (CCNE2) expression by modulating micro RNA (miR)-449a activity, which repressed cellular proliferation. Our data suggested that CircCCNB1may serve as a sponge against miR-449a to delay cellular senescence by targeting CCNE2. Targeting CircCCNB1 may represent a promising strategy for aging and age-related disease interventions. Furthermore, we also identified and characterized several kinds of the CircCCNB1-binding proteins (CBPs), which may contribute to the degradation of CircCCNB1.
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Studies on APP metabolism related to age-associated mitochondrial dysfunction in APP/PS1 transgenic mice

Lizhi Chen, Shicheng Xu, Tong Wu, Yijia Shao, Li Luo, Lingqi Zhou, Shanshan Ou, Hai Tang, Wenhua Huang, Kaihua Guo, Jie Xu,

https://doi.org/10.18632/aging.102451 pp 10242—10251

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Chen L, Xu S, Wu T, Shao Y, Luo L, Zhou L, Ou S, Tang H, Huang W, Guo K, Xu J, . Studies on APP metabolism related to age-associated mitochondrial dysfunction in APP/PS1 transgenic mice. . 11:10242-10251. https://doi.org/10.18632/aging.102451

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                TY  - JOUR
                AU  - Chen, Lizhi 
                AU  - Xu, Shicheng 
                AU  - Wu, Tong 
                AU  - Shao, Yijia 
                AU  - Luo, Li 
                AU  - Zhou, Lingqi 
                AU  - Ou, Shanshan 
                AU  - Tang, Hai 
                AU  - Huang, Wenhua 
                AU  - Guo, Kaihua 
                AU  - Xu, Jie 
                TI  - Studies on APP metabolism related to age-associated mitochondrial dysfunction in APP/PS1 transgenic mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102451
                DO  - 10.18632/aging.102451
                SP  - 10242
                EP  - 10251
                PY  - 
                AB  - The aging brain with mitochondrial dysfunction and a reduced adenosine 5&#x2019;-triphosphate (ATP) has been implicated in the onset and progression of &#x3B2;-Amyloid (A&#x3B2;)-induced neuronal toxicity in AD. To unravel the function of ATP and the underlying mechanisms on AD development, APP/PS1 double transgenic mice and wild-type (WT) C57 mice at 6 and 10 months of age were studied. We demonstrated a decreased ATP release in the hippocampus and platelet of APP/PS1 mice, comparing to C57 mice at a relatively early age. Levels of A&#x3B2; were raised in both hippocampus and platelet of APP/PS1 mice, accompanied by a decrease of &#x3B1;-secretase activity and an increase of &#x3B2;-secretase activity. Moreover, our results presented an age-dependent rise in mitochondrial vulnerability to oxidation in APP/PS1 mice. In addition, we found decreased pSer473-Akt levels, increased GSK3&#x3B2; activity by inhibiting phosphorylation at Ser9 in aged APP/PS1 mice and these dysfunctions probably due to down-regulation of Bcl-2 and up-regulation of cleaved caspase-3. Therefore, we demonstrate that PI3K/Akt/GSK3&#x3B2; signaling pathway could be involved in A&#x3B2;-associated mitochondrial dysfunction of APP/PS1 mice and APP abnormal metabolism in platelet might provide potential biomarkers for early diagnosis of AD.
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Metformin decreases LPS-induced inflammatory response in rabbit annulus fibrosus stem/progenitor cells by blocking HMGB1 release

Yingchao Han, Feng Yuan, Chao Deng, Fan He, Yan Zhang, Hongxing Shen, Zhi Chen, Lie Qian,

https://doi.org/10.18632/aging.102453 pp 10252—10265

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Han Y, Yuan F, Deng C, He F, Zhang Y, Shen H, Chen Z, Qian L, . Metformin decreases LPS-induced inflammatory response in rabbit annulus fibrosus stem/progenitor cells by blocking HMGB1 release. . 11:10252-10265. https://doi.org/10.18632/aging.102453

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                TY  - JOUR
                AU  - Han, Yingchao 
                AU  - Yuan, Feng 
                AU  - Deng, Chao 
                AU  - He, Fan 
                AU  - Zhang, Yan 
                AU  - Shen, Hongxing 
                AU  - Chen, Zhi 
                AU  - Qian, Lie 
                TI  - Metformin decreases LPS-induced inflammatory response in rabbit annulus fibrosus stem/progenitor cells by blocking HMGB1 release
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102453
                DO  - 10.18632/aging.102453
                SP  - 10252
                EP  - 10265
                PY  - 
                AB  - The present study aimed to investigate the mechanism of intervertebral disc degeneration (IVDD) and identify an efficient treatment for low back pain. Rabbit annulus fibrosus stem cells (AFSCs) were treated with metformin and lipopolysaccharide (LPS). The results indicated that LPS induced HMGB1 release from the nuclei of AFSCs and caused cell senescence in a concentration-dependent manner. The production of PGE2 and HMGB1 was increased in the medium of the LPS-treated AFSCs. Certain inflammation-associated genes (IL-&#x3B2;1, IL-6, COX-2 and TNF-&#x3B1;) and proteins (IL-&#x3B2;1, COX-2 and TNF-&#x3B1;) and specific catabolic genes (MMP-3 and MMP-13) exhibited increased expression in LPS-treated AFSCs. However, the expression levels of other anabolic genes, such as collagen I and collagen II were decreased in LPS-treated AFSCs. Following addition of metformin to LPS-containing medium, HMGB1 was retained in the nuclei of AFSCs and the production of PGE2 and HMGB1 was reduced. The expression levels of the catabolic genes and proteins were decreased and those of the anabolic genes were increased. The findings indicated that metformin exerted an anti-inflammatory effect by blocking the HMGB1 translocation and by inhibiting catabolic production and cell senescence in AFSCs. Therefore, metformin may be used as an efficient treatment for the disc degenerative disease.
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Silencing lncRNA FOXD2-AS1 inhibits proliferation, migration, invasion and drug resistance of drug-resistant glioma cells and promotes their apoptosis via microRNA-98-5p/CPEB4 axis

Naibing Gu, Xinlai Wang, Zhengli Di, Jing Xiong, Yue Ma, Yu’e Yan, Yihua Qian, Quanzeng Zhang, Jia Yu,

https://doi.org/10.18632/aging.102455 pp 10266—10283

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Gu N, Wang X, Di Z, Xiong J, Ma Y, Yan Y, Qian Y, Zhang Q, Yu J, . Silencing lncRNA FOXD2-AS1 inhibits proliferation, migration, invasion and drug resistance of drug-resistant glioma cells and promotes their apoptosis via microRNA-98-5p/CPEB4 axis. . 11:10266-10283. https://doi.org/10.18632/aging.102455

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                TY  - JOUR
                AU  - Gu, Naibing 
                AU  - Wang, Xinlai 
                AU  - Di, Zhengli 
                AU  - Xiong, Jing 
                AU  - Ma, Yue 
                AU  - Yan, Yu’e 
                AU  - Qian, Yihua 
                AU  - Zhang, Quanzeng 
                AU  - Yu, Jia 
                TI  - Silencing lncRNA FOXD2-AS1 inhibits proliferation, migration, invasion and drug resistance of drug-resistant glioma cells and promotes their apoptosis via microRNA-98-5p/CPEB4 axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102455
                DO  - 10.18632/aging.102455
                SP  - 10266
                EP  - 10283
                PY  - 
                AB  - Objective: This study was conducted to elucidate the long non-coding RNA FOXD2-AS1 (lncRNA FOXD2-AS1) expression in glioma and its mechanism on the biological features of glioma cells and the drug resistance of temozolomide (TMZ).Results: Highly expressed FOXD2-AS1 was found in glioma. There was more powerful chemotherapeutic resistance of TMZ resistant cell lines than that of the parent cell lines. Silence of FOXD2-AS1 suppressed proliferation and drug resistance and promoted apoptosis of drug-resistant glioma cells. Overexpressed FOXD2-AS1 presented an opposite trend. FOXD2-AS1 could be used as a competing endogenous RNA to adsorb miR-98-5p, thereby up-regulating CPEB4.Conclusion: Our study suggests that down-regulated FOXD2-AS1 repressed invasion, proliferation, migration and drug resistance of drug-resistant glioma cells while stimulating their apoptosis via increasing miR-98-5p and inhibiting CPEB4 expression.Methods: FOXD2-AS1, microRNA-98-5p (miR-98-5p) and cytoplasmic polyadenylation element binding (CPEB4) expression in glioma tissues were tested. Expression of E-cadherin, N-cadherin and Vimentin in glioma cells were explored. A series of assays were conducted to detect the function of FOXD2-AS1 in migration, proliferation, apoptosis, and invasion of glioma cells. Changes in drug-resistance of cells under TMZ treatment were examined, and tumor formation in nude mice was performed to test the changes of drug resistance in vivo.
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The anti-carcinogenesis properties of erianin in the modulation of oxidative stress-mediated apoptosis and immune response in liver cancer

Xinrui Zhang, Yingwu Wang, Xin Li, Anhui Yang, Zhiwen Li, Di Wang,

https://doi.org/10.18632/aging.102456 pp 10284—10300

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Zhang X, Wang Y, Li X, Yang A, Li Z, Wang D, . The anti-carcinogenesis properties of erianin in the modulation of oxidative stress-mediated apoptosis and immune response in liver cancer. . 11:10284-10300. https://doi.org/10.18632/aging.102456

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                TY  - JOUR
                AU  - Zhang, Xinrui 
                AU  - Wang, Yingwu 
                AU  - Li, Xin 
                AU  - Yang, Anhui 
                AU  - Li, Zhiwen 
                AU  - Wang, Di 
                TI  - The anti-carcinogenesis properties of erianin in the modulation of oxidative stress-mediated apoptosis and immune response in liver cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102456
                DO  - 10.18632/aging.102456
                SP  - 10284
                EP  - 10300
                PY  - 
                AB  - In this study, erianin was found to reduce the viability of cancer cells, inhibit their proliferation and migration, induce G2/M phase arrest, enhance cancer cell apoptosis, promote an increase in levels of intracellular reactive oxygen species and a decrease in mitochondrial membrane potential, and regulate the expression levels of anti- and pro-apoptosis-related proteins in HepG2 and SMMC-7721 cells. Erianin inhibited tumor growth in HepG2- and SMMC-7721-xenograft tumor nude mouse models, reduced the expression levels of anti-apoptosis proteins and enhanced the expression levels of pro-apoptosis proteins in tumor tissues. Erianin inhibited tumor growth in immunosuppressed BALB/c mice bearing heterotopic tumors. Among 111 types of cytokines detected in proteome profiling of tumor tissues, erianin substantially influenced levels of 38 types of cytokines in HepG2-xenografted tumors and of 15 types of cytokines in SMMC-7721-xenografted tumors, most of which are related to immune functions. Erianin strongly affected the serum levels of cytokines, and regulated the activation of nuclear factor-kappa B (NF-&#x3BA;B), and the expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream proteins in spleen. The anti-liver cancer properties of erianin were found to be related mostly to its modulation of oxidative stress-mediated mitochondrial apoptosis and immune response.
                ER  -

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Combined test of third lumbar skeletal muscle index and prognostic nutrition index improve prognosis prediction power in resected colorectal cancer liver metastasis

Yang Lv, Mei-Ling Ji, Qing-Yang Feng, De-Xiang Zhu, Song-Bin Lin, Yi-Hao Mao, Yu-Qiu Xu, Peng Zheng, Guo-Dong He, Jian-Min Xu,

https://doi.org/10.18632/aging.102457 pp 10301—10315

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Lv Y, Ji M, Feng Q, Zhu D, Lin S, Mao Y, Xu Y, Zheng P, He G, Xu J, . Combined test of third lumbar skeletal muscle index and prognostic nutrition index improve prognosis prediction power in resected colorectal cancer liver metastasis. . 11:10301-10315. https://doi.org/10.18632/aging.102457

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                TY  - JOUR
                AU  - Lv, Yang 
                AU  - Ji, Mei-Ling 
                AU  - Feng, Qing-Yang 
                AU  - Zhu, De-Xiang 
                AU  - Lin, Song-Bin 
                AU  - Mao, Yi-Hao 
                AU  - Xu, Yu-Qiu 
                AU  - Zheng, Peng 
                AU  - He, Guo-Dong 
                AU  - Xu, Jian-Min 
                TI  - Combined test of third lumbar skeletal muscle index and prognostic nutrition index improve prognosis prediction power in resected colorectal cancer liver metastasis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102457
                DO  - 10.18632/aging.102457
                SP  - 10301
                EP  - 10315
                PY  - 
                AB  - Background: In this paper, we aim to explore clinical value of skeletal muscle index (SMI) and prognostic nutrition index (PNI) on resected colorectal cancer liver metastasis (CRLM).Results: Among the 539 patients, 355 were males. Baseline lower SMI was associated with smaller BMI, smaller PNI, smaller pre-albumin and longer hospitalization days (P&lt;0.05). Patients with lower SMI and PNI had significantly shorter duration of PFS and OS (P&lt;0.05). SMI can reflect the postoperative treatment response. Postoperative 6-month&#x2019;s and 12-month&#x2019;s SMI and PNI can indicate overall prognosis. When combined SMI and PNI, prognostic AUC of ROC curves improved significantly.Conclusion: Combined monitor of SMI and PNI can improve the power at predicting prognosis. Postoperative 6-month&#x2019;s record of SMI and PNI was more accurate and predictive for CRLM prognosis.Method: A total of 539 resected CRLM patients between January 2013 to December 2016 with complete clinical data were included. Computed tomography image was collected from each patient. Receiver-operating characteristic (ROC) curves were constructed; area under curves (AUC) were also determined. All clinical variables were analyzed in proper way.
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Multi-omics analysis reveals epithelial-mesenchymal transition-related gene FOXM1 as a novel prognostic biomarker in clear cell renal carcinoma

Jing Song, Fangzhou Song, Kun Liu, Wanfeng Zhang, Ruihan Luo, Yongyao Tang, Longke Ran,

https://doi.org/10.18632/aging.102459 pp 10316—10337

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Song J, Song F, Liu K, Zhang W, Luo R, Tang Y, Ran L, . Multi-omics analysis reveals epithelial-mesenchymal transition-related gene FOXM1 as a novel prognostic biomarker in clear cell renal carcinoma. . 11:10316-10337. https://doi.org/10.18632/aging.102459

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                TY  - JOUR
                AU  - Song, Jing 
                AU  - Song, Fangzhou 
                AU  - Liu, Kun 
                AU  - Zhang, Wanfeng 
                AU  - Luo, Ruihan 
                AU  - Tang, Yongyao 
                AU  - Ran, Longke 
                TI  - Multi-omics analysis reveals epithelial-mesenchymal transition-related gene FOXM1 as a novel prognostic biomarker in clear cell renal carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102459
                DO  - 10.18632/aging.102459
                SP  - 10316
                EP  - 10337
                PY  - 
                AB  - Identification of novel clinical biomarker in clear cell renal carcinoma (ccRCC) is warranted. Integrating transcriptome (n=1669), DNA methylation (n=577) and copy number data (n=832), we developed a method to identify driver biomarkers by analyzing the omics-level dynamics of Epithelial-Mesenchymal Transition (EMT)-related genes in ccRCC. We first identified 504 expression dynamic changed genes involved in ccRCC-associated key pathways such as EMT, cell cycle, EGFR and PI3K/AKT signaling. Further analysis identified 229 (90 gene promoters) aberrant expression quantitative trait methylation (eQTM) and 256 genes with expression quantitative trait copy number (eQTCN) alterations. Among them, FOXM1 was affected by both eQTM and eQTCN. FOXM1 copy number amplification (115/500, 23% of patients), occurred in an amplified peak in chromosome 12q13.3, was enriched in late-stage ccRCC samples and was associated with worse survival. FOXM1-overexpressed pT3 patients with distant metastasis showed ~25% shorter overall survival in both training (log-rank P=0.006) and validation (log-rank P=0.018) cohorts. The eQTM-gene hybrid signature (cg00044170 and FOXM1), superior to either gene expression or DNA methylation alone, showed great potential in diagnosing localized ccRCC in training (area under curve = 0.958) and validation datasets. FOXM1 could be a novel prognostic biomarker and shed light for early diagnosis at molecular level in ccRCC.
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GBA mutation promotes early mitochondrial dysfunction in 3D neurosphere models

Constanza Morén, Diana Luz Juárez-Flores, Kai-Yin Chau, Matthew Gegg, Glòria Garrabou, Ingrid González-Casacuberta, Mariona Guitart-Mampel, Eduardo Tolosa, María José Martí, Francesc Cardellach, Anthony Henry Vernon Schapira,

https://doi.org/10.18632/aging.102460 pp 10338—10355

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Morén C, Juárez-Flores DL, Chau K, Gegg M, Garrabou G, González-Casacuberta I, Guitart-Mampel M, Tolosa E, Martí MJ, Cardellach F, Schapira AHV, . GBA mutation promotes early mitochondrial dysfunction in 3D neurosphere models. . 11:10338-10355. https://doi.org/10.18632/aging.102460

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                TY  - JOUR
                AU  - Morén, Constanza 
                AU  - Juárez-Flores, Diana Luz 
                AU  - Chau, Kai-Yin 
                AU  - Gegg, Matthew 
                AU  - Garrabou, Glòria 
                AU  - González-Casacuberta, Ingrid 
                AU  - Guitart-Mampel, Mariona 
                AU  - Tolosa, Eduardo 
                AU  - Martí, María José 
                AU  - Cardellach, Francesc 
                AU  - Schapira, Anthony Henry Vernon 
                TI  - <i>GBA</i> mutation promotes early mitochondrial dysfunction in 3D neurosphere models
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102460
                DO  - 10.18632/aging.102460
                SP  - 10338
                EP  - 10355
                PY  - 
                AB  - Glucocerebrosidase (GBA) mutations are the most important genetic risk factor for the development of Parkinson disease (PD). GBA encodes the lysosomal enzyme glucocerebrosidase (GCase). Loss-of-GCase activity in cellular models has implicated lysosomal and mitochondrial dysfunction in PD disease pathogenesis, although the exact mechanisms remain unclear. We hypothesize that GBA mutations impair mitochondria quality control in a neurosphere model.We have characterized mitochondrial content, mitochondrial function and macroautophagy flux in 3D-neurosphere-model derived from neural crest stem cells containing heterozygous and homozygous N370SGBA mutations, under carbonyl cyanide-m-chlorophenyl-hydrazine (CCCP)- induced mitophagy.Our findings on mitochondrial markers and ATP levels indicate that mitochondrial accumulation occurs in mutant N370SGBA neurospheres under basal conditions, and clearance of depolarised mitochondria is impaired following CCCP-treatment. A significant increase in TFEB-mRNA levels, the master regulator of lysosomal and autophagy genes, may explain an unchanged macroautophagy flux in N370SGBA neurospheres. PGC1&#x3B1;-mRNA levels were also significantly increased following CCCP-treatment in heterozygote, but not homozygote neurospheres, and might contribute to the increased mitochondrial content seen in cells with this genotype, probably as a compensatory mechanism that is absent in homozygous lines.Mitochondrial impairment occurs early in the development of GCase-deficient neurons. Furthermore, impaired turnover of depolarised mitochondria is associated with early mitochondrial dysfunction.In summary, the presence of GBA mutation may be associated with higher levels of mitochondrial content in homozygous lines and lower clearance of damaged mitochondria in our neurosphere model.
                ER  -

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Folic acid delays age-related cognitive decline in senescence-accelerated mouse prone 8: alleviating telomere attrition as a potential mechanism

Xin Lv, Xinyan Wang, Yalan Wang, Dezheng Zhou, Wen Li, John X. Wilson, Hong Chang, Guowei Huang,

https://doi.org/10.18632/aging.102461 pp 10356—10373

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Lv X, Wang X, Wang Y, Zhou D, Li W, Wilson JX, Chang H, Huang G, . Folic acid delays age-related cognitive decline in senescence-accelerated mouse prone 8: alleviating telomere attrition as a potential mechanism. . 11:10356-10373. https://doi.org/10.18632/aging.102461

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                TY  - JOUR
                AU  - Lv, Xin 
                AU  - Wang, Xinyan 
                AU  - Wang, Yalan 
                AU  - Zhou, Dezheng 
                AU  - Li, Wen 
                AU  - Wilson, John X. 
                AU  - Chang, Hong 
                AU  - Huang, Guowei 
                TI  - Folic acid delays age-related cognitive decline in senescence-accelerated mouse prone 8: alleviating telomere attrition as a
                potential mechanism
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102461
                DO  - 10.18632/aging.102461
                SP  - 10356
                EP  - 10373
                PY  - 
                AB  - The occurrence of telomere attrition in brain may cause senescence and death of neurons, leading to cognitive
                decline. Folic acid (FA) has been reported to improve cognitive performance in mild cognitive impairment;
                however, its association with telomere remains unclear. The study aimed to investigate if alleviation of telomere
                attrition by FA supplementation could act as a potential mechanism to delay age-related cognitive decline in
                senescence-accelerated mouse prone 8 (SAMP8). Aged SAMP8 mice were assigned to four treatment groups: FAdeficient diet (FA-D) group, FA-normal diet (FA-N) group, low FA-supplemented diet (FA-L) group and high FAsupplemented diet (FA-H) group. There was also an age-matched senescence-accelerated mouse resistant 1
                (SAMR1) control group (Con-R), and a young SAMP8 control group (Con-Y). The results demonstrated that FA
                supplementation delayed age-related cognitive decline and neurodegeneration in SAMP8 mice. Importantly, this
                effect could be attributed to the alleviated telomere attrition, which might be interpreted by the decreased levels
                of reactive oxygen species. Additionally, improved telomere integrity stimulated mitochondrial function via
                telomere-p53-mithondria pathway, consequently delayed neuronal degeneration. In conclusion, we demonstrate
                that FA supplementation delays age-related neurodegeneration and cognitive decline in SAMP8 mice, in which
                alleviated telomere attrition could serve as one influential factor in the process.
                ER  -

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Hypoxia-induced microRNA-10b-3p promotes esophageal squamous cell carcinoma growth and metastasis by targeting TSGA10

Qiang Zhang, Jingjing Zhang, Zhanzhao Fu, Lixin Dong, Yong Tang, Chunlei Xu, Haifeng Wang, Tao Zhang, Yue Wu, Chao Dong, Shasha Shao, Guangxia Wang,

https://doi.org/10.18632/aging.102462 pp 10374—10384

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Zhang Q, Zhang J, Fu Z, Dong L, Tang Y, Xu C, Wang H, Zhang T, Wu Y, Dong C, Shao S, Wang G, . Hypoxia-induced microRNA-10b-3p promotes esophageal squamous cell carcinoma growth and metastasis by targeting TSGA10. . 11:10374-10384. https://doi.org/10.18632/aging.102462

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                TY  - JOUR
                AU  - Zhang, Qiang 
                AU  - Zhang, Jingjing 
                AU  - Fu, Zhanzhao 
                AU  - Dong, Lixin 
                AU  - Tang, Yong 
                AU  - Xu, Chunlei 
                AU  - Wang, Haifeng 
                AU  - Zhang, Tao 
                AU  - Wu, Yue 
                AU  - Dong, Chao 
                AU  - Shao, Shasha 
                AU  - Wang, Guangxia 
                TI  - Hypoxia-induced microRNA-10b-3p promotes esophageal squamous cell carcinoma growth and metastasis by targeting TSGA10
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102462
                DO  - 10.18632/aging.102462
                SP  - 10374
                EP  - 10384
                PY  - 
                AB  - Evidence has shown that hypoxia promotes esophageal squamous cell carcinoma (ESCC) growth and metastasis, but the molecular mechanisms underlying that response remain poorly understood. MicroRNAs (miRNAs) are post-transcriptional regulators that participate in various cancer-related processes. Here, we demonstrated that hypoxia along with hypoxia-inducible factor 1&#x3B1; significantly increased expression of miR-10b-3p. Inhibition of miR-10b-3p weakened the effects of hypoxia on ESCC cell proliferation, migration and invasion, while miR-10b-3p overexpression had the opposite effects. Mechanistically, miR-10b-3p acted as cancer-promoting gene by targeting testis specific 10. Using a xenograft model, we observed that administration of miR-10b-3p agomir to tumors enhanced their growth and metastasis in vivo. These findings verified the potent regulatory role played by hypoxia-induced miR-10b-3p expression in ESCC progression. These results suggest that miR-10b-3p may be a useful therapeutic target for treating ESCC.
                ER  -

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Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegans

Jiangyao Xu, Kan Liu, Tingting Chen, Tianying Zhan, Zijun Ouyang, Yushu Wang, Wen Liu, Xiaoyun Zhang, Yang Sun, Gaixia Xu, Xiaomei Wang,

https://doi.org/10.18632/aging.102466 pp 10385—10408

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Xu J, Liu K, Chen T, Zhan T, Ouyang Z, Wang Y, Liu W, Zhang X, Sun Y, Xu G, Wang X, . Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegans. . 11:10385-10408. https://doi.org/10.18632/aging.102466

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                TY  - JOUR
                AU  - Xu, Jiangyao 
                AU  - Liu, Kan 
                AU  - Chen, Tingting 
                AU  - Zhan, Tianying 
                AU  - Ouyang, Zijun 
                AU  - Wang, Yushu 
                AU  - Liu, Wen 
                AU  - Zhang, Xiaoyun 
                AU  - Sun, Yang 
                AU  - Xu, Gaixia 
                AU  - Wang, Xiaomei 
                TI  - Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of <i>Caenorhabditis elegans</i>
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102466
                DO  - 10.18632/aging.102466
                SP  - 10385
                EP  - 10408
                PY  - 
                AB  - The biological effects of magnetic fields are a research hotspot in the field of biomedical engineering. In this study, we further investigated the effects of a rotating magnetic field (RMF; 0.2 T, 4 Hz) on the growth of human umbilical vein endothelial cells (HUVECs) and Caenorhabditis elegans. The results showed that RMF exposure prolonged the lifespan of C. elegans and slowed the aging of HUVECs. RMF treatment of HUVECs showed that activation of adenosine 5&apos;-monophosphate (AMP)-activated protein kinase (AMPK) was associated with decreased mitochondrial membrane potential (MMP) due to increased intracellular Ca2+ concentrations induced by endoplasmic reticulum stress in anti-aging mechanisms. RMF also promoted the health status of C. elegans by improving activity, reducing age-related pigment accumulation, delaying A&#x3B2;-induced paralysis and increasing resistance to heat and oxidative stress. The prolonged lifespan of C. elegans was associated with decreased levels of daf-16 which related to the insulin/insulin-like growth factor signaling pathway (IIS) activity and reactive oxygen species (ROS), whereas the heat shock transcription factor-1 (hsf-1) pathway was not involved. Moreover, the level of autophagy was increased after RMF treatment. These findings expand our understanding of the potential mechanisms by which RMF treatment prolongs lifespan.
                ER  -

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The anti-inflammation, anti-oxidative and anti-fibrosis properties of swertiamarin in cigarette smoke exposure-induced prostate dysfunction in rats

Jinglou Chen, Jianhua Liu, Yongfang Lei, Min Liu,

https://doi.org/10.18632/aging.102467 pp 10409—10421

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Chen J, Liu J, Lei Y, Liu M, . The anti-inflammation, anti-oxidative and anti-fibrosis properties of swertiamarin in cigarette smoke exposure-induced prostate dysfunction in rats. . 11:10409-10421. https://doi.org/10.18632/aging.102467

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                TY  - JOUR
                AU  - Chen, Jinglou 
                AU  - Liu, Jianhua 
                AU  - Lei, Yongfang 
                AU  - Liu, Min 
                TI  - The anti-inflammation, anti-oxidative and anti-fibrosis properties of swertiamarin in cigarette smoke exposure-induced prostate dysfunction in rats
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102467
                DO  - 10.18632/aging.102467
                SP  - 10409
                EP  - 10421
                PY  - 
                AB  - Chronic cigarette smoke (CS) exposure induces prostate deficits. We previously found that swertiamarin had prostatic protective potential. This study was to investigate the possible protective effect of swertiamarin against CS-induced prostate dysfunction on human prostate epithelial cells, stromal cells and rats. Rat prostate collagen deposition and fibrosis were assessed by sirius red staining and measuring hydroxyproline content, as well as by qPCR and western blot analysis for fibrotic extracellular matrix components. Prostatic levels of oxidative stress and inflammatory-related factors were also analyzed. In order to explore its underling mechanisms, the activities of Hedgehog signaling pathway and epithelial-mesenchymal transition of human prostate cells and rat prostate tissue were estimated. It was found that swertiamarin ameliorated CS-induced prostatic collagen deposition, relieved oxidative stress and local inflammation, inhibited the activation of Hedgehog signaling pathway and attenuated epithelial-mesenchymal transition. It indicated that swertiamarin could ameliorate CS-induced prostatic fibrosis by inhibiting epithelial-mesenchymal transition and Hedgehog pathway.
                ER  -

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Large-scale analyses identify a cluster of novel long noncoding RNAs as potential competitive endogenous RNAs in progression of hepatocellular carcinoma

Mengjia Song, Ailin Zhong, Jieying Yang, Junyi He, Shaoyan Cheng, Jianxiong Zeng, Yue Huang, Qiuzhong Pan, Jingjing Zhao, Ziqi Zhou, Qian Zhu, Yan Tang, Hao Chen, Chaopin Yang, Yuan Liu, Xiaocong Mo, Desheng Weng, Jian-Chuan Xia,

https://doi.org/10.18632/aging.102468 pp 10422—10453

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Song M, Zhong A, Yang J, He J, Cheng S, Zeng J, Huang Y, Pan Q, Zhao J, Zhou Z, Zhu Q, Tang Y, Chen H, et al, . Large-scale analyses identify a cluster of novel long noncoding RNAs as potential competitive endogenous RNAs in progression of hepatocellular carcinoma. . 11:10422-10453. https://doi.org/10.18632/aging.102468

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                TY  - JOUR
                AU  - Song, Mengjia 
                AU  - Zhong, Ailin 
                AU  - Yang, Jieying 
                AU  - He, Junyi 
                AU  - Cheng, Shaoyan 
                AU  - Zeng, Jianxiong 
                AU  - Huang, Yue 
                AU  - Pan, Qiuzhong 
                AU  - Zhao, Jingjing 
                AU  - Zhou, Ziqi 
                AU  - Zhu, Qian 
                AU  - Tang, Yan 
                AU  - Chen, Hao 
                AU  - Yang, Chaopin 
                AU  - Liu, Yuan 
                AU  - Mo, Xiaocong 
                AU  - Weng, Desheng 
                AU  - Xia, Jian-Chuan 
                TI  - Large-scale analyses identify a cluster of novel long noncoding RNAs as potential competitive endogenous RNAs in progression of hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102468
                DO  - 10.18632/aging.102468
                SP  - 10422
                EP  - 10453
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Song, Mengjia 
                AU  - Zhong, Ailin 
                AU  - Yang, Jieying 
                AU  - He, Junyi 
                AU  - Cheng, Shaoyan 
                AU  - Zeng, Jianxiong 
                AU  - Huang, Yue 
                AU  - Pan, Qiuzhong 
                AU  - Zhao, Jingjing 
                AU  - Zhou, Ziqi 
                AU  - Zhu, Qian 
                AU  - Tang, Yan 
                AU  - Chen, Hao 
                AU  - Yang, Chaopin 
                AU  - Liu, Yuan 
                AU  - Mo, Xiaocong 
                AU  - Weng, Desheng 
                AU  - Xia, Jian-Chuan 
                TI  - Large-scale analyses identify a cluster of novel long noncoding RNAs as potential competitive endogenous RNAs in progression of hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102468
                DO  - 10.18632/aging.102468
                SP  - 10422
                EP  - 10453
                PY  - 
                AB  - The abnormal expression of noncoding RNAs has attracted increasing interest in the field of hepatocellular carcinoma progression. However, the underlying molecular mechanisms mediated by noncoding RNAs in these processes are unclear. Here, we obtained the expression profiles of long noncoding RNAs, microRNAs, and mRNAs from the Gene Expression Omnibus database and identified hepatocarcinogenesis-specific differentially expressed transcripts. Next, we identified significant Gene Ontology and pathway terms that the differentially expressed transcripts involved in. Using functional analysis and target prediction, we constructed a hepatocellular carcinoma-associated deregulated competitive endogenous RNA network to reveal the potential mechanisms underlying tumor progression. By analyzing The Cancer Genome Atlas dataset, six key long noncoding RNAs showed significant association with overall survival as well as strong correlation with some microRNAs and mRNAs in the competitive endogenous RNA network. We further validated the above results and determined their diagnostic and prognostic value in clinical samples. Importantly, by large-scale analyses, we identified a cluster of long noncoding RNAs, GBAP1, MCM3AP-AS1, SLC16A1-AS1, C3P1, DIO3OS, and HNF4A-AS1 as candidate biomarkers for the diagnosis and prognosis of hepatocellular carcinoma, which will improve our understanding of competitive endogenous RNA-mediated regulatory mechanisms underlying hepatocellular carcinoma development and will provide novel therapeutic targets in the future.
                ER  -

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Abnormal gut microbiota composition contributes to the development of type 2 diabetes mellitus in db/db mice

Fan Yu, Wei Han, Gaofeng Zhan, Shan Li, Xiaohong Jiang, Long Wang, Shoukui Xiang, Bin Zhu, Ling Yang, Ailin Luo, Fei Hua, Chun Yang,

https://doi.org/10.18632/aging.102469 pp 10454—10467

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Yu F, Han W, Zhan G, Li S, Jiang X, Wang L, Xiang S, Zhu B, Yang L, Luo A, Hua F, Yang C, . Abnormal gut microbiota composition contributes to the development of type 2 diabetes mellitus in db/db mice. . 11:10454-10467. https://doi.org/10.18632/aging.102469

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                TY  - JOUR
                AU  - Yu, Fan 
                AU  - Han, Wei 
                AU  - Zhan, Gaofeng 
                AU  - Li, Shan 
                AU  - Jiang, Xiaohong 
                AU  - Wang, Long 
                AU  - Xiang, Shoukui 
                AU  - Zhu, Bin 
                AU  - Yang, Ling 
                AU  - Luo, Ailin 
                AU  - Hua, Fei 
                AU  - Yang, Chun 
                TI  - Abnormal gut microbiota composition contributes to the development of type 2 diabetes mellitus in db/db mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102469
                DO  - 10.18632/aging.102469
                SP  - 10454
                EP  - 10467
                PY  - 
                AB  - It is well recognized that type 2 diabetes mellitus (T2DM) is an age-related metabolic disease, emerging gradually as a major global health burden that has gained public attention. Meanwhile, increasing attention is paid to the crucial role of gut microbiota in the pathogenesis and therapeutic mechanisms of metabolic disorders, especially T2DM. In this study, we used C57 BL/KS db/db male mice as a T2DM murine model. We found that the &#x3B2;-diversity and relative abundances of gut bacteria were obviously altered in db/db mice, associated with a significant increase in Verrucomicrobia at six levels (phylum, class, order, etc.) and family S24-7 and a significant decrease in Bacteroidaceae at family, genus, and species levels, as well as Prevotellaceae at family and genus levels. Furthermore, fecal bacteria from db/db and m/m mice transplanted into pseudo-germ-free mice showed a significant change in the metabolic parameters, including the body weight, fasting blood glucose, fluid and food intake, and alterations in the composition of the gut microbiota. Taken together, these findings suggest that abnormalities in the composition of the gut microbiota might contribute to the development of T2DM and that potential therapeutic strategies improving gut microbiota might provide beneficial effects for individuals with T2DM and age-related glucose intolerance.
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Genome-wide association study of hippocampal atrophy rate in non-demented elders

Yu Guo, Wei Xu, Jie-Qiong Li, Ya-Nan Ou, Xue-Ning Shen, Yu-Yuan Huang, Qiang Dong, Lan Tan, Jin-Tai Yu,

https://doi.org/10.18632/aging.102470 pp 10468—10484

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Guo Y, Xu W, Li J, Ou Y, Shen X, Huang Y, Dong Q, Tan L, Yu J, . Genome-wide association study of hippocampal atrophy rate in non-demented elders. . 11:10468-10484. https://doi.org/10.18632/aging.102470

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                TY  - JOUR
                AU  - Guo, Yu 
                AU  - Xu, Wei 
                AU  - Li, Jie-Qiong 
                AU  - Ou, Ya-Nan 
                AU  - Shen, Xue-Ning 
                AU  - Huang, Yu-Yuan 
                AU  - Dong, Qiang 
                AU  - Tan, Lan 
                AU  - Yu, Jin-Tai 
                TI  - Genome-wide association study of hippocampal atrophy rate in non-demented elders
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102470
                DO  - 10.18632/aging.102470
                SP  - 10468
                EP  - 10484
                PY  - 
                AB  - Hippocampal atrophy rate has been correlated with cognitive decline and its genetic modifiers are still unclear. Here we firstly performed a genome-wide association study (GWAS) to identify genetic loci that regulate hippocampal atrophy rate. Six hundred and two non-Hispanic Caucasian elders without dementia were included from the Alzheimer&#x2019;s Disease Neuroimaging Initiative cohort. Three single nucleotide polymorphisms (SNPs) (rs4420638, rs56131196, rs157582) in the TOMM40-APOC1 region were associated with hippocampal atrophy rate at genome-wide significance and 3 additional SNPs (in TOMM40 and near MIR302F gene) reached a suggestive level of significance. Strong linkage disequilibrium between rs4420638 and rs56131196 was found. The minor allele of rs4420638 (G) and the minor allele of rs157582 (T) showed associations with lower Mini-mental State Examination score, higher Alzheimer Disease Assessment Scale-cognitive subscale 11 score and smaller entorhinal volume using both baseline and longitudinal measurements, as well as with accelerated cognitive decline. Moreover, rs56131196 (P = 1.96 &#xD7; 10-454) and rs157582 (P = 9.70 &#xD7; 10-434) were risk loci for Alzheimer&#x2019;s disease. Collectively, rs4420638, rs56131196 and rs157582 were found to be associated with hippocampal atrophy rate. Besides, they were also identified as genetic loci for cognitive decline.
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Identification of functional tRNA-derived fragments in senescence-accelerated mouse prone 8 brain

Shuai Zhang, Hejian Li, Ling Zheng, Hong Li, Chengqiang Feng, Wensheng Zhang,

https://doi.org/10.18632/aging.102471 pp 10485—10498

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Zhang S, Li H, Zheng L, Li H, Feng C, Zhang W, . Identification of functional tRNA-derived fragments in senescence-accelerated mouse prone 8 brain. . 11:10485-10498. https://doi.org/10.18632/aging.102471

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                TY  - JOUR
                AU  - Zhang, Shuai 
                AU  - Li, Hejian 
                AU  - Zheng, Ling 
                AU  - Li, Hong 
                AU  - Feng, Chengqiang 
                AU  - Zhang, Wensheng 
                TI  - Identification of functional tRNA-derived fragments in senescence-accelerated mouse prone 8 brain
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102471
                DO  - 10.18632/aging.102471
                SP  - 10485
                EP  - 10498
                PY  - 
                AB  - Transfer RNA-derived fragments (tRFs) are known to contribute to multiple illnesses, including cancers, viral infections, and age-related neurodegeneration. In this study, we used senescence-accelerated mouse prone 8 (SAMP8) as a model of neurodegenerative disorders such as Alzheimer&#x2019;s disease and Parkinson&#x2019;s disease, and a control, the senescence-accelerated mouse resistant 1 (SAMR1) model, to comprehensively explore differences in tRF expression between them. We discovered 570 tRF transcripts among which eight were differentially expressed. We then obtained 110 potential target genes in a miRNA-like pattern. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) annotation suggest that these target genes participate in a variety of brain functions; e.g., synapse formation (GO: 0045202) and the synaptic vesicle cycle pathway. We further assessed in detail those tRFs whose miRNA-like pattern was most likely to promote the progression of either Alzheimer&#x2019;s or Parkinson&#x2019;s disease, such as AS-tDR-011775 acting on Mobp and Park2. Our findings suggest the eight dysregulated tRFs we uncovered here may be beneficially exploited as potential diagnostic biomarkers and/or therapeutic targets to treat age-related brain diseases.
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Melatonin modulates IL-1β-induced extracellular matrix remodeling in human nucleus pulposus cells and attenuates rat intervertebral disc degeneration and inflammation

Yan Zhang, Fan He, Zhi Chen, Qihang Su, Meijun Yan, Qiang Zhang, Jun Tan, Lie Qian, Yingchao Han,

https://doi.org/10.18632/aging.102472 pp 10499—10512

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Zhang Y, He F, Chen Z, Su Q, Yan M, Zhang Q, Tan J, Qian L, Han Y, . Melatonin modulates IL-1β-induced extracellular matrix remodeling in human nucleus pulposus cells and attenuates rat intervertebral disc degeneration and inflammation. . 11:10499-10512. https://doi.org/10.18632/aging.102472

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                TY  - JOUR
                AU  - Zhang, Yan 
                AU  - He, Fan 
                AU  - Chen, Zhi 
                AU  - Su, Qihang 
                AU  - Yan, Meijun 
                AU  - Zhang, Qiang 
                AU  - Tan, Jun 
                AU  - Qian, Lie 
                AU  - Han, Yingchao 
                TI  - Melatonin modulates IL-1β-induced extracellular matrix remodeling in human nucleus pulposus cells and attenuates rat intervertebral disc degeneration and inflammation
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102472
                DO  - 10.18632/aging.102472
                SP  - 10499
                EP  - 10512
                PY  - 
                AB  - The inflammatory-associated factors interleukin-1&#x3B2; (IL-1&#x3B2;), interleukin-6 (IL-6) and tumor necrosis factor-&#x3B1; (TNF-&#x3B1;) are widely reported to be associated with intervertebral disc (IVD) degeneration (IVDD). N-acetyl-5-methoxytryptamine (melatonin) is a natural hormone secreted by the pineal gland which has been shown to participate in several physiological and pathological progresses, such as aging, anti-inflammation, anti-apoptosis and autophagy regulation. However, the effects of melatonin on IVD remain unclear. In the present study, we treated human nucleus pulposus cells (NPCs) with melatonin and discovered that melatonin could modulate extracellular matrix (ECM) remodeling induced by IL-1&#x3B2; by enhancing collagen II and aggrecan expression levels and by downregulating matrix metalloproteinase-3 (MMP-3) levels. These findings were verified by western blot and immunofluorescence assays. Intraperitoneal injection of melatonin mitigated IVDD in the rat tail puncture model. X-ray and magnetic resonance imaging (MRI), as well as hematoxylin-eosin (H&amp;E), Safranine O-Green, Alcian blue and Celium red staining methods were adopted to evaluate IVDD grades, the structural integrity of nucleus pulposus (NP) and annulus fibrosus (AF) and the damage and calcification of the cartilage endplate. Melatonin reduced inflammatory cell aggregation and the release of the inflammatory factors IL-1&#x3B2;, IL-6, TNF-&#x3B1; as determined by immunohistochemistry. In conclusion, the present study demonstrated that melatonin could modulate ECM remodeling by IL-1&#x3B2; in vitro and attenuate the IVDD and induction of inflammation in a rat tail puncture model in vivo. The data demonstrated that melatonin may contribute to the restoration processs of IVD following damage and may be used as a potential novel therapy for IVDD.
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Astaxanthin protects against osteoarthritis via Nrf2: a guardian of cartilage homeostasis

Kai Sun, Jiahui Luo, Xingzhi Jing, Jiachao Guo, Xudong Yao, Xiaoxia Hao, Yaping Ye, Shuang Liang, Jiamin Lin, Genchun Wang, Fengjing Guo,

https://doi.org/10.18632/aging.102474 pp 10513—10531

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Sun K, Luo J, Jing X, Guo J, Yao X, Hao X, Ye Y, Liang S, Lin J, Wang G, Guo F, . Astaxanthin protects against osteoarthritis via Nrf2: a guardian of cartilage homeostasis. . 11:10513-10531. https://doi.org/10.18632/aging.102474

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                TY  - JOUR
                AU  - Sun, Kai 
                AU  - Luo, Jiahui 
                AU  - Jing, Xingzhi 
                AU  - Guo, Jiachao 
                AU  - Yao, Xudong 
                AU  - Hao, Xiaoxia 
                AU  - Ye, Yaping 
                AU  - Liang, Shuang 
                AU  - Lin, Jiamin 
                AU  - Wang, Genchun 
                AU  - Guo, Fengjing 
                TI  - Astaxanthin protects against osteoarthritis via Nrf2: a guardian of cartilage homeostasis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102474
                DO  - 10.18632/aging.102474
                SP  - 10513
                EP  - 10531
                PY  - 
                AB  - Scope: Osteoarthritis (OA) is a progressive disease characterized by cartilage degradation. Astaxanthin (Ast), a natural compound with remarkable antioxidant activity and multiple medical applications due to its activation of Nrf2 signaling, has been studied for application to various degenerative diseases. Currently, however, little is known about its efficacy in treating OA. This study reports the effects of Ast on cartilage homeostasis in OA progression.Methods: IL-1&#x3B2;, TNF-&#x3B1;, and tert-butyl hydroperoxide (TBHP) were used to impair cartilage homeostasis. Modulating effects of Ast on the Nrf2 signaling pathway, and damage-associated events including extracellular matrix (ECM) degradation, inflammation, oxidative stress, chondrocyte apoptosis, and in vivo cartilage degradation were examined.Results: Ast attenuated ECM degradation of OA chondrocytes through the Nrf2 signaling, and ameliorated the IL-1&#x3B2;-induced inflammatory response and ECM degradation via blockade of MAPK signaling. Additionally, Ast alleviated TNF-&#x3B1;-induced ECM degradation and chondrocyte apoptosis by inhibiting the NF-&#x3BA;B signaling, suppressed TBHP-induced oxidative stress, and subsequently reduced chondrocyte apoptosis. In vitro results were finally corroborated in vivo by demonstrating that Ast attenuates the severity of cartilage destruction in a mouse model of OA.Conclusions: Ast could protect against osteoarthritis via the Nrf2 signaling, suggesting Ast might be a potential therapeutic supplement for OA treatment.
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Distinct effects of epirubicin, cisplatin and cyclophosphamide on ovarian somatic cells of prepuberal ovaries

Serena Marcozzi, Valerio Rossi, Giulia Salvatore, Francesca Di Rella, Massimo De Felici, Francesca Gioia Klinger,

https://doi.org/10.18632/aging.102476 pp 10532—10556

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Marcozzi S, Rossi V, Salvatore G, Di Rella F, De Felici M, Klinger FG, . Distinct effects of epirubicin, cisplatin and cyclophosphamide on ovarian somatic cells of prepuberal ovaries. . 11:10532-10556. https://doi.org/10.18632/aging.102476

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                TY  - JOUR
                AU  - Marcozzi, Serena 
                AU  - Rossi, Valerio 
                AU  - Salvatore, Giulia 
                AU  - Di Rella, Francesca 
                AU  - De Felici, Massimo 
                AU  - Klinger, Francesca Gioia 
                TI  - Distinct effects of epirubicin, cisplatin and cyclophosphamide on ovarian somatic cells of prepuberal ovaries
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102476
                DO  - 10.18632/aging.102476
                SP  - 10532
                EP  - 10556
                PY  - 
                AB  - In vitro culture models were used to characterize the effects of chemotherapeutic drugs and of LH on somatic cells from prepuberal mouse ovaries. All cell types (pre- and granulosa cells, pre-thecal and OSE cells) underwent apoptosis following Epirubicin (0.5&#x3BC;M) exposure for 24hrs (about 60%) and 48hrs (&gt;80%). Cisplatin (10&#x3BC;M) and the Cyclophosphamide active metabolite, Phosphoramide Mustard (10&#x3BC;M), didn&#x2019;t cause apoptosis in 90% of pre-thecal and pre-granulosa cells up to 72hrs of exposure, although they suffered extensive DNA damage and cell cycle arrest, and acquired stress induced premature senescence (SIPS) features. Cultured granulosa cells didn&#x2019;t show evident DNA damage and remained viable without acquiring SIPS features; OSE cells were resistant to apoptosis and SIPS but not to DNA damage. These latter, like pre-thecal and pre-granulosa cells, were able of efficient DNA repair involving MLH1-dependent MMR pathways. SIPS features were also observed in ovary after in vivo treatment with Cisplatin. LH (200mIU/mL) didn&#x2019;t significantly influence apoptosis, SIPS and DNA damage but favoured DNA repair. These results show that somatic cells of prepuberal ovary response to drugs in different ways, either undergoing apoptosis or SIPS, either showing resistance to Cisplatin and Phosphoramide Mustard. Moreover, a new role of LH in promoting DNA repair was shown.
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Identification of prognostic genes in the acute myeloid leukemia microenvironment

Shaoxin Huang, Biyu Zhang, Wenyan Fan, Qihan Zhao, Lei Yang, Wang Xin, Denggang Fu,

https://doi.org/10.18632/aging.102477 pp 10557—10580

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Huang S, Zhang B, Fan W, Zhao Q, Yang L, Xin W, Fu D, . Identification of prognostic genes in the acute myeloid leukemia microenvironment. . 11:10557-10580. https://doi.org/10.18632/aging.102477

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                TY  - JOUR
                AU  - Huang, Shaoxin 
                AU  - Zhang, Biyu 
                AU  - Fan, Wenyan 
                AU  - Zhao, Qihan 
                AU  - Yang, Lei 
                AU  - Xin, Wang 
                AU  - Fu, Denggang 
                TI  - Identification of prognostic genes in the acute myeloid leukemia microenvironment
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102477
                DO  - 10.18632/aging.102477
                SP  - 10557
                EP  - 10580
                PY  - 
                AB  - The tumor microenvironment (TME) has a strong influence on the progression, therapeutic response, and clinical outcome of acute myeloid leukemia (AML), one of the most common hematopoietic malignancies in adults. In this study, we identified TME-related genes associated with AML prognosis. Gene expression profiles from AML patients were downloaded from TCGA database, and immune and stromal scores were calculated using the ESTIMATE algorithm. Immune scores were correlated with clinical features such as FAB subtypes and patient&#x2019;s age. After categorizing AML cases into high and low score groups, an association between several differentially expressed genes (DEGs) and overall survival was identified. Functional enrichment analysis of the DEGs showed that they were primarily enriched in the immune response, inflammatory response, and cytokine activity, and were involved in signaling processes related to hematopoietic cell lineage, B cell receptor, and chemokine pathways. Two significant modules, dominated respectively by CCR5 and ITGAM nodes, were identified from the PPI network, and 20 hub genes were extracted. A total of 112 DEGs correlated with poor overall survival of AML patients, and 11 of those genes were validated in a separate TARGET-AML cohort. By identifying TME-associated genes, our findings may lead to improved prognoses and therapies for AML.
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Mixed-location cerebral microbleeds as a biomarker of neurodegeneration in a memory clinic population

Bibek Gyanwali, Muhammad Amin Shaik, Chuen Seng Tan, Henri Vrooman, Narayanaswamy Venketasubramanian, Christopher Chen, Saima Hilal,

https://doi.org/10.18632/aging.102478 pp 10581—10596

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Gyanwali B, Shaik MA, Tan CS, Vrooman H, Venketasubramanian N, Chen C, Hilal S, . Mixed-location cerebral microbleeds as a biomarker of neurodegeneration in a memory clinic population. . 11:10581-10596. https://doi.org/10.18632/aging.102478

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                TY  - JOUR
                AU  - Gyanwali, Bibek 
                AU  - Shaik, Muhammad Amin 
                AU  - Tan, Chuen Seng 
                AU  - Vrooman, Henri 
                AU  - Venketasubramanian, Narayanaswamy 
                AU  - Chen, Christopher 
                AU  - Hilal, Saima 
                TI  - Mixed-location cerebral microbleeds as a biomarker of neurodegeneration in a memory clinic population
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102478
                DO  - 10.18632/aging.102478
                SP  - 10581
                EP  - 10596
                PY  - 
                AB  - Cerebral microbleeds (CMBs) in the lobar and deep locations are associated with two distinct pathologies: cerebral amyloid angiopathy and hypertensive arteriopathy. However, the role of mixed-location CMBs in neurodegeneration remains unexplored. We investigated the associations between strictly lobar, strictly deep and mixed-location CMBs with markers of neurodegeneration. This study recruited 477 patients from a memory clinic who underwent 3T MRI scans. CMBs were categorized into strictly lobar, strictly deep and mixed-location. Cortical thickness, white matter volume and subcortical structural volumes were quantified using Free-Surfer. Linear regression models were performed to assess the association between CMBs and cerebral atrophy, and the mean difference (&#x3B2;) and 95% confidence intervals (CIs) were reported. In the regression analyses, mixed-location CMBs were associated with smaller cortical thickness of limbic region [&#x3B2;= -0.01; 95% CI= -0.02, -0.00, p=0.007) as well as with smaller accumbens volume [&#x3B2;= -0.01; 95% CI= -0.02, -0.00, p=0.004) and presubiculum region of hippocampus [&#x3B2;= -0.01; 95% CI= -0.02, -0.00, p=0.002). Strictly lobar CMBs were associated with smaller total white matter volume [&#x3B2;= -0.03; 95% CI= -0.04, -0.01, p&lt;0.001] and with region specific white matter volumes. The underlying mechanism requires further research and may involve shared mechanisms of vascular dysfunction and neurodegeneration.
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Crucial role of serum response factor in renal tubular epithelial cell epithelial-mesenchymal transition in hyperuricemic nephropathy

Long Zhao, Chenyu Li, Bin Zhou, Congjuan Luo, Yanfei Wang, Lin Che, Jun Zhao, Yan Xu,

https://doi.org/10.18632/aging.102479 pp 10597—10609

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Zhao L, Li C, Zhou B, Luo C, Wang Y, Che L, Zhao J, Xu Y, . Crucial role of serum response factor in renal tubular epithelial cell epithelial-mesenchymal transition in hyperuricemic nephropathy. . 11:10597-10609. https://doi.org/10.18632/aging.102479

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                TY  - JOUR
                AU  - Zhao, Long 
                AU  - Li, Chenyu 
                AU  - Zhou, Bin 
                AU  - Luo, Congjuan 
                AU  - Wang, Yanfei 
                AU  - Che, Lin 
                AU  - Zhao, Jun 
                AU  - Xu, Yan 
                TI  - Crucial role of serum response factor in renal tubular epithelial cell epithelial-mesenchymal transition in hyperuricemic nephropathy
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102479
                DO  - 10.18632/aging.102479
                SP  - 10597
                EP  - 10609
                PY  - 
                AB  - Objective: To explore the regulation and function of serum response factor (SRF) in epithelial-mesenchymal transition (EMT) in renal tubular epithelial cells (TECs) in hyperuricemic nephropathy (HN).Results: In NRK-52E cells treated with UA and renal medulla tissue samples from hyperuricemic rats, SRF, fibronectin, &#x3B1;-SMA and FSP-1 expression was upregulated, while ZO-1 and E-cadherin expression was downregulated. SRF upregulation in NRK-52E cells increased slug expression. Blockade of SRF by an SRF-specific siRNA or CCG-1423 reduced slug induction and protected TECs from undergoing EMT both in vitro and in vivo.Conclusion: Increased SRF activity promotes EMT and dysfunction in TECs in HN. Targeting SRF with CCG-1423 may be an attractive therapeutic strategy in HN.Methods: The expression of SRF, mesenchymal markers (fibronectin, &#x3B1;-SMA, and FSP-1), epithelial markers (ZO-1 and E-cadherin) and was examined in rat renal TECs (NRK-52E cells) or renal medulla tissue samples following uric acid (UA) treatment. SRF overexpressed with pcDNA-SRF plasmid and suppressed by CCG-1423 (a small molecule inhibitor of SRF) to study how SRF influences EMT in TECs in HN. Oxonic acid (OA) was used to establish HN in rats.
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Ets2 suppresses inflammatory cytokines through MAPK/NF-κB signaling and directly binds to the IL-6 promoter in macrophages

Xianwei Ma, Zhengyu Jiang, Na Li, Wei Jiang, Peng Gao, Mingjin Yang, Xiya Yu, Guifang Wang, Yan Zhang,

https://doi.org/10.18632/aging.102480 pp 10610—10625

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Ma X, Jiang Z, Li N, Jiang W, Gao P, Yang M, Yu X, Wang G, Zhang Y, . Ets2 suppresses inflammatory cytokines through MAPK/NF-κB signaling and directly binds to the IL-6 promoter in macrophages. . 11:10610-10625. https://doi.org/10.18632/aging.102480

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                TY  - JOUR
                AU  - Ma, Xianwei 
                AU  - Jiang, Zhengyu 
                AU  - Li, Na 
                AU  - Jiang, Wei 
                AU  - Gao, Peng 
                AU  - Yang, Mingjin 
                AU  - Yu, Xiya 
                AU  - Wang, Guifang 
                AU  - Zhang, Yan 
                TI  - Ets2 suppresses inflammatory cytokines through MAPK/NF-κB signaling and directly binds to the IL-6 promoter in macrophages
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102480
                DO  - 10.18632/aging.102480
                SP  - 10610
                EP  - 10625
                PY  - 
                AB  - Proper activation of Toll-like receptor (TLR)-mediated signaling and production of proinflammatory cytokines are critical for the initiation of innate immunity, while the specific mechanism maintaining inflammatory homeostasis remains mostly unknown. Here, we show that Ets2 is upregulated following LPS and VSV stimulation. Ets2 knockdown or knockout leads to increased IL-6, TNF-&#x3B1;, and IFN-&#x3B2; production in macrophages. Consistently, Ets2-deficient mice show exacerbated inflammatory cytokine production and are more susceptible to CLP-induced sepsis. Mechanistically, Ets2 inhibits the LPS- and VSV-induced activation of ERK1/2, JNK, p38, and p65. Ets2 also binds to the promoter of IL-6 to inhibit transcription. Collectively, the results of the present study show the negative regulatory role of Ets2 in LPS- and VSV-induced inflammation through the suppression of MAPK/NF-&#x3BA;B signaling, direct binding to the IL-6 promoter and inhibition of transcription.
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Circ_0006332 promotes growth and progression of bladder cancer by modulating MYBL2 expression via miR-143

Mingshan Li, Yili Liu, Jie Liu, Wei Li, Ning Li, Dongwei Xue, Xiling Zhang, Ping Wang,

https://doi.org/10.18632/aging.102481 pp 10626—10643

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Li M, Liu Y, Liu J, Li W, Li N, Xue D, Zhang X, Wang P, . Circ_0006332 promotes growth and progression of bladder cancer by modulating MYBL2 expression via miR-143. . 11:10626-10643. https://doi.org/10.18632/aging.102481

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                TY  - JOUR
                AU  - Li, Mingshan 
                AU  - Liu, Yili 
                AU  - Liu, Jie 
                AU  - Li, Wei 
                AU  - Li, Ning 
                AU  - Xue, Dongwei 
                AU  - Zhang, Xiling 
                AU  - Wang, Ping 
                TI  - Circ_0006332 promotes growth and progression of bladder cancer by modulating MYBL2 expression via miR-143
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102481
                DO  - 10.18632/aging.102481
                SP  - 10626
                EP  - 10643
                PY  - 
                AB  - In this study, we analyzed the role of circular RNAs in the growth and progression of bladder cancer. Direct Sanger sequencing and quantitative RT-PCR analysis showed that circ_0006332 was significantly upregulated in bladder cancer tissues. Sequencing analysis showed that circ_0006332 is generated from splicing of exons 8 and 9 of the MYBL2 transcript. Fluorescence in situ hybridization analysis showed that circ_0006332 was localized to the cytoplasm of bladder cancer cells. Dual luciferase reporter assays showed that miR-143 specifically bound to circ_0006332 and the 3&#x2019;UTR of MYBL2. High expression of circ_006332 correlated with tumor-node-metastasis stages and muscular invasion in bladder cancer patients. Knockdown of circ_0006332 in bladder cancer cells decreased proliferation, colony formation and invasiveness. Circ_0006332 knockdown increased E-cadherin levels and decreased Vimentin, CCNB1 and P21 protein expression. This suggests that circ_0006332 promotes epithelial&#x2013;mesenchymal transition and cell cycle progression. In vivo experiments in nude mice showed that circ_0006332 knockdown bladder cancer cells form significantly smaller tumors than the controls. Our study demonstrates that circ_0006332 promotes the growth and progression of bladder cancer by modulating MYBL2 expression by acting as a sponge for miR-143. Circ_0006332 is thus a potential early diagnostic marker of bladder cancer.
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MYSM1-AR complex-mediated repression of Akt/c-Raf/GSK-3β signaling impedes castration-resistant prostate cancer growth

Jinbo Sun, Xiangnan Hu, Yongheng Gao, Qisheng Tang, Zhining Zhao, Wenjin Xi, Fan Yang, Wei Zhang, Yue Song, Bin Song, Tao Wang, He Wang,

https://doi.org/10.18632/aging.102482 pp 10644—10663

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Sun J, Hu X, Gao Y, Tang Q, Zhao Z, Xi W, Yang F, Zhang W, Song Y, Song B, Wang T, Wang H, . MYSM1-AR complex-mediated repression of Akt/c-Raf/GSK-3β signaling impedes castration-resistant prostate cancer growth. . 11:10644-10663. https://doi.org/10.18632/aging.102482

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                TY  - JOUR
                AU  - Sun, Jinbo 
                AU  - Hu, Xiangnan 
                AU  - Gao, Yongheng 
                AU  - Tang, Qisheng 
                AU  - Zhao, Zhining 
                AU  - Xi, Wenjin 
                AU  - Yang, Fan 
                AU  - Zhang, Wei 
                AU  - Song, Yue 
                AU  - Song, Bin 
                AU  - Wang, Tao 
                AU  - Wang, He 
                TI  - MYSM1-AR complex-mediated repression of Akt/c-Raf/GSK-3β signaling impedes castration-resistant prostate cancer growth
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102482
                DO  - 10.18632/aging.102482
                SP  - 10644
                EP  - 10663
                PY  - 
                AB  - Epigenetic alterations that lead to dysregulated gene expression in the progression of castration-resistant prostate cancer (CRPC) remain elusive. Here, we investigated the role of histone deubiquitinase MYSM1 in the pathogenesis of prostate cancer (PCa). Tissues and public datasets of PCa were evaluated for MYSM1 levels. We explored the effects of MYSM1 on cell proliferation, senescence and viability both in vitro and in vivo. Integrative database analyses and co-immunoprecipitation assays were performed to elucidate genomic association of MYSM1 and MYSM1-involved biological interaction network in PCa. We observed that MYSM1 were downregulated in CRPC compared to localized prostate tumors. Knockdown of MYSM1 promoted cell proliferation and suppressed senescence of CRPC cells under condition of androgen ablation. MYSM1 downregulation enhanced the tumorigenic ability in nude mice. Integrative bioinformatic analyses of the significantly associated genes with MYSM1 revealed MYSM1-correlated pathways, providing substantial clues as to the role of MYSM1 in PCa. MYSM1 was able to bind to androgen receptor instead of increasing its expression and knockdown of MYSM1 resulted in activation of Akt/c-Raf/GSK-3&#x3B2; signaling. Together, our findings indicate that MYSM1 is pivotal in CRPC pathogenesis and may be established as a potential target for future treatment.
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Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis

Nan Zhang, Zhou Zhong, Yujia Wang, Li Yang, Fengbo Wu, Cheng Peng, Wei Huang, Gu He,

https://doi.org/10.18632/aging.102483 pp 10664—10683

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Zhang N, Zhong Z, Wang Y, Yang L, Wu F, Peng C, Huang W, He G, . Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis. . 11:10664-10683. https://doi.org/10.18632/aging.102483

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                TY  - JOUR
                AU  - Zhang, Nan 
                AU  - Zhong, Zhou 
                AU  - Wang, Yujia 
                AU  - Yang, Li 
                AU  - Wu, Fengbo 
                AU  - Peng, Cheng 
                AU  - Huang, Wei 
                AU  - He, Gu 
                TI  - Competing endogenous network analysis identifies lncRNA Meg3 activates inflammatory damage in UVB induced murine skin lesion by sponging miR-93-5p/epiregulin axis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102483
                DO  - 10.18632/aging.102483
                SP  - 10664
                EP  - 10683
                PY  - 
                AB  - In this study, we obtained the RNA expression data of murine skin tissues of control, and UVB irradiated groups. After the re-annotation of lncRNAs, a gene expression similarity analysis was done by WGCNA. The target mRNA prediction of lncRNAs, miRNAs, and ceRNA regulatory networks were constructed by five lncRNAs, 14 miRNAs and 54 mRNAs, respectively. Based on the ceRNA network of UVB-induced skin lesions, it was evident that the dysregulation of Meg3 has critical effects on the UVB-induced inflammatory lesion of murine skin tissues. The overexpression of Meg3 after UVB irradiation was observed in primary murine skin fibroblasts, and the up-regulated Meg3 expression was related to the activation of the inflammatory cytokines. These functional experiments demonstrated that the RNA silencing of Meg3 in murine skin fibroblasts could suppress the expression of the cytokines (in vitro) and UVB-induced skin lesions (in vivo). Moreover, the Meg3 functioned as a competing endogenous RNA (ceRNA) that acted as a sponge for miR-93-5p and thereby modulated the expression of Epiregulin (Ereg). Our results proved that Meg3 was involved in UVB-induced skin inflammation and that the ceRNA networks, which includes miR-93-5p and Ereg, could prove to be a potential therapeutic target for UVB-induced skin damage.
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Disrupted brain functional hub and causal connectivity in acute mild traumatic brain injury

Fengfang Li, Liyan Lu, Huiyou Chen, Peng Wang, Yu-Chen Chen, Hong Zhang, Xindao Yin,

https://doi.org/10.18632/aging.102484 pp 10684—10696

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Li F, Lu L, Chen H, Wang P, Chen Y, Zhang H, Yin X, . Disrupted brain functional hub and causal connectivity in acute mild traumatic brain injury. . 11:10684-10696. https://doi.org/10.18632/aging.102484

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                TY  - JOUR
                AU  - Li, Fengfang 
                AU  - Lu, Liyan 
                AU  - Chen, Huiyou 
                AU  - Wang, Peng 
                AU  - Chen, Yu-Chen 
                AU  - Zhang, Hong 
                AU  - Yin, Xindao 
                TI  - Disrupted brain functional hub and causal connectivity in acute mild traumatic brain injury
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102484
                DO  - 10.18632/aging.102484
                SP  - 10684
                EP  - 10696
                PY  - 
                AB  - There have been an increasing number of functional magnetic resonance imaging (fMRI) reports on brain abnormalities in mild traumatic brain injury (mTBI) at different phases. However, the neural bases and cognitive impairment after acute mTBI are unclear. This study aimed to identify brain functional hubs and connectivity abnormalities in acute mTBI patients and their correlations with deficits in cognitive performance. Within seven days after brain injury, mTBI patients (n=55) and age-, sex-, and educational -matched healthy controls (HCs) (n=41) underwent resting-state fMRI scans and cognitive assessments. We derived functional connectivity (FC) strength of the whole-brain network using degree centrality (DC) and performed Granger causality analysis (GCA) to analyze causal connectivity patterns in acute mTBI. Compared with HCs, acute mTBI patients had significantly decreased network centrality in the left middle frontal gyrus (MFG). Additionally, acute mTBI showed decreased inflows from the left MFG to bilateral middle temporal gyrus (MTG), left medial superior frontal gyrus (mSFG), and left anterior cingulate cortex (ACC). Correlation analyses revealed that changes in network centrality and causal connectivity were associated with deficits in cognitive performance in mTBI. Our findings may help to provide a new perspective for understanding the neuropathophysiological mechanism of acute cognitive impairment after mTBI.
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MAP2K4 interacts with Vimentin to activate the PI3K/AKT pathway and promotes breast cancer pathogenesis

Shu Liu, Juan Huang, Yewei Zhang, Yiyi Liu, Shi Zuo, Rong Li,

https://doi.org/10.18632/aging.102485 pp 10697—10710

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Liu S, Huang J, Zhang Y, Liu Y, Zuo S, Li R, . MAP2K4 interacts with Vimentin to activate the PI3K/AKT pathway and promotes breast cancer pathogenesis. . 11:10697-10710. https://doi.org/10.18632/aging.102485

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                TY  - JOUR
                AU  - Liu, Shu 
                AU  - Huang, Juan 
                AU  - Zhang, Yewei 
                AU  - Liu, Yiyi 
                AU  - Zuo, Shi 
                AU  - Li, Rong 
                TI  - MAP2K4 interacts with Vimentin to activate the PI3K/AKT pathway and promotes breast cancer pathogenesis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102485
                DO  - 10.18632/aging.102485
                SP  - 10697
                EP  - 10710
                PY  - 
                AB  - Mitogen-activated protein kinase kinase 4 (MAP2K4) is a member of the mitogen-activated protein kinase (MAPK) activator family. MAPK signaling plays a significant role in cell proliferation, differentiation, transcriptional regulation, and development. However, specific function and mechanism of MAP2K4 in breast cancer have not been clarified. According to our study, overexpressed MAP2K4 in breast cancer cells increased proliferation, migration, and invasion in vivo and in vitro, while MAP2K4 knockdown restored the effects. Subsequent mechanistic analyses demonstrated that MAP2K4 promoted cell proliferation, migration, and invasion by activating phosphoinositide-3-kinase (PI3K)/AKT signaling, the downstream proteins, c-JUN, the G1/S cell cycle, and the epithelial-to-mesenchymal transition (EMT). Meanwhile, MAP2K4 interacted with Vimentin and further propagated the malignant phenotype. Furthermore, patients with high MAP2K4 and Vimentin expression levels had poorer overall survival rates than those with low expression levels of both proteins. Our studies demonstrated that MAP2K4 has the potential to serve as an oncogene in breast cancer and it activates the phosphorylated PI3K/AKT signaling pathway to activate downstream cycle-associated proteins and EMT signals while interacting with Vimentin to promote breast cancer cells proliferation, migration, and invasion. In our study, MAP2K4 and Vimentin co-expression is confirmed to be an unfavorable factor in breast cancer.
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p62-DNA-encoding plasmid reverts tumor grade, changes tumor stroma, and enhances anticancer immunity

Franco M. Venanzi, Vladimir Gabai, Francesca Mariotti, Gian Enrico Magi, Cecilia Vullo, Albert A. Sufianov, Sergey I. Kolesnikov, Alexander Shneider,

https://doi.org/10.18632/aging.102486 pp 10711—10722

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Venanzi FM, Gabai V, Mariotti F, Magi GE, Vullo C, Sufianov AA, Kolesnikov SI, Shneider A, . p62-DNA-encoding plasmid reverts tumor grade, changes tumor stroma, and enhances anticancer immunity. . 11:10711-10722. https://doi.org/10.18632/aging.102486

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                TY  - JOUR
                AU  - Venanzi, Franco M. 
                AU  - Gabai, Vladimir 
                AU  - Mariotti, Francesca 
                AU  - Magi, Gian Enrico 
                AU  - Vullo, Cecilia 
                AU  - Sufianov, Albert A. 
                AU  - Kolesnikov, Sergey I. 
                AU  - Shneider, Alexander 
                TI  - p62-DNA-encoding plasmid reverts tumor grade, changes tumor stroma, and enhances anticancer immunity
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102486
                DO  - 10.18632/aging.102486
                SP  - 10711
                EP  - 10722
                PY  - 
                AB  - Previously, we reported that the administration of a p62/SQSTM1-encoding plasmid demonstrates high safety and signs of clinical benefits for human cancer patients. The treatment also suppressed tumor growth and metastasis in dogs and mouse models. Here we investigated some mechanistic aspects of these effects. In mammary tumors bearing-dogs, i.m. injections of p62 plasmid reduced tumor sizes and their aggressive potential in 5 out of 6 animals, with one carcinoma switching to adenoma. The treatment increased levels of smooth muscle actin in stroma cells and type III collagen in the extracellular matrix, which correlate with a good clinical prognosis. The p62 treatment also increased the abundance of intratumoral T-cells. Because of the role of adaptive immunity cannot be tested in dogs, we compared the protective effects of the p62 plasmid against B16 melanoma in wild type C57BL/6J mice versus their SCID counterpart lacking lymphocytes. The plasmid was only protective in the wild type strain. Also, p62 plasmid amplified the anti-tumor effect of T-cell transfer from tumor-bearing animals to animals challenged with the same tumors. We conclude that the plasmid acts via re-modeling of the tumor microenvironment, making it more favorable for increased anti-cancer immunity. Thus, the p62-encoding plasmid might be a new adjuvant for cancer treatments.
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T cells and immune functions of plasma extracellular vesicles are differentially modulated from adults to centenarians

Ainhoa Alberro, Iñaki Osorio-Querejeta, Lucía Sepúlveda, Gorka Fernández-Eulate, Maider Mateo-Abad, Maider Muñoz-Culla, Susana Carregal-Romero, Ander Matheu, Itziar Vergara, Adolfo López de Munain, Matías Sáenz-Cuesta, David Otaegui,

https://doi.org/10.18632/aging.102517 pp 10723—10741

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Alberro A, Osorio-Querejeta I, Sepúlveda L, Fernández-Eulate G, Mateo-Abad M, Muñoz-Culla M, Carregal-Romero S, Matheu A, Vergara I, López de Munain A, Sáenz-Cuesta M, Otaegui D, . T cells and immune functions of plasma extracellular vesicles are differentially modulated from adults to centenarians. . 11:10723-10741. https://doi.org/10.18632/aging.102517

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                TY  - JOUR
                AU  - Alberro, Ainhoa 
                AU  - Osorio-Querejeta, Iñaki 
                AU  - Sepúlveda, Lucía 
                AU  - Fernández-Eulate, Gorka 
                AU  - Mateo-Abad, Maider 
                AU  - Muñoz-Culla, Maider 
                AU  - Carregal-Romero, Susana 
                AU  - Matheu, Ander 
                AU  - Vergara, Itziar 
                AU  - López de Munain, Adolfo 
                AU  - Sáenz-Cuesta, Matías 
                AU  - Otaegui, David 
                TI  - T cells and immune functions of plasma extracellular vesicles are differentially modulated from adults to centenarians
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102517
                DO  - 10.18632/aging.102517
                SP  - 10723
                EP  - 10741
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Alberro, Ainhoa 
                AU  - Osorio-Querejeta, Iñaki 
                AU  - Sepúlveda, Lucía 
                AU  - Fernández-Eulate, Gorka 
                AU  - Mateo-Abad, Maider 
                AU  - Muñoz-Culla, Maider 
                AU  - Carregal-Romero, Susana 
                AU  - Matheu, Ander 
                AU  - Vergara, Itziar 
                AU  - López de Munain, Adolfo 
                AU  - Sáenz-Cuesta, Matías 
                AU  - Otaegui, David 
                TI  - T cells and immune functions of plasma extracellular vesicles are differentially modulated from adults to centenarians
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102517
                DO  - 10.18632/aging.102517
                SP  - 10723
                EP  - 10741
                PY  - 
                AB  - Aging is a universal and complex process that affects all tissues and cells types, including immune cells, in a process known as immunosenescence. However, many aspects of immunosenescence are not completely understood, as the characteristics of the immune cells of nonagenarians and centenarians or the features and implications of extracellular vesicles (EVs). In this study, we analyzed blood samples from 51 individuals aged 20-49 and 70-104 years. We found that senescent CD8 cells accumulate with age, while there is a partial reduction of senescent CD4 cells in nonagenarians and centenarians. Moreover, plasma EVs carry T cell specific markers, but no accumulation of &#x201C;senescent-like EVs&#x201D; was found within any of analyzed age groups. Our functional studies of cocultures of peripheral blood mononuclear cells and EVs showed that EVs enhance T cell viability and, under phytohemagglutinin stimulation, they influence cytokine secretion and cell activation in an age-dependent manner. These results underline the importance of EVs on the immune system functioning, and open new perspectives to further study their implication in human aging.
                ER  -

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Association of genes with phenotype in autism spectrum disorder

Sabah Nisar, Sheema Hashem, Ajaz A. Bhat, Najeeb Syed, Santosh Yadav, Muhammad Waqar Azeem, Shahab Uddin, Puneet Bagga, Ravinder Reddy, Mohammad Haris,

https://doi.org/10.18632/aging.102473 pp 10742—10770

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Nisar S, Hashem S, Bhat AA, Syed N, Yadav S, Azeem MW, Uddin S, Bagga P, Reddy R, Haris M, . Association of genes with phenotype in autism spectrum disorder. . 11:10742-10770. https://doi.org/10.18632/aging.102473

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                TY  - JOUR
                AU  - Nisar, Sabah 
                AU  - Hashem, Sheema 
                AU  - Bhat, Ajaz A. 
                AU  - Syed, Najeeb 
                AU  - Yadav, Santosh 
                AU  - Azeem, Muhammad Waqar 
                AU  - Uddin, Shahab 
                AU  - Bagga, Puneet 
                AU  - Reddy, Ravinder 
                AU  - Haris, Mohammad 
                TI  - Association of genes with phenotype in autism spectrum disorder
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102473
                DO  - 10.18632/aging.102473
                SP  - 10742
                EP  - 10770
                PY  - 
                AB  - Autism spectrum disorder (ASD) is a genetic heterogeneous neurodevelopmental disorder that is characterized by impairments in social interaction and speech development and is accompanied by stereotypical behaviors such as body rocking, hand flapping, spinning objects, sniffing and restricted behaviors. The considerable significance of the genetics associated with autism has led to the identification of many risk genes for ASD used for the probing of ASD specificity and shared cognitive features over the past few decades. Identification of ASD risk genes helps to unravel various genetic variants and signaling pathways which are involved in ASD. This review highlights the role of ASD risk genes in gene transcription and translation regulation processes, as well as neuronal activity modulation, synaptic plasticity, disrupted key biological signaling pathways, and the novel candidate genes that play a significant role in the pathophysiology of ASD. The current emphasis on autism spectrum disorders has generated new opportunities in the field of neuroscience, and further advancements in the identification of different biomarkers, risk genes, and genetic pathways can help in the early diagnosis and development of new clinical and pharmacological treatments for ASD.
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Deep biomarkers of aging and longevity: from research to applications

Alex Zhavoronkov, Ricky Li, Candice Ma, Polina Mamoshina,

https://doi.org/10.18632/aging.102475 pp 10771—10780

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Zhavoronkov A, Li R, Ma C, Mamoshina P, . Deep biomarkers of aging and longevity: from research to applications. . 11:10771-10780. https://doi.org/10.18632/aging.102475

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                TY  - JOUR
                AU  - Zhavoronkov, Alex 
                AU  - Li, Ricky 
                AU  - Ma, Candice 
                AU  - Mamoshina, Polina 
                TI  - Deep biomarkers of aging and longevity: from research to applications
                JO  - 
                JA  - 
                VL  - 11
                IS  - 22
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.102475
                DO  - 10.18632/aging.102475
                SP  - 10771
                EP  - 10780
                PY  - 
                AB  - Multiple recent advances in machine learning enabled computer systems to exceed human performance in many tasks including voice, text, and speech recognition and complex strategy games. Aging is a complex multifactorial process driven by and resulting in the many minute changes transpiring at every level of the human organism. Deep learning systems trained on the many measurable features changing in time can generalize and learn the many biological processes on the population and individual levels. The deep age predictors can help advance aging research by establishing causal relationships in non-linear systems. Deep aging clocks can be used for identification of novel therapeutic targets, evaluating the efficacy of the various interventions, data quality control, data economics, prediction of health trajectories, mortality, and many other applications. Here we present the current state of development of the deep aging clocks in the context of the pharmaceutical research and development and clinical applications.
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Correction for: Proteomics-based identification of different training adaptations of aged skeletal muscle following long-term high-intensity interval and moderate-intensity continuous training in aged rats

Fang-Hui Li, Lei Sun, Da-Shuai Wu, Hao-En Gao, Zhu Min,

https://doi.org/10.18632/aging.102596 pp 10781—10782

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Li F, Sun L, Wu D, Gao H, Min Z, . Correction for: Proteomics-based identification of different training adaptations of aged skeletal muscle following long-term high-intensity interval and moderate-intensity continuous training in aged rats. . 11:10781-10782. https://doi.org/10.18632/aging.102596

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Volume 11, Issue 22

About the Cover

Editorials

Cecile Lambe, Olivier Goulet, Lorenzo Norsa,

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Chi Kin Ip, Herbert Herzog, Lei Zhang,

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Susana Ravassa, Gabriel Ballesteros, Javier Díez,

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Cristina Aguayo-Mazzucato, Ayush Midha,

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Gaurav Baranwal, Joseph M. Rutkowski,

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Meeting Report

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Research Papers

Qiu Tang, Zhigang Chen, Liangping Zhao, Hai Xu,

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Pan Sun, Wutao Lou, Jianghong Liu, Lin Shi, Kuncheng Li, Defeng Wang, Vincent CT Mok, Peipeng Liang,

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Yongyao Yang, Feng Tang, Fang Wei, Long Yang, Chunyan Kuang, Hongming Zhang, Jiusheng Deng, Qiang Wu,

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Xiaohui Wu, Weidan Chen, Fangqin Lin, Qingsheng Huang, Jiayong Zhong, Huan Gao, Yanyan Song, Huiying Liang,

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Chen Xu, Yalan Liu, Dongxian Jiang, Xiaowen Ge, Jie Huang, Jieakesu Su, Xue Zhang, Shaohua Lu, Yuan Ji, Jun Hou, Tianshu Liu, Yingyong Hou,

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Dong Liu, Zhiqiang Ma, Liqun Xu, Xiaoyan Zhang, Shubin Qiao, Jiansong Yuan,

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Huanhuan Liu, Yi Sun, Huan Tian, Xiaolian Xiao, Jiaqi Zhang, Yongzhen Wang, Fengyan Yu,

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Qunlin Chen, Yunman Xia, Kaixiang Zhuang, Xinran Wu, Guangyuan Liu, Jiang Qiu,

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Runzhi Huang, Tong Meng, Rui Chen, Penghui Yan, Jie Zhang, Peng Hu, Xiaolong Zhu, Huabin Yin, Dianwen Song, Zongqiang Huang,

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Wenying Zhou, Jiao Gong, Yaqiong Chen, Jiahao Chen, Qi Zhuang, Jing Cao, Zhixiong Mei, Bo Hu,

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Xin-Bin Pan, Yan Lu, Jian-Li Huang, Ying Long, De-Sheng Yao,

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Eryan Yang, Ying Cai, Xiuhua Yao, Ji Liu, Qixue Wang, Weili Jin, Qiaoli Wu, Weijia Fan, Lina Qiu, Chunsheng Kang, Jialing Wu,

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Chuanjie Zhang, Hongchao He, Xin Hu, Ao Liu, Da Huang, Yang Xu, Lu Chen, Danfeng Xu,

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