Volume 12, Issue 18

Tan J, Wang X, Hwang B, Gonzales R, Konen O, Lan L, Lu A, . An ordered assembly of MYH glycosylase, SIRT6 protein deacetylase, and Rad9-Rad1-Hus1 checkpoint clamp at oxidatively damaged telomeres. . 12:17761-17785. https://doi.org/10.18632/aging.103934

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                TY  - JOUR
                AU  - Tan, Jun 
                AU  - Wang, Xiangyu 
                AU  - Hwang, Bor-Jang 
                AU  - Gonzales, Rex 
                AU  - Konen, Olivia 
                AU  - Lan, Li 
                AU  - Lu, A-Lien 
                TI  - An ordered assembly of MYH glycosylase, SIRT6 protein deacetylase, and Rad9-Rad1-Hus1 checkpoint clamp at oxidatively damaged telomeres
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103934
                DO  - 10.18632/aging.103934
                SP  - 17761
                EP  - 17785
                PY  - 
                AB  - In the base excision repair pathway, MYH/MUTYH DNA glycosylase prevents mutations by removing adenine mispaired with 8-oxoG, a frequent oxidative lesion. MYH glycosylase activity is enhanced by Rad9-Rad1-Hus1 (9-1-1) checkpoint clamp and SIRT6 histone/protein deacetylase. Here, we show that MYH, SIRT6, and 9-1-1 are recruited to confined oxidatively damaged regions on telomeres in mammalian cells. Using different knockout cells, we show that SIRT6 responds to damaged telomeres very early, and then recruits MYH and Hus1 following oxidative stress. However, the recruitment of Hus1 to damaged telomeres is partially dependent on SIRT6. The catalytic activities of SIRT6 are not important for SIRT6 response but are essential for MYH recruitment to damaged telomeres. Compared to wild-type MYH, the recruitment of hMYHV315A mutant (defective in both SIRT6 and Hus1 interactions), but not hMYHQ324H mutant (defective in Hus1 interaction only), to damaged telomeres is severely reduced. The formation of MYH/SIRT6/9-1-1 complex is of biological significance as interrupting their interactions can increase cell&#x2019;s sensitivity to H2O2 and/or elevate cellular 8-oxoG levels after H2O2 treatment. Our results establish that SIRT6 acts as an early sensor of BER enzymes and both SIRT6 and 9-1-1 serve critical roles in DNA repair to maintain telomere integrity.
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Rapamycin maintains NAD⁺/NADH redox homeostasis in muscle cells

Zhigang Zhang, He N. Xu, Siyu Li, Antonio Davila Jr, Karthikeyani Chellappa, James G. Davis, Yuxia Guan, David W. Frederick, Weiqing Chu, Huaqing Zhao, Lin Z. Li, Joseph A. Baur,

https://doi.org/10.18632/aging.103954 pp 17786—17799

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Zhang Z, Xu HN, Li S, Jr AD, Chellappa K, Davis JG, Guan Y, Frederick DW, Chu W, Zhao H, Li LZ, Baur JA, . Rapamycin maintains NAD⁺/NADH redox homeostasis in muscle cells. . 12:17786-17799. https://doi.org/10.18632/aging.103954

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 TY - JOUR
 AU - Zhang, Zhigang 
 AU - Xu, He N. 
 AU - Li, Siyu 
 AU - Jr, Antonio Davila 
 AU - Chellappa, Karthikeyani 
 AU - Davis, James G. 
 AU - Guan, Yuxia 
 AU - Frederick, David W. 
 AU - Chu, Weiqing 
 AU - Zhao, Huaqing 
 AU - Li, Lin Z. 
 AU - Baur, Joseph A. 
 TI - Rapamycin maintains NAD+/NADH redox homeostasis in muscle cells
 JO - 
 JA - 
 VL - 12
 IS - 18
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103954
 DO - 10.18632/aging.103954
 SP - 17786
 EP - 17799
 PY - 
 AB - Rapamycin delays multiple age-related conditions and extends lifespan in organisms ranging from yeast to mice. However, the mechanisms by which rapamycin influences longevity are incompletely understood. The objective of this study was to investigate the effect of rapamycin on NAD+/NADH redox balance. We report that the NAD+/NADH ratio of C2C12 myoblasts or differentiated myotubes significantly decreases over time in culture, and that rapamycin prevents this effect. Despite lowering the NADH available to support ATP generation, rapamycin increases ATP availability, consistent with lowering energetic demand. Although rapamycin did not change the NAD+/NADH ratio or steady-state ATP concentration in the livers, kidneys, or muscles of young mice, optical redox imaging revealed that rapamycin caused a substantial decline in the NADH content and an increase in the optical redox ratio (a surrogate of NAD+/NADH redox ratio) in muscles from aged mice. Collectively, these data suggest that rapamycin favors a more oxidized NAD+/NADH ratio in aged muscle, which may influence metabolism and the activity of NAD+-dependent enzymes. This study provides new insight into the mechanisms by which rapamycin might influence the aging process to improve health and longevity among the aging population.
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p21 can be a barrier to ferroptosis independent of p53

Divya Venkatesh, Brent R. Stockwell, Carol Prives,

https://doi.org/10.18632/aging.103961 pp 17800—17814

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Venkatesh D, Stockwell BR, Prives C, . p21 can be a barrier to ferroptosis independent of p53. . 12:17800-17814. https://doi.org/10.18632/aging.103961

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                TY  - JOUR
                AU  - Venkatesh, Divya 
                AU  - Stockwell, Brent R. 
                AU  - Prives, Carol 
                TI  - p21 can be a barrier to ferroptosis independent of p53
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103961
                DO  - 10.18632/aging.103961
                SP  - 17800
                EP  - 17814
                PY  - 
                AB  - Traditionally, the p21 protein has been viewed as limiting cancer progression and promoting aging. In contrast, there are reports that p21 can enhance cancer survival and limit tissue damage, depending on the tissue of origin and type of stressor involved. Here, we provide evidence to support these latter two roles of p21 by exploring its ability to regulate ferroptosis. Ferroptosis is a form of cell death that is associated with certain degenerative diseases, some of which are aging-related. Our results reveal a correlation between p21 protein levels in cell lines that are resistant to ferroptosis (p21 high) versus cell lines that are sensitive and easily undergo ferroptosis (p21 low). We also show that p21 levels themselves are differentially regulated in response to ferroptosis in a p53-independent manner. Further, experimentally altering the abundance of p21 protein inverts the ferroptosis-sensitivity of both resistant and sensitive human cancer cell lines. Our data also indicate that the interaction of p21 with CDKs is crucial for its ability to restrict the progression of ferroptosis. While this study was performed in cancer cell lines, our results support the potential of p21 to aid in maintenance of healthy tissues by blocking the damage incurred due to ferroptosis.
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Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics

Alexei Kurakin, Dale E. Bredesen,

https://doi.org/10.18632/aging.103883 pp 17815—17844

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Kurakin A, Bredesen DE, . Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics. . 12:17815-17844. https://doi.org/10.18632/aging.103883

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                TY  - JOUR
                AU  - Kurakin, Alexei 
                AU  - Bredesen, Dale E. 
                TI  - Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103883
                DO  - 10.18632/aging.103883
                SP  - 17815
                EP  - 17844
                PY  - 
                AB  - Ineffective results of clinical trials of over 200 anti-Alzheimer&apos;s drug candidates, with a 99.6% attrition rate, suggest that the current paradigm of Alzheimer&apos;s disease (AD) may be incomplete, necessitating exploration of alternative and complementary frameworks.Using algorithms for hypothesis independent search and expert-assisted synthesis of heterogeneous data, we attempted to reconcile multimodal clinical profiles of early-stage AD patients and accumulated research data within a parsimonious framework. Results of our analysis suggest that Alzheimer&#x2019;s may not be a brain disease but a progressive system-level network disorder, which is driven by chronic network stress and dyshomeostasis. The latter can be caused by various endogenous and exogenous factors, such as chronic inflammatory conditions, infections, vascular dysfunction, head trauma, environmental toxicity, and immune disorders. Whether originating in the brain or on the periphery, chronic stress, toxicity, and inflammation are communicated to the central nervous system (CNS) via humoral and neural routes, preferentially targeting high-centrality regulatory nodes and circuits of the nervous system, and eventually manifesting as a neurodegenerative CNS disease.In this report, we outline an alternative perspective on AD as a systems network disorder and discuss biochemical and genetic evidence suggesting the central role of chronic tissue injury/dyshomeostasis, innate immune reactivity, and inflammation in the etiopathobiology of Alzheimer&#x2019;s disease.
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Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis

Xiaoqi Zhu, Junyan Shen, Shengyu Feng, Ce Huang, Zhongmin Liu, Yi Eve Sun, Hailiang Liu,

https://doi.org/10.18632/aging.103693 pp 17845—17862

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Zhu X, Shen J, Feng S, Huang C, Liu Z, Sun YE, Liu H, . Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis. . 12:17845-17862. https://doi.org/10.18632/aging.103693

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                TY  - JOUR
                AU  - Zhu, Xiaoqi 
                AU  - Shen, Junyan 
                AU  - Feng, Shengyu 
                AU  - Huang, Ce 
                AU  - Liu, Zhongmin 
                AU  - Sun, Yi Eve 
                AU  - Liu, Hailiang 
                TI  - Metformin improves cognition of aged mice by promoting cerebral angiogenesis and neurogenesis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103693
                DO  - 10.18632/aging.103693
                SP  - 17845
                EP  - 17862
                PY  - 
                AB  - Metformin is a widely used drug for type 2 diabetes that is considered to have potential anti-aging effects. However, the beneficial effects of metformin in middle-aged normoglycemic mice are less explored. Here, we report that metformin treated by tail vein injection improved cognitive function of aged mice better than oral administration, which seem to show a dose-dependent manner. Correspondingly, long-term oral administration of metformin was associated with significant disability rates. Further, metformin restored cerebral blood flow and brain vascular density and promoted neurogenic potential of the subependymal zone/subventricular zone both in vivo and in vitro. RNA-Seq and q-PCR results indicated that metformin could enhance relative mRNA glycolysis expression in blood and hippocampal tissue, respectively. Mechanistically, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a key enzyme in glycolysis pathway, may contribute to angiogenic and neurogenic potentials of NSCs. Interestingly, the relative GAPDH mRNA expression of peripheral blood mononuclear cell was gradually decreased with aging. Meanwhile its expression level positively correlated with cognitive levels. Our results indicated that metformin represents a candidate pharmacological approach for recruitment of NSCs in aged mouse brain by enhancing glycolysis and promoting neurovascular generation, a strategy that might be of therapeutic value for anti-aging in humans.
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Epigenetic mutation load is weakly correlated with epigenetic age acceleration

Qi Yan, Kimberly C. Paul, Ake T. Lu, Cynthia Kusters, Alexandra M. Binder, Steve Horvath, Beate Ritz,

https://doi.org/10.18632/aging.103950 pp 17863—17894

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Yan Q, Paul KC, Lu AT, Kusters C, Binder AM, Horvath S, Ritz B, . Epigenetic mutation load is weakly correlated with epigenetic age acceleration. . 12:17863-17894. https://doi.org/10.18632/aging.103950

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                TY  - JOUR
                AU  - Yan, Qi 
                AU  - Paul, Kimberly C. 
                AU  - Lu, Ake T. 
                AU  - Kusters, Cynthia 
                AU  - Binder, Alexandra M. 
                AU  - Horvath, Steve 
                AU  - Ritz, Beate 
                TI  - Epigenetic mutation load is weakly correlated with epigenetic age acceleration
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103950
                DO  - 10.18632/aging.103950
                SP  - 17863
                EP  - 17894
                PY  - 
                AB  - DNA methylation (DNAm) age estimators are widely used to study aging-related conditions. It is not yet known whether DNAm age is associated with the accumulation of stochastic epigenetic mutations (SEMs), which reflect dysfunctions of the epigenetic maintenance system. Here, we defined epigenetic mutation load (EML) as the total number of SEMs per individual. We assessed associations between EML and DNAm age acceleration estimators using biweight midcorrelations in four population-based studies (total n = 6,388). EML was not only positively associated with chronological age (meta r = 0.171), but also with four measures of epigenetic age acceleration: the Horvath pan tissue clock, intrinsic epigenetic age acceleration, the Hannum clock, and the GrimAge clock (meta-analysis correlation ranging from r = 0.109 to 0.179). We further conducted pathway enrichment analyses for each participant&#x2019;s SEMs. The enrichment result demonstrated the stochasticity of epigenetic mutations, meanwhile implicated several pathways: signaling, neurogenesis, neurotransmitter, glucocorticoid, and circadian rhythm pathways may contribute to faster DNAm age acceleration. Finally, investigating genomic-region specific EML, we found that EMLs located within regions of transcriptional repression (TSS1500, TSS200, and 1stExon) were associated with faster age acceleration. Overall, our findings suggest a role for the accumulation of epigenetic mutations in the aging process.
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Developmentally-programmed cellular senescence is conserved and widespread in zebrafish

Sabela Da Silva-Álvarez, Jorge Guerra-Varela, Daniel Sobrido-Cameán, Ana Quelle, Antón Barreiro-Iglesias, Laura Sánchez, Manuel Collado,

https://doi.org/10.18632/aging.103968 pp 17895—17901

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Da Silva-Álvarez S, Guerra-Varela J, Sobrido-Cameán D, Quelle A, Barreiro-Iglesias A, Sánchez L, Collado M, . Developmentally-programmed cellular senescence is conserved and widespread in zebrafish. . 12:17895-17901. https://doi.org/10.18632/aging.103968

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                TY  - JOUR
                AU  - Da Silva-Álvarez, Sabela 
                AU  - Guerra-Varela, Jorge 
                AU  - Sobrido-Cameán, Daniel 
                AU  - Quelle, Ana 
                AU  - Barreiro-Iglesias, Antón 
                AU  - Sánchez, Laura 
                AU  - Collado, Manuel 
                TI  - Developmentally-programmed cellular senescence is conserved and widespread in zebrafish
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103968
                DO  - 10.18632/aging.103968
                SP  - 17895
                EP  - 17901
                PY  - 
                AB  - Cellular senescence is considered a stress response imposing a stable cell cycle arrest to restrict the growth of damaged cells. More recently however, cellular senescence was identified during mouse embryo development at particular structures during specific periods of time. This programmed cell senescence has been proposed to serve developmental and morphogenetic functions and to potentially represent an evolutionary origin of senescence. Cellular senescence has also been described to take place during bird (chick and quail) and amphibian (xenopus and axoltl) development. Fish however, have been described to show a very narrow and restricted pattern of developmental cell senescence. Here we carried out a detailed characterization of senescence during zebrafish development and found it to be conserved and widespread. Apart from yolk and cloaca, previously described structures, we also identified senescence in the developing central nervous system, intestine, liver, pronephric ducts, and crystalline. Interestingly, senescence at these developing structures disappeared upon treatment with senolytic compound ABT-263, supporting their senescent identity and opening the possibility of studying the contribution of this process to development. In summary, our findings extend the description of developmentally-programmed cell senescence to lower vertebrates contributing to the notion of the relevance of this process for embryo development.
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Long noncoding RNA SBF2-AS1 contributes to the growth and metastatic phenotypes of NSCLC via regulating miR-338-3p/ADAM17 axis

Qi Chen, Sheng Min Guo, Hou Qiang Huang, Guo Ping Huang, Yi Li, Zi Hui Li, Run Huang, Lu Xiao, Chun Rong Fan, Qing Yuan, Si Lin Zheng,

https://doi.org/10.18632/aging.103332 pp 17902—17920

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Chen Q, Guo SM, Huang HQ, Huang GP, Li Y, Li ZH, Huang R, Xiao L, Fan CR, Yuan Q, Zheng SL, . Long noncoding RNA SBF2-AS1 contributes to the growth and metastatic phenotypes of NSCLC via regulating miR-338-3p/ADAM17 axis. . 12:17902-17920. https://doi.org/10.18632/aging.103332

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                TY  - JOUR
                AU  - Chen, Qi 
                AU  - Guo, Sheng Min 
                AU  - Huang, Hou Qiang 
                AU  - Huang, Guo Ping 
                AU  - Li, Yi 
                AU  - Li, Zi Hui 
                AU  - Huang, Run 
                AU  - Xiao, Lu 
                AU  - Fan, Chun Rong 
                AU  - Yuan, Qing 
                AU  - Zheng, Si Lin 
                TI  - Long noncoding RNA SBF2-AS1 contributes to the growth and metastatic phenotypes of NSCLC via regulating miR-338-3p/ADAM17 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103332
                DO  - 10.18632/aging.103332
                SP  - 17902
                EP  - 17920
                PY  - 
                AB  - Non-small cell lung cancer (NSCLC) is a type of refractory malignant lung cancer with a high rate of metastasis and mortality. Currently, long non-coding RNA (lncRNA) SBF2 Antisense RNA 1 (SBF2-AS1) is considered as a biomarker for a variety of tumors. However, the function of SBF2-AS1 in the growth and metastasis of NSCLC needs to be further studied. In this study, we revealed that SBF2-AS1 was overexpressed in NSCLC tissues compared with that in normal tissues. SBF2-AS1 silencing restrained the growth and aggressive phenotypes of NSCLC cell in vitro. Consistently, SBF2-AS1 knockdown hindered the growth of NSCLC cell in nude mice. The following luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay suggested the relationship between miR-338-3p and SBF2-AS1. The rescue experiments showed that miR-338-3p inhibitor abolished SBF2-AS1 silencing caused inhibition on the growth, migration and invasiveness of NSCLC cell. The luciferase reporter assay and immunoblotting assay validated that A Disintegrin and Metalloprotease 17 (ADAM17) was a target of miR-338-3p. In addition, SBF2-AS1 positively regulated the level of ADAM17 through sponging for miR-338-3p. Finally, we revealed that SBF2-AS1 contributed to the proliferation and metastatic phenotypes of NSCLC cell via regulating miR-338-3p/ADAM17 axis.
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circKIF4A sponges miR-127 to promote ovarian cancer progression

Shunliang Sheng, Yi Hu, Furong Yu, Wenjuan Tong, Shufen Wang, Yanlin Cai, Jiayu Zhu,

https://doi.org/10.18632/aging.103389 pp 17921—17929

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Sheng S, Hu Y, Yu F, Tong W, Wang S, Cai Y, Zhu J, . circKIF4A sponges miR-127 to promote ovarian cancer progression. . 12:17921-17929. https://doi.org/10.18632/aging.103389

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                TY  - JOUR
                AU  - Sheng, Shunliang 
                AU  - Hu, Yi 
                AU  - Yu, Furong 
                AU  - Tong, Wenjuan 
                AU  - Wang, Shufen 
                AU  - Cai, Yanlin 
                AU  - Zhu, Jiayu 
                TI  - circKIF4A sponges miR-127 to promote ovarian cancer progression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103389
                DO  - 10.18632/aging.103389
                SP  - 17921
                EP  - 17929
                PY  - 
                AB  - Ovarian cancer is a major gynecologic cancer and common cause of gynecologic cancer death worldwide. However, the molecular mechanisms of ovarian cancer progression are still unclear. circular RNAs (circRNAs) are recently reported to be involved in cancer progression regulation but the potential functions of circRNAs in ovarian cancer remains unknown. In this study, we explored the expression of circKIF4A in ovarian cancer tissues. Then, a series of experiments were conducted to investigate how circKIF4A functioned in ovarian cancer in vitro and in vivo. The results revealed that circKIF4A was highly expressed in ovarian cancer tissues. Knockdown of circKIF4A suppressed cell proliferation and migration in ovarian cancer. Subsequent mechanism study revealed that circKIF4A acted as a competitive endogenous RNA (ceRNA) to promoted ovarian cancer progression by sponging miR-127 and upregulated the expression of Junctional adhesion molecule 3 (JAM3). Therefore, circKIF4A could be a novel biomarker and therapeutic target for ovarian cancer.
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Modulating redox homeostasis and cellular reprogramming through inhibited methylenetetrahydrofolate dehydrogenase 2 enzymatic activities in lung cancer

Chun-Hao Chan, Chia-Yu Wu, Navneet Kumar Dubey, Hong-Jian Wei, Jui-Hua Lu, Samantha Mao, Joy Liang, Yu-Hsuan Liang, Hsin-Chung Cheng, Win-Ping Deng,

https://doi.org/10.18632/aging.103471 pp 17930—17947

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Chan C, Wu C, Dubey NK, Wei H, Lu J, Mao S, Liang J, Liang Y, Cheng H, Deng W, . Modulating redox homeostasis and cellular reprogramming through inhibited methylenetetrahydrofolate dehydrogenase 2 enzymatic activities in lung cancer. . 12:17930-17947. https://doi.org/10.18632/aging.103471

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                TY  - JOUR
                AU  - Chan, Chun-Hao 
                AU  - Wu, Chia-Yu 
                AU  - Dubey, Navneet Kumar 
                AU  - Wei, Hong-Jian 
                AU  - Lu, Jui-Hua 
                AU  - Mao, Samantha 
                AU  - Liang, Joy 
                AU  - Liang, Yu-Hsuan 
                AU  - Cheng, Hsin-Chung 
                AU  - Deng, Win-Ping 
                TI  - Modulating redox homeostasis and cellular reprogramming through inhibited methylenetetrahydrofolate dehydrogenase 2 enzymatic activities in lung cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103471
                DO  - 10.18632/aging.103471
                SP  - 17930
                EP  - 17947
                PY  - 
                AB  - Recent reports have indicated the role of highly expressed methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) enzyme in cancers, showing poor survival; however, detailed mechanistic insight of metabolic functions of MTHFD2 have not been well-defined. Therefore, we aimed to examine the metabolic functions and cellular reprograming potential of MTHFD2 in lung cancer (LCa). In this study, we initially confirmed the expression levels of MTHFD2 in LCa not only in tissue and OncomineTM database, but also at molecular levels. Further, we reprogrammed metabolic activities in these cells through MTHFD2 gene knockdown via lentiviral transduction, and assessed their viability, transformation and self-renewal ability. In vivo tumorigenicity was also evaluated in NOD/SCID mice. Results showed that MTHFD2 was highly expressed in stage-dependent LCa tissues as well in cell lines, A549, H1299 and H441. Cellular viability, transformation and self-renewal abilities were significantly inhibited in MTHFD2-knockdown LCa cell lines. These cells also showed suppressed tumor-initiating ability and reduced tumor size compared to vector controls. Under low oxygen tension, MTHFD2-knockdown groups showed no significant increase in sphere formation, and hence the stemness. Conclusively, the suppressed levels of MTHFD2 is essential for cellular metabolic reprogramming leading to inhibited LCa growth and tumor aggressiveness.
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Constructing a global transcriptional regulatory landscape for early non-small cell lung cancer to identify hub genes and key pathways

Jianlong Bu, Pinyi Zhang, Kaibin Zhu, Yubo Yan, Bowen Shi, Junfeng Wang, Shidong Xu,

https://doi.org/10.18632/aging.103475 pp 17948—17957

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Bu J, Zhang P, Zhu K, Yan Y, Shi B, Wang J, Xu S, . Constructing a global transcriptional regulatory landscape for early non-small cell lung cancer to identify hub genes and key pathways. . 12:17948-17957. https://doi.org/10.18632/aging.103475

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                TY  - JOUR
                AU  - Bu, Jianlong 
                AU  - Zhang, Pinyi 
                AU  - Zhu, Kaibin 
                AU  - Yan, Yubo 
                AU  - Shi, Bowen 
                AU  - Wang, Junfeng 
                AU  - Xu, Shidong 
                TI  - Constructing a global transcriptional regulatory landscape for early non-small cell lung cancer to identify hub genes and key pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103475
                DO  - 10.18632/aging.103475
                SP  - 17948
                EP  - 17957
                PY  - 
                AB  - This study aimed to investigate the potential pathogenesis of early non-small cell lung cancer (NSCLC), including lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC), by constructing a global transcriptional regulatory landscape to identify hub genes and key pathways. A total of 1,206 differentially expressed genes (DEGs) in early NSCLC were identified compared to normal lung tissue samples in GSE33532 and GSE29013. DEGs-related protein-protein interaction networks (PPIs) were constructed based on the STRING database and were then modularly analyzed using the ClusterOne tool. The enrichment analysis revealed that multiple modules were significantly involved in pathways such as the TNF signaling pathway, PPAR signaling pathway and PI3K/AKt signaling pathway. Ten genes were identified as hub genes in the PPIs and also found up-regulated at protein level. The prognostic value of the hub genes and the ten hub gene set variation score varied according to the different pathological types of NSCLC, which suggested the ten hub gene expression patterns can reflect the heterogeneity of two types of NSCLC. In conclusion, by carrying out a series of in-depth analyses, hub genes and key pathways associated with early NSCLC were identified by a global transcriptional regulatory landscape.
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Prognostic landscape of tumor-infiltrating immune cells and immune-related genes in the tumor microenvironment of gastric cancer

Shichao Zhang, Zhu Zeng, Yongfen Liu, Jiangtao Huang, Jinhua Long, Yun Wang, Xiaoyan Peng, Zuquan Hu, Yan Ouyang,

https://doi.org/10.18632/aging.103519 pp 17958—17975

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Zhang S, Zeng Z, Liu Y, Huang J, Long J, Wang Y, Peng X, Hu Z, Ouyang Y, . Prognostic landscape of tumor-infiltrating immune cells and immune-related genes in the tumor microenvironment of gastric cancer. . 12:17958-17975. https://doi.org/10.18632/aging.103519

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                TY  - JOUR
                AU  - Zhang, Shichao 
                AU  - Zeng, Zhu 
                AU  - Liu, Yongfen 
                AU  - Huang, Jiangtao 
                AU  - Long, Jinhua 
                AU  - Wang, Yun 
                AU  - Peng, Xiaoyan 
                AU  - Hu, Zuquan 
                AU  - Ouyang, Yan 
                TI  - Prognostic landscape of tumor-infiltrating immune cells and immune-related genes in the tumor microenvironment of gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103519
                DO  - 10.18632/aging.103519
                SP  - 17958
                EP  - 17975
                PY  - 
                AB  - The tumor microenvironment is closely related to the progression and immune escape of tumor cells. Tumor-infiltrating immune cells (TIICs) and immune-related genes (IRGs) are indispensable components of the tumor microenvironment and have been demonstrated to be highly valuable in determining the prognosis of multiple cancers. To elucidate the prognostic value of TIICs and IRGs in gastric cancer, we conducted a comprehensive analysis focusing on the abundances of 22 types of TIICs and differentially expressed IRGs based on a dataset from The Cancer Genome Atlas (TCGA). The results showed that great composition differences in TIICs and immune cell subfractions were associated with survival outcomes in different stages. Additionally, 29 hub genes were characterized from 345 differentially expressed IRGs and found to be significantly associated with survival outcomes. Then, an independent prognostic indicator based on ten IRGs was successfully constructed after multivariate adjustment for some clinical parameters. Further validation revealed that these hub IRGs could reflect the infiltration levels of immune cells. Thus, our results confirmed the clinical significance of TIICs and IRGs in gastric cancer and may establish a foundation for further exploring immune cell and gene targets for personalized treatment.
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Prothrombotic effects of high uric acid in mice via activation of MEF2C-dependent NF-κB pathway by upregulating let-7c

Xiaoyu Cheng, Tian Liu, Lidan Ma, Zhen Liu, Ying Xin, Zhaotong Jia, Ying Chen, Changgui Li, Ruixia Sun,

https://doi.org/10.18632/aging.103540 pp 17976—17989

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Cheng X, Liu T, Ma L, Liu Z, Xin Y, Jia Z, Chen Y, Li C, Sun R, . Prothrombotic effects of high uric acid in mice via activation of MEF2C-dependent NF-κB pathway by upregulating let-7c. . 12:17976-17989. https://doi.org/10.18632/aging.103540

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 TY - JOUR
 AU - Cheng, Xiaoyu 
 AU - Liu, Tian 
 AU - Ma, Lidan 
 AU - Liu, Zhen 
 AU - Xin, Ying 
 AU - Jia, Zhaotong 
 AU - Chen, Ying 
 AU - Li, Changgui 
 AU - Sun, Ruixia 
 TI - Prothrombotic effects of high uric acid in mice via activation of MEF2C-dependent NF-κB pathway by upregulating let-7c
 JO - 
 JA - 
 VL - 12
 IS - 18
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103540
 DO - 10.18632/aging.103540
 SP - 17976
 EP - 17989
 PY - 
 AB - Serum uric acid is reportedly associated with thrombosis development. However, still unclear is the mechanism of high uric acid in thrombosis with the involvement of let-7c. In an aim to fill this void, we conducted this study by treating mice and human umbilical vein endothelial cells with high uric acid. Analysis indicated that let-7c was upregulated in hyperuricemia patients as well as in mice and human umbilical vein endothelial cells treated with high uric acid. Furthermore, high uric acid inhibited myocyte enhancer factor-2C, but activated nuclear factor-kappa B pathway in human umbilical vein endothelial cells. Then the targeting relationship between let-7c and myocyte enhancer factor-2C was verified. On the one hand, high uric acid shortened activated partial thromboplastin time and prothrombin time of mice and declined tissue plasminogen activator level. Additionally, the treatment prolonged thrombin time and elevated the levels of thrombosis related molecules or proteins such as Fibrinogen and D-dimer. Nevertheless, these alternations could be reversed by inhibition of let-7c and nuclear factor-kappa B pathway or overexpressing myocyte enhancer factor-2C. To sum up, our results uncovered the pro-thrombotic effect of high uric acid in mice by activating myocyte enhancer factor-2C-dependent nuclear factor-kappa B pathway via let-7c upregulation.
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SIRT1 activation by minocycline on regulation of microglial polarization homeostasis

Ling-Hsuan Wu, Bor-Ren Huang, Sheng-Wei Lai, Chingju Lin, Hsiao-Yun Lin, Liang-Yo Yang, Dah-Yuu Lu,

https://doi.org/10.18632/aging.103542 pp 17990—18007

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Wu L, Huang B, Lai S, Lin C, Lin H, Yang L, Lu D, . SIRT1 activation by minocycline on regulation of microglial polarization homeostasis. . 12:17990-18007. https://doi.org/10.18632/aging.103542

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                TY  - JOUR
                AU  - Wu, Ling-Hsuan 
                AU  - Huang, Bor-Ren 
                AU  - Lai, Sheng-Wei 
                AU  - Lin, Chingju 
                AU  - Lin, Hsiao-Yun 
                AU  - Yang, Liang-Yo 
                AU  - Lu, Dah-Yuu 
                TI  - SIRT1 activation by minocycline on regulation of microglial polarization homeostasis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103542
                DO  - 10.18632/aging.103542
                SP  - 17990
                EP  - 18007
                PY  - 
                AB  - Sirtuin 1 (SIRT1) has been reported to be involved in the mechanisms underlying longevity and has also been indicated as a valuable regulator of age-related neurological disorders. Some natural products increase SIRT1 activity and stimulate deacetylation of various proteins. In the present study, SIRT1 overexpression by genetic modification or treatment with SIRT1 activators significantly inhibited the secretion of nitric oxide and expression of inducible nitric oxide synthase, cyclooxygenase 2, and proinflammatory mediator&#x2014;interleukin 1&#x3B2;&#x2014;in microglia. SIRT1 activation also decreased the levels of K379 acetyl-p53 and the protein inhibitor of activated Stat 1 expression in microglial cells. In addition, it dramatically promoted M2 polarization of microglia, which enhanced cell motility and altered phagocytic ability. We also used minocycline, a well-known inhibitor of microglial activation, to study the mechanism of SIRT1 signaling. Minocycline treatment decreased neuroinflammatory responses and promoted M2 polarization of microglia. It also reduced the acetyl-p53 level in the brain tissues in an inflammatory mouse model. Our findings demonstrated that SIRT1 participates in the maintenance of microglial polarization homeostasis and that minocycline exerts regulatory effects on SIRT1 activation. Therefore, our results indicate that SIRT1 activation may be a useful therapeutic target for the treatment of neuroinflammation-associated disorders.
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Pre-incubation with human umbilical cord derived mesenchymal stem cells-exosomes prevents cisplatin-induced renal tubular epithelial cell injury

Zongying Li, Shuyi Cao,

https://doi.org/10.18632/aging.103545 pp 18008—18018

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Li Z, Cao S, . Pre-incubation with human umbilical cord derived mesenchymal stem cells-exosomes prevents cisplatin-induced renal tubular epithelial cell injury. . 12:18008-18018. https://doi.org/10.18632/aging.103545

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                TY  - JOUR
                AU  - Li, Zongying 
                AU  - Cao, Shuyi 
                TI  - Pre-incubation with human umbilical cord derived mesenchymal stem cells-exosomes prevents cisplatin-induced renal tubular epithelial cell injury
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103545
                DO  - 10.18632/aging.103545
                SP  - 18008
                EP  - 18018
                PY  - 
                AB  - Purpose: The administration of cisplatin is limited due to its nephrotoxicity, and prevention of this nephrotoxicity of cisplatin is difficult. Mesenchymal stem cell (MSC)-derived exosomes have been implicated as a novel therapeutic approach for tissue injury.
                Results: In vitro, the NRK cells pre-incubated with HUMSC-exosomes increased the Cp-inhibited cell viability, proliferation activity, and the cell proportion in G1-phase and inhibited Cp-induced cell apoptosis. Furthermore, the expression levels of apoptotic marker proteins Bim, Bad, Bax, cleaved caspase-3, and cleaved caspase-9 induced by Cp in the NRK cells were decreased by pre-incubating with HUMSC-exosomes.
                Conclusion: Our findings indicated that the exosomes from HUMSCs can effectively increase the survival rate and inhibit cell apoptosis of NRK cells. Therefore, pre-treatment of HUMSC-exosomes may be a new method to improve the therapeutic effect of cisplatin.
                Patients and methods: Exosomes were isolated from human umbilical cord derived mesenchymal stem cells (HUMSCs). Co-culture of normal rat renal tubular epithelial cells (NRK) and the absorption of exogenous exosomes by NRK cells were examined in vitro. Then the NRK cells were incubated with exosomes from HUMSCs and cisplatin (Cp). Cells were harvested for MTT assay, cloning formation, flow cytometry, and Western blot.
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Long non-coding RNA AGAP2-AS1 increases the invasiveness of papillary thyroid cancer

Liang Shao, Wei Sun, Hao Zhang, Ping Zhang, Zhihong Wang, Wenwu Dong, Liang He, Ting Zhang, Yuan Qin,

https://doi.org/10.18632/aging.103570 pp 18019—18032

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Shao L, Sun W, Zhang H, Zhang P, Wang Z, Dong W, He L, Zhang T, Qin Y, . Long non-coding RNA AGAP2-AS1 increases the invasiveness of papillary thyroid cancer. . 12:18019-18032. https://doi.org/10.18632/aging.103570

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 TY - JOUR
 AU - Shao, Liang 
 AU - Sun, Wei 
 AU - Zhang, Hao 
 AU - Zhang, Ping 
 AU - Wang, Zhihong 
 AU - Dong, Wenwu 
 AU - He, Liang 
 AU - Zhang, Ting 
 AU - Qin, Yuan 
 TI - Long non-coding RNA AGAP2-AS1 increases the invasiveness of papillary thyroid cancer
 JO - 
 JA - 
 VL - 12
 IS - 18
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103570
 DO - 10.18632/aging.103570
 SP - 18019
 EP - 18032
 PY - 
 AB - Papillary thyroid cancer (PTC) is considered a low hazard endocrine system cancer, but a considerable number of patients have poor prognosis because of lymph node metastasis and invasion of surrounding tissues. In this study, we analyzed the expression and function of the long non-coding RNA (lncRNA) AGAP2-AS1 in PTC. We found that AGAP2-AS1 expression was significantly higher in human PTC tissues than adjacent noncancerous tissues (n=110; p&lt;0.01) and correlated with lymph node metastasis (p=0.01) and tumor-node-metastasis stage (p=0.006). AGAP2-AS1 downregulation decreased migration and invasion by PTC cells, and reduced expression of matrix metalloproteinase-2 (MMP2). AGAP2-AS1 upregulated MMP2 expression by competitively binding to microRNA-425-5p. In addition, miR-424-5p expression was decreased in PTC tissues and correlates negatively with the AGAP2-AS1 levels. These results demonstrate that AGAP2-AS1 expression is significantly elevated in PTC tissues and that, by binding to miRNA-425-5p, it upregulates the MMP2 expression, thereby increasing the invasiveness and migration capacity of PTC cells.
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Insulin sensitivity in long-lived growth hormone-releasing hormone knockout mice

Fang Zhang, Mert Icyuz, Zhenghui Liu, Michael Fitch, Liou Y. Sun,

https://doi.org/10.18632/aging.103588 pp 18033—18051

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Zhang F, Icyuz M, Liu Z, Fitch M, Sun LY, . Insulin sensitivity in long-lived growth hormone-releasing hormone knockout mice. . 12:18033-18051. https://doi.org/10.18632/aging.103588

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                TY  - JOUR
                AU  - Zhang, Fang 
                AU  - Icyuz, Mert 
                AU  - Liu, Zhenghui 
                AU  - Fitch, Michael 
                AU  - Sun, Liou Y. 
                TI  - Insulin sensitivity in long-lived growth hormone-releasing hormone knockout mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103588
                DO  - 10.18632/aging.103588
                SP  - 18033
                EP  - 18051
                PY  - 
                AB  - Our previous studies showed that loss-of-function mutation of growth hormone releasing hormone (GHRH) results in increased longevity and enhanced insulin sensitivity in mice. However, the details of improved insulin action and tissue-specific insulin signaling are largely unknown in this healthy-aging mouse model. We conducted hyperinsulinemic-euglycemic clamp to investigate mechanisms underlying enhanced insulin sensitivity in growth hormone (GH) deficient mice. Further, we assessed in vivo tissue-specific insulin activity via activation of PI3K-AKT and MAPK-ERK1/2 cascades using western blot. Clamp results showed that the glucose infusion rate required for maintaining euglycemia was much higher in GHRH-/- mice compared to WT controls. Insulin-mediated glucose production was largely suppressed, whereas glucose uptake in skeletal muscle and brown adipose tissue were significant enhanced in GHRH-/- mice compared to WT controls. Enhanced capacity of insulin-induced activation of the PI3K-AKT and MAPK-ERK1/2 signaling were observed in a tissue-specific manner in GHRH-/- mice. Enhanced systemic insulin sensitivity in long-lived GHRH-/- mice is associated with differential activation of insulin signaling cascades among various organs. Improved action of insulin in the insulin sensitive tissues is likely to mediate the prolonged longevity and healthy-aging effects of GH deficiency in mice.
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Caloric restriction alleviates aging-related fibrosis of kidney through downregulation of miR-21 in extracellular vesicles

Jin-rui Liu, Guang-yan Cai, Yi-chun Ning, Jing-chao Wang, Yang Lv, Ya-nan Guo, Bo Fu, Quan Hong, Xue-feng Sun, Xiang-mei Chen,

https://doi.org/10.18632/aging.103591 pp 18052—18072

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Liu J, Cai G, Ning Y, Wang J, Lv Y, Guo Y, Fu B, Hong Q, Sun X, Chen X, . Caloric restriction alleviates aging-related fibrosis of kidney through downregulation of miR-21 in extracellular vesicles. . 12:18052-18072. https://doi.org/10.18632/aging.103591

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                TY  - JOUR
                AU  - Liu, Jin-rui 
                AU  - Cai, Guang-yan 
                AU  - Ning, Yi-chun 
                AU  - Wang, Jing-chao 
                AU  - Lv, Yang 
                AU  - Guo, Ya-nan 
                AU  - Fu, Bo 
                AU  - Hong, Quan 
                AU  - Sun, Xue-feng 
                AU  - Chen, Xiang-mei 
                TI  - Caloric restriction alleviates aging-related fibrosis of kidney through downregulation of miR-21 in extracellular vesicles
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103591
                DO  - 10.18632/aging.103591
                SP  - 18052
                EP  - 18072
                PY  - 
                AB  - Glomerulosclerosis and renal interstitial fibrosis occur with the aging kidney. In this study, we examined the expression of miR-21, peroxisome proliferator-activated receptor(PPAR&#x3B1;), hypoxia-inducible factor(HIF-1&#x3B1;) in the kidney of 3-month-old rats fed ad libitum (YAL), 24-month-old rats fed ad libitum (OAL) and 24-month-old rats subjected to a 70% calorie-restricted diet for 8 months (OCR). We found long-term caloric restriction (CR) ameliorated aging and aging-related fibrosis. CR ameliorated the increment of miR-21 and HIF-1&#x3B1;, as well as the decrement of PPAR&#x3B1; in old ad libitum group. Human proximal tubular cells (HPTCs) presented phenotypes of senescence and epithelial to mesenchymal transition (EMT) under high-glucose conditions, in which senescence occurred earlier than EMT. Senescent cells secreted extracellular vesicles (EVs) which contained miR-21 into the recipient cells. Inhibiting miR-21 of donor cells prevented the occurrence of EMT in recipient cells. In addition, miR-21 induced EMT through targeting PPAR&#x3B1; protein and consequently enhancing HIF-1&#x3B1; expression, although other pathways cannot be ruled out. These findings demonstrated that miR-21-containing EVs derived from the senescent cells could facilitate EMT of HPTCs via PPAR&#x3B1;-HIF-1&#x3B1; signaling pathway. Long-term caloric restriction and caloric restriction mimetics alleviated aging-related-fibrosis of kidney through downregulation of miR-21.
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MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis

Xiang Li, Ying Wang, Yijiang Wang, Xingbo He,

https://doi.org/10.18632/aging.103608 pp 18073—18083

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Li X, Wang Y, Wang Y, He X, . MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis. . 12:18073-18083. https://doi.org/10.18632/aging.103608

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                TY  - JOUR
                AU  - Li, Xiang 
                AU  - Wang, Ying 
                AU  - Wang, Yijiang 
                AU  - He, Xingbo 
                TI  - MiR-141-3p ameliorates RIPK1-mediated necroptosis of intestinal epithelial cells in necrotizing enterocolitis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103608
                DO  - 10.18632/aging.103608
                SP  - 18073
                EP  - 18083
                PY  - 
                AB  - Aim: To explore the effects of miR-141-3p on intestinal epithelial cells in necrotizing enterocolitis and the underlying mechanism.
Results: The expression of miR-141-3p was significantly downregulated in serum samples of patients with NEC and LPS-treated Caco-2 cells. The in vitro assays showed that miR-141-3p mimics inhibited expression of IL-6 and TNF-&#x3B1; and reduced PI positive rate of the LPS-treated Caco-2 cells. Next, receptor interacting protein kinase 1 (RIPK1) was identified as the downstream molecule of miR-141-3p, and RIPK1 overexpression aggravated LPS-induced Caco-2 cell injury, which was ameliorated by miR-141-3p mimics. Finally, we found miR-141-3p mimics inhibited upregulation of necroptosis-related molecules and interaction of RIPK1 and RIPK3 in LPS-treated Caco-2 cells.
Conclusion: Our research indicated that miR-141-3p protected intestinal epithelial cells from LPS damage by suppressing RIPK1-mediated inflammation and necroptosis, providing an alternative perspective to explore the pathogenesis of NEC.
Methods: Quantitative real time-polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-141-3p in serum samples of participants and lipopolysaccharide (LPS)-treated Caco-2 cells. Cell Counting Kit-8 (CCK-8) assay, Propidium Iodide (PI) staining and detection of inflammatory cytokines were performed to evaluate the role of miR-141-3p in LPS-treated Caco-2 cells. TargetScanHuman database and luciferase reporter gene assay were utilized to confirm the direct downstream molecule of miR-141-3p. Western blot analysis was used to explore the mechanism.
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RAI14 silencing suppresses progression of esophageal cancer via the STAT3 pathway

Jianlin Wang, Yun Cai, Judong Luo, Zhiqiang Sun, Jingping Yu, Feng Yan, Xia He,

https://doi.org/10.18632/aging.103613 pp 18084—18098

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Wang J, Cai Y, Luo J, Sun Z, Yu J, Yan F, He X, . RAI14 silencing suppresses progression of esophageal cancer via the STAT3 pathway. . 12:18084-18098. https://doi.org/10.18632/aging.103613

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                TY  - JOUR
                AU  - Wang, Jianlin 
                AU  - Cai, Yun 
                AU  - Luo, Judong 
                AU  - Sun, Zhiqiang 
                AU  - Yu, Jingping 
                AU  - Yan, Feng 
                AU  - He, Xia 
                TI  - RAI14 silencing suppresses progression of esophageal cancer via the STAT3 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103613
                DO  - 10.18632/aging.103613
                SP  - 18084
                EP  - 18098
                PY  - 
                AB  - Esophageal cancer (EC) is an aggressive malignancy that has an unclear molecular pathogenesis. Although retinoic acid induced 14 (RAI14) is involved in various cancer processes, the relationship between EC and RAI14 has not been elucidated. Our study reported the oncogenic function of RAI14 and its underlying mechanisms in EC. The Cancer Genome Atlas (TCGA) database revealed that RAI14 was upregulated in EC, and this upregulation correlated with T stage, histologic grade, and poor clinical prognosis. RAI14 was evaluated in EC cell lines, and the overexpression of RAI14 promoted cell proliferation, migration, and invasion in vitro. Conversely, RAI14 knockdown induced apoptosis and cell cycle arrest. RAI14 activated STAT3, upregulated Mcl-1 and cyclin D1, and inhibited cleaved caspase-3. Inhibition of STAT3 restored the oncogenic effect of RAI14, and RAI14 silencing restrained tumor growth and the protein level of Ki67 in vivo. Our results suggest that RAI14 regulates the STAT3 pathway and acts as an oncogene during EC progression.
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Early-life exposure to bisphenol A and reproductive-related outcomes in rodent models: a systematic review and meta-analysis

Xiaohan Ren, Tongtong Zhang, Xinglin Chen, Xiyi Wei, Ye Tian, Guangyao Li, Xu Zhang, Wei Zhang, Zebing You, Shangqian Wang, Chao Qin,

https://doi.org/10.18632/aging.103620 pp 18099—18126

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Ren X, Zhang T, Chen X, Wei X, Tian Y, Li G, Zhang X, Zhang W, You Z, Wang S, Qin C, . Early-life exposure to bisphenol A and reproductive-related outcomes in rodent models: a systematic review and meta-analysis. . 12:18099-18126. https://doi.org/10.18632/aging.103620

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                TY  - JOUR
                AU  - Ren, Xiaohan 
                AU  - Zhang, Tongtong 
                AU  - Chen, Xinglin 
                AU  - Wei, Xiyi 
                AU  - Tian, Ye 
                AU  - Li, Guangyao 
                AU  - Zhang, Xu 
                AU  - Zhang, Wei 
                AU  - You, Zebing 
                AU  - Wang, Shangqian 
                AU  - Qin, Chao 
                TI  - Early-life exposure to bisphenol A and reproductive-related outcomes in rodent models: a systematic review and meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103620
                DO  - 10.18632/aging.103620
                SP  - 18099
                EP  - 18126
                PY  - 
                AB  - We performed this meta-analysis to elucidate the associations between early-life BPA exposure and reproductive-related outcome indicators. The standardized mean differences (SMDs) and its 95% confidence intervals (CIs) were measured by fixed-effects or random-effects models. The results revealed that BPA exposure at extremely-high dose (&gt;50mg/kg/day) was significantly associated with negative reproductive-related outcomes (Prostate weight: SMD: -4.21; 95% Cl: -5.97, -2.44; Testis weight: SMD: -1.92; 95% Cl: -2.61, -1.23; Epididymis weight: SMD: -2.16; 95% Cl: -3.47, -0.86; Daily sperm production; SMD: -1.90; 95% Cl: -3.27, -0.53; Epididymal sperm count; SMD: -3.42; 95% Cl: -3.87, -2.97). Meanwhile, regardless of the dose, early-life BPA exposure could result in an adverse effect on sperm parameters of F1 generation male rodents at any period. Also, we found the non-monotonic dose response curves of BPA in specific tissues or organs, which may challenge the traditional mindset of &quot;safe dose&quot;. This study demonstrated that bisphenol A exposure was relevant to adverse reproductive-related outcomes at specially appointed dose and period of life. Yet the assumption that no adverse effects can occur below the &quot;safe&quot; dose is suspected.
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GHR knockdown enhances the sensitivity of HCC cells to sorafenib

Shuang Gao, Qianwen Ni, Xiuli Wu, Tieliu Cao,

https://doi.org/10.18632/aging.103625 pp 18127—18136

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Gao S, Ni Q, Wu X, Cao T, . GHR knockdown enhances the sensitivity of HCC cells to sorafenib. . 12:18127-18136. https://doi.org/10.18632/aging.103625

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                TY  - JOUR
                AU  - Gao, Shuang 
                AU  - Ni, Qianwen 
                AU  - Wu, Xiuli 
                AU  - Cao, Tieliu 
                TI  - GHR knockdown enhances the sensitivity of HCC cells to sorafenib
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103625
                DO  - 10.18632/aging.103625
                SP  - 18127
                EP  - 18136
                PY  - 
                AB  - Sorafenib is approved for treatment of advanced hepatocellular carcinoma (HCC) by the Drug Administration. However, the efficacy of sorafenib has become very limited because most tumors have developed resistance to this drug. In this study, we found that sorafenib stimulated GHR expression in HCC cell lines. Thus, GHR might be linked to sorafenib resistance. To verify this hypothesis, we researched the roles of GHR knockdown and sorafenib combination in cell viability, apoptosis, cycle, and migration. The results showed that GHR blockage enhanced sorafenib blocking of cell cycle progression, leading to inhibition of this drug on HCC cell viability, and the improved promoting ability of sorafenib on cell apoptosis. In addition, it was found that GHR knockdown enhanced sorafenib inhibition of cell migration. The synergistic antitumor effects of sorafenib and GHR knockdown combination may be attributed to inhibition of PI3K/AKT/ERK1/2 signaling pathway. In conclusion, the findings suggest that GHR knockdown enhances the sensitivity of HCC cells to sorafenib. and the inactivation of PI3K/AKT/ERK1/2 signaling pathway may be the underlying mechanisms. This highlights the absence of GHR as a promising way to enhance sorafenib efficacy in HCC.
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The clinicopathological characteristics and genetic alterations between younger and older gastric cancer patients with curative surgery

Chew-Wun Wu, Ming-Huang Chen, Kuo-Hung Huang, Shih-Ching Chang, Wen-Liang Fang, Chien-Hsing Lin, Yee Chao, Su-Shun Lo, Anna Fen-Yau Li, Yi-Ming Shyr,

https://doi.org/10.18632/aging.103627 pp 18137—18150

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Wu C, Chen M, Huang K, Chang S, Fang W, Lin C, Chao Y, Lo S, Li AF, Shyr Y, . The clinicopathological characteristics and genetic alterations between younger and older gastric cancer patients with curative surgery. . 12:18137-18150. https://doi.org/10.18632/aging.103627

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                TY  - JOUR
                AU  - Wu, Chew-Wun 
                AU  - Chen, Ming-Huang 
                AU  - Huang, Kuo-Hung 
                AU  - Chang, Shih-Ching 
                AU  - Fang, Wen-Liang 
                AU  - Lin, Chien-Hsing 
                AU  - Chao, Yee 
                AU  - Lo, Su-Shun 
                AU  - Li, Anna Fen-Yau 
                AU  - Shyr, Yi-Ming 
                TI  - The clinicopathological characteristics and genetic alterations between younger and older gastric cancer patients with curative surgery
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103627
                DO  - 10.18632/aging.103627
                SP  - 18137
                EP  - 18150
                PY  - 
                AB  - Few reports have investigated different genetic alterations according to age in various cancers. In total, 1749 GC patients receiving curative surgery were enrolled. The clinicopathological features, and prognoses were compared between younger (&lt;65 years) and older (&#x2265;65 years) patients. Genetic mutations were analyzed using mass spectrometric single nucleotide polymorphism genotyping technology, including 68 validated mutations within eight genes (TP53, ARID1A, BRAF, and the PI3K/AKT pathway) previously reported in relation to age. Younger patients were more likely to be female and have poor cell differentiation, diffuse-type tumors, less lymphovascular invasion, fewer liver metastases, and better 5-year overall survival (OS) (68.0% vs. 54.6%, P&lt;0.001) and disease-free survival (DFS) (65.4% vs. 53.0%, P&lt;0.001) rates than older patients. Regarding the genetic alterations, older patients had more microsatellite instability-high (MSI-H) tumors and more ARID1A mutations than younger patients. Younger patients had significantly better OS and DFS rates than older patients for each pathological Tumor, Node, Metastasis (TNM) stage. Older patients had a significantly higher non-cancer related death rate than younger patients (36.2% vs. 12.3%, P&lt;0.001). Age was an independent prognostic factor in GC. In conclusion, age was associated with different clinicopathological features and genetic alterations in GC with curative surgery.
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Distant metastasis prediction via a multi-feature fusion model in breast cancer

Wenjuan Ma, Xin Wang, Guijun Xu, Zheng Liu, Zhuming Yin, Yao Xu, Haixiao Wu, Vladimir P. Baklaushev, Karl Peltzer, Henian Sun, Natalia V. Kharchenko, Lisha Qi, Min Mao, Yanbo Li, Peifang Liu, Vladimir P. Chekhonin, Chao Zhang,

https://doi.org/10.18632/aging.103630 pp 18151—18162

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Ma W, Wang X, Xu G, Liu Z, Yin Z, Xu Y, Wu H, Baklaushev VP, Peltzer K, Sun H, Kharchenko NV, Qi L, Mao M, et al, . Distant metastasis prediction via a multi-feature fusion model in breast cancer. . 12:18151-18162. https://doi.org/10.18632/aging.103630

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                TY  - JOUR
                AU  - Ma, Wenjuan 
                AU  - Wang, Xin 
                AU  - Xu, Guijun 
                AU  - Liu, Zheng 
                AU  - Yin, Zhuming 
                AU  - Xu, Yao 
                AU  - Wu, Haixiao 
                AU  - Baklaushev, Vladimir P. 
                AU  - Peltzer, Karl 
                AU  - Sun, Henian 
                AU  - Kharchenko, Natalia V. 
                AU  - Qi, Lisha 
                AU  - Mao, Min 
                AU  - Li, Yanbo 
                AU  - Liu, Peifang 
                AU  - Chekhonin, Vladimir P. 
                AU  - Zhang, Chao 
                TI  - Distant metastasis prediction via a multi-feature fusion model in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103630
                DO  - 10.18632/aging.103630
                SP  - 18151
                EP  - 18162
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ma, Wenjuan 
                AU  - Wang, Xin 
                AU  - Xu, Guijun 
                AU  - Liu, Zheng 
                AU  - Yin, Zhuming 
                AU  - Xu, Yao 
                AU  - Wu, Haixiao 
                AU  - Baklaushev, Vladimir P. 
                AU  - Peltzer, Karl 
                AU  - Sun, Henian 
                AU  - Kharchenko, Natalia V. 
                AU  - Qi, Lisha 
                AU  - Mao, Min 
                AU  - Li, Yanbo 
                AU  - Liu, Peifang 
                AU  - Chekhonin, Vladimir P. 
                AU  - Zhang, Chao 
                TI  - Distant metastasis prediction via a multi-feature fusion model in breast cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103630
                DO  - 10.18632/aging.103630
                SP  - 18151
                EP  - 18162
                PY  - 
                AB  - This study aimed to develop a model that fused multiple features (multi-feature fusion model) for predicting metachronous distant metastasis (DM) in breast cancer (BC) based on clinicopathological characteristics and magnetic resonance imaging (MRI). A nomogram based on clinicopathological features (clinicopathological-feature model) and a nomogram based on the multi-feature fusion model were constructed based on BC patients with DM (n=67) and matched patients (n=134) without DM. DM was diagnosed on average (17.31&#xB1;13.12) months after diagnosis. The clinicopathological-feature model included seven features: reproductive history, lymph node metastasis, estrogen receptor status, progesterone receptor status, CA153, CEA, and endocrine therapy. The multi-feature fusion model included the same features and an additional three MRI features (multiple masses, fat-saturated T2WI signal, and mass size). The multi-feature fusion model was relatively better at predicting DM. The sensitivity, specificity, diagnostic accuracy and AUC of the multi-feature fusion model were 0.746 (95% CI: 0.623-0.841), 0.806 (0.727-0.867), 0.786 (0.723-0.841), and 0.854 (0.798-0.911), respectively. Both internal and external validations suggested good generalizability of the multi-feature fusion model to the clinic. The incorporation of MRI factors significantly improved the specificity and sensitivity of the nomogram. The constructed multi-feature fusion nomogram may guide DM screening and the implementation of prophylactic treatment for BC.
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Bioinformatics analysis of the clinical value and potential mechanisms of AHNAK2 in papillary thyroid carcinoma

Zhenyu Xie, Yu Lun, Xin Li, Yuzhen He, Song Wu, Shiyue Wang, Jianjian Sun, Yuchen He, Jian Zhang,

https://doi.org/10.18632/aging.103645 pp 18163—18180

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Xie Z, Lun Y, Li X, He Y, Wu S, Wang S, Sun J, He Y, Zhang J, . Bioinformatics analysis of the clinical value and potential mechanisms of AHNAK2 in papillary thyroid carcinoma. . 12:18163-18180. https://doi.org/10.18632/aging.103645

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                TY  - JOUR
                AU  - Xie, Zhenyu 
                AU  - Lun, Yu 
                AU  - Li, Xin 
                AU  - He, Yuzhen 
                AU  - Wu, Song 
                AU  - Wang, Shiyue 
                AU  - Sun, Jianjian 
                AU  - He, Yuchen 
                AU  - Zhang, Jian 
                TI  - Bioinformatics analysis of the clinical value and potential mechanisms of AHNAK2 in papillary thyroid carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103645
                DO  - 10.18632/aging.103645
                SP  - 18163
                EP  - 18180
                PY  - 
                AB  - Background: AHNAK2 has been recently reported as a biomarker in many cancers. However, a systematic investigation of AHNAK2 in papillary thyroid carcinoma (PTC) has not been conducted.Results: AHNAK2 is overexpressed in PTC tissues and could be an independent prognostic factor. AHNAK2 expression was significantly high in patients with advanced stage, advanced T classification, lymph node metastasis, increased BRAF mutations and decreased RAS mutations. Cell adhesion-, cell junction-, and immune-related pathways were the most frequently noted in gene set enrichment analysis. AHNAK2 expression in PTC was positively correlated with immune infiltration and negatively correlated with AHNAK2 methylation. AHNAK2 expression was significantly positively correlated with tumor progression and poor overall survival (OS) in pan-cancer patients.Conclusions: AHNAK2 is a good biomarker for the diagnosis and prognosis of PTC. AHNAK2 may promote thyroid cancer progression through cell adhesion-, cell junction-, and immune-related pathways. Methylation may act as an upstream regulator to inhibit the expression and biological function of AHNAK2. Additionally, AHNAK2 has broad prognostic value in pan-cancer.Methods: Based on The Cancer Genome Atlas (TCGA) data, we screened AHNAK2-related genes through weighted gene coexpression network analysis and explored the clinical value and the potential mechanism of AHNAK2 in PTC by multiomics analysis.
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NLRP3 activation in endothelia promotes development of diabetes-associated atherosclerosis

Dong Huang, Wei Gao, Xin Zhong, Junbo Ge,

https://doi.org/10.18632/aging.103666 pp 18181—18191

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Huang D, Gao W, Zhong X, Ge J, . NLRP3 activation in endothelia promotes development of diabetes-associated atherosclerosis. . 12:18181-18191. https://doi.org/10.18632/aging.103666

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                TY  - JOUR
                AU  - Huang, Dong 
                AU  - Gao, Wei 
                AU  - Zhong, Xin 
                AU  - Ge, Junbo 
                TI  - NLRP3 activation in endothelia promotes development of diabetes-associated atherosclerosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103666
                DO  - 10.18632/aging.103666
                SP  - 18181
                EP  - 18191
                PY  - 
                AB  - Inflammatory damage to endothelial cells plays a pivotal role in the diabetes-provoked atherosclerosis (AS). PYD domains-containing protein 3 (NLRP3) induces formation of inflammasome activates caspase-1, which subsequently cleaves the precursor form of IL-1&#x3B2; (pro-IL-1&#x3B2;) into the processed, secreted form IL-1&#x3B2; to promote the immune responses in AS. However, it is not known whether NLRP3 activation specifically in endothelial cells causes AS. Here, in an in vitro model for AS, we showed that NLRP3-depleted human aortic endothelial cells (HAECs) became resistant to apoptotic cell death, maintained proliferative potential and reduced reactive oxygen species (ROS) production upon treatment with oxidized low-density lipoprotein (ox-LDL). Next, the role of NLRP3 in endothelial cells in the development of diabetes-associated AS was assessed in endothelial cell-specific NLRP3 mutant, ApoE (-/-) mice (APOEKO/Tie2p-Cre/NLRP3MKO), compared to control ApoE (-/-) mice (APOEKO), supplied with either high-fat diet (HFD), or normal diet (ND). We found that endothelia-specific NLRP3-depletion significantly attenuated AS severity in mice treated with HFD, likely through reduced apoptotic death of endothelial cells and production of ROS. Together, our data suggest that NLRP3 activation in endothelial cells promotes development of diabetes-associated AS.
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MicroRNA-216a-3p promotes sorafenib sensitivity in hepatocellular carcinoma by downregulating MAPK14 expression

Zhong Wan, Tingyu Liu, Liang Wang, Rong Wang, Hai Zhang,

https://doi.org/10.18632/aging.103670 pp 18192—18208

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Wan Z, Liu T, Wang L, Wang R, Zhang H, . MicroRNA-216a-3p promotes sorafenib sensitivity in hepatocellular carcinoma by downregulating MAPK14 expression. . 12:18192-18208. https://doi.org/10.18632/aging.103670

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                TY  - JOUR
                AU  - Wan, Zhong 
                AU  - Liu, Tingyu 
                AU  - Wang, Liang 
                AU  - Wang, Rong 
                AU  - Zhang, Hai 
                TI  - MicroRNA-216a-3p promotes sorafenib sensitivity in hepatocellular carcinoma by downregulating MAPK14 expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103670
                DO  - 10.18632/aging.103670
                SP  - 18192
                EP  - 18208
                PY  - 
                AB  - We investigated MAPK14-dependent resistance to sorafenib in hepatocellular carcinoma (HCC). Bioinformatics analysis and dual luciferase reporter assays in HCC cell lines showed that miR-216a-3p directly binds to the 3&#x2019;UTR of MAPK14 mRNA and downregulates MAPK14 protein expression. Consequently, miR-216a-3p expression correlates inversely with MAPK14 protein levels in HCC patient tissues. miR-216a-3p overexpression significantly increases the sorafenib sensitivity of HCC cells by suppressing MAPK14 expression and reducing the subsequent activation of the MEK/ERK and ATF2 signaling pathways. The growth of xenograft tumors derived from miR-216a-3p-overexpression HCC cells was significantly diminished in sorafenib-treated Balb/c nude mice compared to controls. High miR-216a-3p levels in HCC tissue samples prior to treatment correlated with a better sorafenib response and favorable prognosis. Our findings thus demonstrate that miR-216a-3p enhances sorafenib sensitivity in HCC cells and tumor tissues by decreasing MAPK14 levels, thereby inhibiting the MAPK14-dependent MEK/ERK and ATF2 signaling.
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piR-19166 inhibits migration and metastasis through CTTN/MMPs pathway in prostate carcinoma

Tingyue Qi, Haiyan Cao, Hongguang Sun, Hao Feng, Nianfeng Li, Chenghai Wang, Lei Wang,

https://doi.org/10.18632/aging.103677 pp 18209—18220

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Qi T, Cao H, Sun H, Feng H, Li N, Wang C, Wang L, . piR-19166 inhibits migration and metastasis through CTTN/MMPs pathway in prostate carcinoma. . 12:18209-18220. https://doi.org/10.18632/aging.103677

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                TY  - JOUR
                AU  - Qi, Tingyue 
                AU  - Cao, Haiyan 
                AU  - Sun, Hongguang 
                AU  - Feng, Hao 
                AU  - Li, Nianfeng 
                AU  - Wang, Chenghai 
                AU  - Wang, Lei 
                TI  - piR-19166 inhibits migration and metastasis through CTTN/MMPs pathway in prostate carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103677
                DO  - 10.18632/aging.103677
                SP  - 18209
                EP  - 18220
                PY  - 
                AB  - Tumor metastasis is one of death causes for patients of prostate carcinoma. PIWI-interacting RNAs (piRNAs) are a subtype of noncoding protein RNAs that are involved in tumorigenesis, but the effect of piRNAs in prostate carcinoma (PCa) remains unclear. This article showed the identification of piRNAs was performed using a piRNA microarray screen in PCa tissues and several piRNAs were identified as dysregulated. The two up-regulated piRNAs (piR-19004 and piR-2878) and one down-regulated piR-19166 have been validated in the tissues and cell lines of PCa using quantitative reverse transcription polymerase chain reaction (qRT-PCR). Further studies showed that piR-19166 is transfected into PCa cells to suppress its migration and metastasis. Mechanistically, cortactin (CTTN) 3&apos; untranslated region (UTR) was complementary combined with piR-19166 by bioinformatic prediction and identified as a direct target of piR-19166 through dual-luciferase reporter assay. Over-expression and knockdown of CTTN could respectively rescue and simulate the effects induced by piR-19166. Finally, piR-19166 suppresses migration and metastasis by the CTTN/matrix metalloproteinases (MMPs) pathway in PCa cells. Thus, these findings suggested that piR-19166 targets the CTTN of prostate cancer cells to inhibit migration and distant metastasis, and may represent a new marker of diagnosis and treatment for PCa patients in early stages.
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High pulse pressure is a risk factor for prodromal Alzheimer’s disease: a longitudinal study

Wen-Yan Shi, Zuo-Teng Wang, Fu-Rong Sun, Ya-Hui Ma, Wei Xu, Xue-Ning Shen, Qiang Dong, Lan Tan, Jin-Tai Yu, Yang Yu, Alzheimer’s Disease Neuroimaging Initiative,

https://doi.org/10.18632/aging.103678 pp 18221—18237

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Shi W, Wang Z, Sun F, Ma Y, Xu W, Shen X, Dong Q, Tan L, Yu J, Yu Y, , . High pulse pressure is a risk factor for prodromal Alzheimer’s disease: a longitudinal study. . 12:18221-18237. https://doi.org/10.18632/aging.103678

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                TY  - JOUR
                AU  - Shi, Wen-Yan 
                AU  - Wang, Zuo-Teng 
                AU  - Sun, Fu-Rong 
                AU  - Ma, Ya-Hui 
                AU  - Xu, Wei 
                AU  - Shen, Xue-Ning 
                AU  - Dong, Qiang 
                AU  - Tan, Lan 
                AU  - Yu, Jin-Tai 
                AU  - Yu, Yang 
                AU  - ,  
                TI  - High pulse pressure is a risk factor for prodromal Alzheimer’s disease: a longitudinal study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103678
                DO  - 10.18632/aging.103678
                SP  - 18221
                EP  - 18237
                PY  - 
                AB  - It has been increasingly evident that pulse pressure (PP) is associated with Alzheimer&apos;s disease (AD) but whether PP increases AD risk and the mechanism responsible for this association remains unclear. To investigate the effects of PP in the process of AD, we have evaluated the cross-sectional and longitudinal associations of PP with AD biomarkers, brain structure and cognition and have assessed the effect of PP on AD risk in a large sample (n= 1,375) from the Alzheimer&#x2019;s Disease Neuroimaging Initiative (ADNI). Multiple linear regression and mixed-model regression were employed in cross-sectional and longitudinal analyses respectively. Clinical disease progression was assessed using Cox proportional hazards models. High PP was associated with lower &#x3B2;-amyloid 42 (A&#x3B2;42) (P= .015), and higher total tau (T-tau) (P= .011), phosphorylated tau (P-tau) (P= .003), T-tau/A&#x3B2;42 (P= .004) and P-tau/A&#x3B2;42 (P = .001), as well as heavier cortical amyloid-beta burden (P= .011). Longitudinally, baseline high PP was significantly associated with hippocampal atrophy (P= .039), entorhinal atrophy (P= .031) and worse memory performance (P= .058). Baseline high PP showed more rapid progression than those with normal PP (P &lt;.001). These results suggest PP elevation could increase AD risk, which may be driven by amyloid plaques and subclinical neurodegeneration.
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The mitochondrial-targeted peptide SBT-20 ameliorates inflammation and oxidative stress in chronic renal failure

Lina Sun, Haiping Xu, Yunfei Wang, Xiaoying Ma, Yan Xu, Fuyun Sun,

https://doi.org/10.18632/aging.103681 pp 18238—18250

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Sun L, Xu H, Wang Y, Ma X, Xu Y, Sun F, . The mitochondrial-targeted peptide SBT-20 ameliorates inflammation and oxidative stress in chronic renal failure. . 12:18238-18250. https://doi.org/10.18632/aging.103681

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                TY  - JOUR
                AU  - Sun, Lina 
                AU  - Xu, Haiping 
                AU  - Wang, Yunfei 
                AU  - Ma, Xiaoying 
                AU  - Xu, Yan 
                AU  - Sun, Fuyun 
                TI  - The mitochondrial-targeted peptide SBT-20 ameliorates inflammation and oxidative stress in chronic renal failure
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103681
                DO  - 10.18632/aging.103681
                SP  - 18238
                EP  - 18250
                PY  - 
                AB  - Chronic renal failure (CRF) is the final outcome of the development of chronic kidney disease with different causes. Although CRF is a common clinical disease, its pathogenesis remains to be improved. SBT-20 belongs to a class of cell-permeable peptides that target the inner mitochondrial membrane, reduce reactive oxygen species (ROS), normalize electron transport chain function, and ATP generation. Our experiment was to evaluate whether SBT-20 affected the oxidative stress and inflammatory process of CRF. The levels of ROS production, mitochondrial membrane potential, NF- &#x3BA;B-p65, TNF-&#x3B1;, Drp1, and mfn2 were measured before and after SBT-20 treatment. We observed that SBT-20 treatment inhibited H2O2-induced mitochondrial ROS production. SBT-20 could also restore the mitochondrial membrane potential and reduce the elevated levels of NF-&#x3BA;B-p65 and TNF-&#x3B1; in HK-2 cells. In vivo, the renal function of CRF mice recovered after treating with SBT-20, the levels of necrotic cells and inflammation decreased, and the morphology of mitochondria recovered. The results showed that SBT-20 had a protective effect on CRF by reducing oxidative stress, inflammation progression via down-regulating of NF-&#x3BA;B-p65, TNF-&#x3B1;, and Drp1 and upregulating of Mfn2. These data support SBT-20 could be used as a potential preparation for CRF.
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Transcriptomic analysis reveals gender differences in gene expression profiling of the hypothalamus of rhesus macaque with aging

Yong Fan, Congru Li, Wendi Pei, Tao Tan, Rong Li, Jie Qiao, Yang Yu,

https://doi.org/10.18632/aging.103682 pp 18251—18273

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Fan Y, Li C, Pei W, Tan T, Li R, Qiao J, Yu Y, . Transcriptomic analysis reveals gender differences in gene expression profiling of the hypothalamus of rhesus macaque with aging. . 12:18251-18273. https://doi.org/10.18632/aging.103682

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                TY  - JOUR
                AU  - Fan, Yong 
                AU  - Li, Congru 
                AU  - Pei, Wendi 
                AU  - Tan, Tao 
                AU  - Li, Rong 
                AU  - Qiao, Jie 
                AU  - Yu, Yang 
                TI  - Transcriptomic analysis reveals gender differences in gene expression profiling of the hypothalamus of rhesus macaque with aging
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103682
                DO  - 10.18632/aging.103682
                SP  - 18251
                EP  - 18273
                PY  - 
                AB  - Due to the current delay in childbearing, the importance of elucidating the underlying mechanisms for reproductive aging has increased. Human fertility is considered to be controlled by hormones secreted by the hypothalamic-pituitary-gonadal axis. To clarify the changes in hypothalamic gene expression with increasing age, we performed paired-end strand-specific total RNA sequencing for the hypothalamus tissues of rhesus. We found that hypothalamic gene expression in females was more susceptible to aging than that in males, and reproductive aging in females and males might have different regulatory mechanisms. Intriguingly, the expression of most of the hormones secreted by hypothalamus showed no significant difference among the macaques grouped by age and gender. Moreover, the age-related housekeeping genes in females were enriched in neurodegenerative disorders- and metabolic-related pathways. This study provides evidence that aging may influence hypothalamic gene expression through different mechanisms in females and males and may involve some nonhormonal pathways, which helps further elucidate the process of reproductive aging and improve clinical fertility assessment in mid-aged women.
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MSC-derived exosomes promote recovery from traumatic brain injury via microglia/macrophages in rat

Yunfei Chen, Jing Li, Baitao Ma, Na Li, Shihua Wang, Zhao Sun, Chunling Xue, Qin Han, Junji Wei, Robert Chunhua Zhao,

https://doi.org/10.18632/aging.103692 pp 18274—18296

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Chen Y, Li J, Ma B, Li N, Wang S, Sun Z, Xue C, Han Q, Wei J, Zhao RC, . MSC-derived exosomes promote recovery from traumatic brain injury via microglia/macrophages in rat. . 12:18274-18296. https://doi.org/10.18632/aging.103692

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Provider: 
                TY  - JOUR
                AU  - Chen, Yunfei 
                AU  - Li, Jing 
                AU  - Ma, Baitao 
                AU  - Li, Na 
                AU  - Wang, Shihua 
                AU  - Sun, Zhao 
                AU  - Xue, Chunling 
                AU  - Han, Qin 
                AU  - Wei, Junji 
                AU  - Zhao, Robert Chunhua 
                TI  - MSC-derived exosomes promote recovery from traumatic brain injury via microglia/macrophages in rat
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103692
                DO  - 10.18632/aging.103692
                SP  - 18274
                EP  - 18296
                PY  - 
                AB  - Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in young individuals worldwide. There is currently no effective clinical treatment for TBI, but mesenchymal stem cell-derived exosomes have exhibited promising therapeutic effects. In this study, we performed intracerebroventricular microinjection of human adipose mesenchymal stem cell (hADSC)-derived exosomes (hADSC-ex) in a weight-drop-induced TBI rat model. We found that hADSC-ex promoted functional recovery, suppressed neuroinflammation, reduced neuronal apoptosis, and increased neurogenesis in TBI rats. The therapeutic effects of hADSC-ex were comparable to those of hADSC. Sequential in vivo imaging revealed increasing aggregation of DiR-labeled hADSC-ex in the lesion area. Immunofluorescent staining of coronal brain sections and primary mixed neural cell cultures revealed distinct overlap between CM-DiI-labeled hADSC-ex and microglia/macrophages, indicating that hADSC-ex were mainly taken up by microglia/macrophages. In a lipopolysaccharide-induced inflammatory model, hADSC-ex suppressed microglia/macrophage activation by inhibiting nuclear factor &#x3BA;B and P38 mitogen-activated protein kinase signaling. These data suggest that hADSC-ex specifically enter microglia/macrophages and suppress their activation during brain injury, thereby inhibiting inflammation and facilitating functional recovery. They also offer new insight into the cellular targeting, uptake and migration of hADSC-ex, and provide a theoretical basis for new therapeutic strategies for central nervous system diseases.
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Glioblastoma cell differentiation trajectory predicts the immunotherapy response and overall survival of patients

Zihao Wang, Xiaopeng Guo, Lu Gao, Yu Wang, Wenbin Ma, Bing Xing,

https://doi.org/10.18632/aging.103695 pp 18297—18321

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Wang Z, Guo X, Gao L, Wang Y, Ma W, Xing B, . Glioblastoma cell differentiation trajectory predicts the immunotherapy response and overall survival of patients. . 12:18297-18321. https://doi.org/10.18632/aging.103695

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                TY  - JOUR
                AU  - Wang, Zihao 
                AU  - Guo, Xiaopeng 
                AU  - Gao, Lu 
                AU  - Wang, Yu 
                AU  - Ma, Wenbin 
                AU  - Xing, Bing 
                TI  - Glioblastoma cell differentiation trajectory predicts the immunotherapy response and overall survival of patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103695
                DO  - 10.18632/aging.103695
                SP  - 18297
                EP  - 18321
                PY  - 
                AB  - Glioblastoma (GBM) is the most common and lethal primary brain tumor. In this study, we aimed to investigate the differentiation states of GBM cells and their clinical relevance. Integrated single-cell RNA-sequencing (scRNA-seq) data and bulk RNA-seq data from GBM samples were used for analysis. Two subsets of GBM cells in distinct differentiation states were characterized, and 498 GBM cell differentiation-related genes (GDRGs) were identified. GDRGs were significantly correlated with immune regulation and metabolic pathways. We classified the GBM patients into two groups based on the expression of GDRGs in tumors and found that the cell differentiation-based classification successfully predicted patient overall survival (OS), immune checkpoint expression and likelihood of immunotherapy response in GBMs. FN1, APOE, RPL7A and GSTM2 were the 4 most significant survival-predicting GDRGs, and patients with different expression levels of each of these genes had distinct survival outcomes. Finally, a nomogram composed of the GDRG signature, age, pharmacotherapy, radiotherapy, IDH mutations and MGMT promoter methylation was generated and validated in two large GBM cohorts to predict GBM prognosis. This study highlights the significant roles of cell differentiation in predicting the clinical outcomes of GBM patients and their potential response to immunotherapy, suggesting promising therapeutic targets for GBM.
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A two-gene-based prognostic signature for pancreatic cancer

Shuyi Zhou, Yuanliang Yan, Xi Chen, Shuangshuang Zeng, Jie Wei, Xiang Wang, Zhicheng Gong, Zhijie Xu,

https://doi.org/10.18632/aging.103698 pp 18322—18342

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Zhou S, Yan Y, Chen X, Zeng S, Wei J, Wang X, Gong Z, Xu Z, . A two-gene-based prognostic signature for pancreatic cancer. . 12:18322-18342. https://doi.org/10.18632/aging.103698

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                TY  - JOUR
                AU  - Zhou, Shuyi 
                AU  - Yan, Yuanliang 
                AU  - Chen, Xi 
                AU  - Zeng, Shuangshuang 
                AU  - Wei, Jie 
                AU  - Wang, Xiang 
                AU  - Gong, Zhicheng 
                AU  - Xu, Zhijie 
                TI  - A two-gene-based prognostic signature for pancreatic cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103698
                DO  - 10.18632/aging.103698
                SP  - 18322
                EP  - 18342
                PY  - 
                AB  - The purpose of this study was to identify a vital gene signature that has prognostic value for pancreatic cancer based on gene expression datasets from the Cancer Genome Atlas and Gene Expression Omnibus. A total of 34 genes were obtained by the univariate analysis, which were significantly associated with the overall survival of PC patients. After further analysis, Anillin (ANLN) and Histone H1c (HIST1H1C) were identified and considered to be the most significant prognostic genes among the 34 genes. A prognostic model based on these two genes was constructed, and successfully distinguished pancreatic cancer survival into high-risk and low-risk groups in the training set and testing set. Subsequently, independent predictive factors, including the age, margin condition and risk score, were then employed to construct the nomogram model. The area under curve for the nomogram model was 0.826 at 0.5 years and 0.726 at 1 year, and the C-index of the nomogram model was 0.664 higher than the others variables alone. These findings have indicated that high expression of ANLN and HIST1H1C predicted poor outcomes for patients with pancreatic cancer. The nomogram model based on the expression of two genes could be valuable for the guidance of clinical treatment.
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Modeling mtDNA hypermethylation vicious circle mediating Aβ-induced endothelial damage memory in HCMEC/D3 cell

HaoChen Liu, Hong Zhang, Yixuan Zhang, Sheng Xu, Huimin Zhao, Hua He, XiaoQuan Liu,

https://doi.org/10.18632/aging.103699 pp 18343—18362

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Liu H, Zhang H, Zhang Y, Xu S, Zhao H, He H, Liu X, . Modeling mtDNA hypermethylation vicious circle mediating Aβ-induced endothelial damage memory in HCMEC/D3 cell. . 12:18343-18362. https://doi.org/10.18632/aging.103699

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                TY  - JOUR
                AU  - Liu, HaoChen 
                AU  - Zhang, Hong 
                AU  - Zhang, Yixuan 
                AU  - Xu, Sheng 
                AU  - Zhao, Huimin 
                AU  - He, Hua 
                AU  - Liu, XiaoQuan 
                TI  - Modeling mtDNA hypermethylation vicious circle mediating Aβ-induced endothelial damage memory in HCMEC/D3 cell
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103699
                DO  - 10.18632/aging.103699
                SP  - 18343
                EP  - 18362
                PY  - 
                AB  - It is well accepted that accumulation of beta-amyloid (A&#x3B2;) may involve in endothelial dysfunction during the Alzheimer&#x2019;s disease (AD) progression. However, cerebrovascular function cannot be improved by removing A&#x3B2; in AD animal models. The reasons for these paradoxical results still remain to be further investigated. We hypothesize that A&#x3B2; exposure may cause persistence damage to cerebral endothelial cell even after A&#x3B2; is removed (termed as cerebrovascular endothelial damage memory) mitochondria DNA (mtDNA) hypermethylation is assumed to be involved in this process. The aim of this study is to investigate whether A&#x3B2; exposure induces cerebrovascular endothelial damage memory in endothelial cells and mtDNA hypermethylation involves in this process. The hCMEC/D3 cell is treated with A&#x3B2;1&#x2013;42 for 12h and then withdraw A&#x3B2;1&#x2013;42 for another 12h incubation to investigate whether cerebrovascular endothelial damage memory exists in endothelial cells. The levels of mtDNA methylation and cell vitality were not improved by removing A&#x3B2;1&#x2013;42 after 12h A&#x3B2;1&#x2013;42 incubation which suggested that the cerebrovascular endothelial damage memory may exist in endothelial cells. Kinetics model analysis suggested that mtDNA hypermethylation involves in initiating the cerebrovascular endothelial damage memory otherwise &#x3B1;-oxoglutarate (AKG) exhaustion plays a vital role in maintaining this process. DNA methylation inhibitor decitabine and AKG supplement may relieve the cerebrovascular endothelial damage memory dose dependently. This study provides a novel feature of cerebrovascular endothelial damage induced by A&#x3B2;.
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A 12-immune cell signature to predict relapse and guide chemotherapy for stage II colorectal cancer

Xianglong Tian, Xiaoqiang Zhu, Wenying Meng, Shiguang Bai, Min Shi, Shihao Xiang, Chen Zhao, Yugang Wang,

https://doi.org/10.18632/aging.103707 pp 18363—18383

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Tian X, Zhu X, Meng W, Bai S, Shi M, Xiang S, Zhao C, Wang Y, . A 12-immune cell signature to predict relapse and guide chemotherapy for stage II colorectal cancer. . 12:18363-18383. https://doi.org/10.18632/aging.103707

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                TY  - JOUR
                AU  - Tian, Xianglong 
                AU  - Zhu, Xiaoqiang 
                AU  - Meng, Wenying 
                AU  - Bai, Shiguang 
                AU  - Shi, Min 
                AU  - Xiang, Shihao 
                AU  - Zhao, Chen 
                AU  - Wang, Yugang 
                TI  - A 12-immune cell signature to predict relapse and guide chemotherapy for stage II colorectal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103707
                DO  - 10.18632/aging.103707
                SP  - 18363
                EP  - 18383
                PY  - 
                AB  - The management of stage II colorectal cancer is still difficult. We aimed to construct a new immune cell-associated signature for prognostic evaluation and guiding chemotherapy in stage II colorectal cancer. We used the &#x201C;Cell Type Identification by Estimating Relative Subsets of RNA Transcripts&#x201D; (CIBERSORT) method to estimate the fraction of 22 immune cells by analyzing bulk tumor transcriptomes and a LASSO Cox regression model to select the prognostic immune cells. A 12-immune cell prognostic classifier, ISCRC, was built, which could successfully discriminate the high-risk patients in the training cohort (GSE39582: HR = 3.16, 95% CI: 1.85&#x2013;5.40, P &lt; 0.0001) and another independent cohorts (GSE14333: HR = 3.47, 95% CI: 1.18&#x2013;10.15, P =0.0167). The receiver operating characteristic analysis revealed that the AUC of the ISCRC model was significantly greater than that of oncotypeDX model (0.7111 versus 0.5647, p=0.0152). We introduced the propensity score matching analysis to eliminate the selection bias; survival analysis showed relatively poor prognosis after chemotherapy in stage II CRC patients. Furthermore, a nomogram was built for clinicians and did well in the calibration plots. In conclusion, this immune cell-based signature could improve prognostic prediction and may help guide chemotherapy in stage II colorectal cancer patients.
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p38γ overexpression promotes osteosarcoma cell progression

Ce Shi, Wei-Nan Cheng, Yin Wang, Da-Zhuang Li, Li-Na Zhou, Yu-Cheng Zhu, Xiao-Zhong Zhou,

https://doi.org/10.18632/aging.103708 pp 18384—18395

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Shi C, Cheng W, Wang Y, Li D, Zhou L, Zhu Y, Zhou X, . p38γ overexpression promotes osteosarcoma cell progression. . 12:18384-18395. https://doi.org/10.18632/aging.103708

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                TY  - JOUR
                AU  - Shi, Ce 
                AU  - Cheng, Wei-Nan 
                AU  - Wang, Yin 
                AU  - Li, Da-Zhuang 
                AU  - Zhou, Li-Na 
                AU  - Zhu, Yu-Cheng 
                AU  - Zhou, Xiao-Zhong 
                TI  - p38γ overexpression promotes osteosarcoma cell progression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103708
                DO  - 10.18632/aging.103708
                SP  - 18384
                EP  - 18395
                PY  - 
                AB  - Osteosarcoma (OS) is the most common primary bone malignancy in the adolescent population. Recent studies demonstrate that p38 gamma (p38&#x3B3;) phosphorylates retinoblastoma (Rb) to promote cyclin expression, cell-cycle entry and tumorigenesis. Studying the potential function of p38&#x3B3; in human OS, we show that p38&#x3B3; mRNA and protein expression are significantly elevated in OS tissues and OS cells, whereas its expression is relatively low in normal bone tissue and in human osteoblasts/osteoblastic cells. Knockdown of p38&#x3B3; in established (U2OS) and primary human OS cells potently inhibited cell growth, proliferation, migration and invasion, while promoting cell apoptosis. Furthermore, CRISPR/Cas9-induced p38&#x3B3; knockout inhibited human OS cell progression in vitro. Conversely, ectopic overexpression of p38&#x3B3; in primary human OS cells augmented cell growth, proliferation and migration. Signaling studies show that retinoblastoma (Rb) phosphorylation and cyclin E1/cyclin A expression were decreased following p38&#x3B3; shRNA knockdown and knockout, but increased after ectopic p38&#x3B3; overexpression. Collectively, these results show that p38&#x3B3; overexpression promotes human OS cell progression.
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Elevated serum IL-21 levels are associated with stable immune status in kidney transplant recipients and a mouse model of kidney transplantation

Luying Guo, Junhao Lv, Jian Zhang, Hao Deng, Shi Feng, Shuaihui Liu, Pengpeng Yan, Jingyi Zhou, Hui Chen, Meifang Wang, Qin Zhou, Huiping Wang, Jianghua Chen, Yu Kuang, Jia Shen, Rending Wang,

https://doi.org/10.18632/aging.103713 pp 18396—18414

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Guo L, Lv J, Zhang J, Deng H, Feng S, Liu S, Yan P, Zhou J, Chen H, Wang M, Zhou Q, Wang H, Chen J, et al, . Elevated serum IL-21 levels are associated with stable immune status in kidney transplant recipients and a mouse model of kidney transplantation. . 12:18396-18414. https://doi.org/10.18632/aging.103713

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                TY  - JOUR
                AU  - Guo, Luying 
                AU  - Lv, Junhao 
                AU  - Zhang, Jian 
                AU  - Deng, Hao 
                AU  - Feng, Shi 
                AU  - Liu, Shuaihui 
                AU  - Yan, Pengpeng 
                AU  - Zhou, Jingyi 
                AU  - Chen, Hui 
                AU  - Wang, Meifang 
                AU  - Zhou, Qin 
                AU  - Wang, Huiping 
                AU  - Chen, Jianghua 
                AU  - Kuang, Yu 
                AU  - Shen, Jia 
                AU  - Wang, Rending 
                TI  - Elevated serum IL-21 levels are associated with stable immune status in kidney transplant recipients and a mouse model of kidney transplantation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103713
                DO  - 10.18632/aging.103713
                SP  - 18396
                EP  - 18414
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Guo, Luying 
                AU  - Lv, Junhao 
                AU  - Zhang, Jian 
                AU  - Deng, Hao 
                AU  - Feng, Shi 
                AU  - Liu, Shuaihui 
                AU  - Yan, Pengpeng 
                AU  - Zhou, Jingyi 
                AU  - Chen, Hui 
                AU  - Wang, Meifang 
                AU  - Zhou, Qin 
                AU  - Wang, Huiping 
                AU  - Chen, Jianghua 
                AU  - Kuang, Yu 
                AU  - Shen, Jia 
                AU  - Wang, Rending 
                TI  - Elevated serum IL-21 levels are associated with stable immune status in kidney transplant recipients and a mouse model of kidney transplantation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103713
                DO  - 10.18632/aging.103713
                SP  - 18396
                EP  - 18414
                PY  - 
                AB  - Allograft rejection after renal transplantation remains a challenge to overcome. Interleukin (IL)-21, a cytokine with pleiotropic effects, maintains immune homeostasis post-transplantation. Here, we report higher levels of IL-21 in kidney transplant recipients with non-rejection (NR) than in recipients with T cell-mediated rejection (TCMR, P &lt; 0.001) and antibody-mediated rejection (ABMR, P = 0.005). We observed a negative correlation between IL-21 and creatinine (Cr) levels (P = 0.016). The receiving operating characteristic (ROC) curve showed a promising diagnostic value of IL-21 to identify acute rejection with an area under the curve (AUC) of 0.822 (P &lt; 0.001). In contrast, exogenous administration of IL-21 accelerated acute rejection in a comparative translational kidney transplant (KT) mouse model. Reduced IL-21 levels in the peripheral blood were observed in KT mice after IL-21 injection. Further analysis revealed that increased IL-21 levels in the spleen induced proliferation of CD4+ T cells and CD19+ B cells after IL-21 treatment. Our findings suggest a critical function of IL-21 in kidney transplantation and the potential involvement of the IL-21/IL-21R pathway in acute rejection management.
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Association of vitamin C intake with breast cancer risk and mortality: a meta-analysis of observational studies

Dai Zhang, Peng Xu, Yiche Li, Bajin Wei, Si Yang, Yi Zheng, Lijuan Lyu, Yujiao Deng, Zhen Zhai, Na Li, Nan Wang, Jun Lyu, Zhijun Dai,

https://doi.org/10.18632/aging.103769 pp 18415—18435

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Zhang D, Xu P, Li Y, Wei B, Yang S, Zheng Y, Lyu L, Deng Y, Zhai Z, Li N, Wang N, Lyu J, Dai Z, . Association of vitamin C intake with breast cancer risk and mortality: a meta-analysis of observational studies. . 12:18415-18435. https://doi.org/10.18632/aging.103769

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                TY  - JOUR
                AU  - Zhang, Dai 
                AU  - Xu, Peng 
                AU  - Li, Yiche 
                AU  - Wei, Bajin 
                AU  - Yang, Si 
                AU  - Zheng, Yi 
                AU  - Lyu, Lijuan 
                AU  - Deng, Yujiao 
                AU  - Zhai, Zhen 
                AU  - Li, Na 
                AU  - Wang, Nan 
                AU  - Lyu, Jun 
                AU  - Dai, Zhijun 
                TI  - Association of vitamin C intake with breast cancer risk and mortality: a meta-analysis of observational studies
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103769
                DO  - 10.18632/aging.103769
                SP  - 18415
                EP  - 18435
                PY  - 
                AB  - The association between vitamin C intake and breast cancer is unclear. This meta-analysis aimed to precisely assess the association of vitamin C intake with breast cancer risk and mortality. We searched the PubMed, Embase, and Web of Science databases up to June 2020 and found 69 studies relevant to breast cancer risk (54 studies) and survival (15 studies). Relative risks and 95% confidence intervals were calculated using the random-effects models. Pooled results suggested that the highest versus lowest vitamin C intake was significantly associated with a lower risk of breast cancer incidence (Relative Risk = 0.86; 95% confidence interval, 0.81&#x2013;0.92). Dietary vitamin C but not supplements was found to reduce breast cancer risk (Relative Risk = 0.89; 95% confidence interval, 0.82&#x2013;0.96). For the highest versus lowest vitamin C intake, the pooled hazard risk for breast cancer-specific mortality was 0.78 (95% confidence interval, 0.69&#x2013;0.88), totality mortality was 0.82 (95% confidence interval, 0.74&#x2013;0.91), and recurrence was 0.81 (95% confidence interval, 0.67&#x2013;0.99). Our analysis suggests that higher vitamin C intake is significantly associated with reduced breast cancer incidence and mortality. However, the intake of vitamin C supplements has no significant effect on breast cancer prevention.
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Nudt21-mediated alternative polyadenylation of HMGA2 3′-UTR impairs stemness of human tendon stem cell

Yangbai Sun, Hua Chen, Hui Ye, Wenqing Liang, Kun-kuan Lam, Biao Cheng, Yong Lu, Chaoyin Jiang,

https://doi.org/10.18632/aging.103771 pp 18436—18452

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Sun Y, Chen H, Ye H, Liang W, Lam K, Cheng B, Lu Y, Jiang C, . Nudt21-mediated alternative polyadenylation of HMGA2 3′-UTR impairs stemness of human tendon stem cell. . 12:18436-18452. https://doi.org/10.18632/aging.103771

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                TY  - JOUR
                AU  - Sun, Yangbai 
                AU  - Chen, Hua 
                AU  - Ye, Hui 
                AU  - Liang, Wenqing 
                AU  - Lam, Kun-kuan 
                AU  - Cheng, Biao 
                AU  - Lu, Yong 
                AU  - Jiang, Chaoyin 
                TI  - Nudt21-mediated alternative polyadenylation of HMGA2 3′-UTR impairs stemness of human tendon stem cell
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103771
                DO  - 10.18632/aging.103771
                SP  - 18436
                EP  - 18452
                PY  - 
                AB  - Tendon-derived stem cells (TSCs) play a primary role in tendon physiology, pathology, as well as tendon repair and regeneration after injury. TSCs are often exposed to mechanical loading-related cellular stresses such as oxidative stress, resulting in loss of stemness and multipotent differentiation potential. Cytoprotective autophagy has previously been identified as an important mechanism to protect human TSCs (hTSCs) from oxidative stress induced impairments. In this study, we found that high-mobility AT-hook 2 (HMGA2) overexpression protects hTSCs against H2O2-induced loss of stemness through autophagy activation. Evidentially, H2O2 treatment increases the expression of Nudt21, a protein critical to polyadenylation site selection in alternative polyadenylation (APA) of mRNA transcripts. This leads to increased cleavage and polyadenylation of HMGA2 3&#x2032;-UTR at the distal site, resulting in increased HMGA2 silencing by the microRNA let-7 and reduced HMGA2 expression. In conclusion, Nudt21-regulated APA of HMGA2 3&#x2032;-UTR and subsequent HMGA2 downregulation mediates oxidative stress induced hTSC impairments.
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A newly defined risk signature, consisting of three m⁶A RNA methylation regulators, predicts the prognosis of ovarian cancer

Lili Fan, Ying Lin, Han Lei, Guang Shu, Liuer He, Zhipeng Yan, Hai Rihan, Gang Yin,

https://doi.org/10.18632/aging.103811 pp 18453—18475

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Fan L, Lin Y, Lei H, Shu G, He L, Yan Z, Rihan H, Yin G, . A newly defined risk signature, consisting of three m⁶A RNA methylation regulators, predicts the prognosis of ovarian cancer. . 12:18453-18475. https://doi.org/10.18632/aging.103811

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Provider: 
 TY - JOUR
 AU - Fan, Lili 
 AU - Lin, Ying 
 AU - Lei, Han 
 AU - Shu, Guang 
 AU - He, Liuer 
 AU - Yan, Zhipeng 
 AU - Rihan, Hai 
 AU - Yin, Gang 
 TI - A newly defined risk signature, consisting of three m6A RNA methylation regulators, predicts the prognosis of ovarian cancer
 JO - 
 JA - 
 VL - 12
 IS - 18
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.103811
 DO - 10.18632/aging.103811
 SP - 18453
 EP - 18475
 PY - 
 AB - N6-methyladenosine (m6A) RNA methylation, involved in cancer initiation and progression, is dynamically regulated by the m6A RNA methylation regulators. However, the expression of m6A RNA methylation regulators in ovarian cancer and their correlation with prognosis remain elusive. Here, we demonstrated that the 18 central m6A RNA methylation regulators were expressed differently between ovarian cancer (OC) and normal tissues. By applying consensus clustering, all ovarian cancer patient cases can be divided into three subgroups (cluster1/2/3) based on overall expression levels of all 18 m6A RNA methylation regulators. We systematically analyzed the prognostic value of transcription levels of 18 m6A RNA methylation regulators in ovarian cancer and found that insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1), vir like m6A methyltransferase associated (VIRMA), and zinc finger CCCH-type containing 13 (ZC3H13) yield the highest scores for predicting the prognosis of ovarian cancer. Accordingly, we derived a risk signature consisting of transcription levels of these three selected m6A RNA methylation regulators as an independent prognostic marker for OC and validated our findings with data derived from a different ovarian cancer cohort. Moreover, by the Gene Set Enrichment Analysis (GSEA), we demonstrated that the three selected regulators were all correlated with pathways in cancer and WNT signaling pathways. In conclusion, m6A RNA methylation regulators are vital participants in ovarian cancer pathology; and IGF2BP1, VIRMA, and ZC3H13 mRNA levels are valuable factors for prognosis prediction and treatment strategy development.
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YTHDF2 correlates with tumor immune infiltrates in lower-grade glioma

Xiangan Lin, Zhichao Wang, Guangda Yang, Guohua Wen, Hailiang Zhang,

https://doi.org/10.18632/aging.103812 pp 18476—18500

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Lin X, Wang Z, Yang G, Wen G, Zhang H, . YTHDF2 correlates with tumor immune infiltrates in lower-grade glioma. . 12:18476-18500. https://doi.org/10.18632/aging.103812

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                TY  - JOUR
                AU  - Lin, Xiangan 
                AU  - Wang, Zhichao 
                AU  - Yang, Guangda 
                AU  - Wen, Guohua 
                AU  - Zhang, Hailiang 
                TI  - YTHDF2 correlates with tumor immune infiltrates in lower-grade glioma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103812
                DO  - 10.18632/aging.103812
                SP  - 18476
                EP  - 18500
                PY  - 
                AB  - Immunotherapy is an effective treatment for many cancer types. However, YTHDF2 effects on the prognosis of different tumors and correlation with tumor immune infiltration are unclear. Here, we analyzed The Cancer Genome Atlas and Gene Expression Omnibus data obtained through various web-based platforms. The analyses showed that YTHDF2 expression and associated prognoses may depend on cancer type. High YTHDF2 expression was associated with poor overall survival in lower-grade glioma (LGG). In addition, YTHDF2 expression positively correlated with expression of several immune cell markers, including PD-1, TIM-3, and CTLA-4, as well as tumor-associated macrophage gene markers, and isocitrate dehydrogenase 1 in LGG. These findings suggest that YTHDF2 is a potential prognostic biomarker that correlates with LGG tumor-infiltrating immune cells.
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D-galactose induces senescence of glioblastoma cells through YAP-CDK6 pathway

Xingxing Xu, Xiya Shen, Wenjin Feng, Danlu Yang, Lingting Jin, Jiaojiao Wang, Mianxian Wang, Zhang Ting, Feng Xue, Jingjing Zhang, Chaobo Meng, Roumeng Chen, Xinru Zheng, Leilei Du, Lina Xuan, Ying Wang, Tian Xie, Zhihui Huang,

https://doi.org/10.18632/aging.103819 pp 18501—18521

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Xu X, Shen X, Feng W, Yang D, Jin L, Wang J, Wang M, Ting Z, Xue F, Zhang J, Meng C, Chen R, Zheng X, et al, . D-galactose induces senescence of glioblastoma cells through YAP-CDK6 pathway. . 12:18501-18521. https://doi.org/10.18632/aging.103819

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                TY  - JOUR
                AU  - Xu, Xingxing 
                AU  - Shen, Xiya 
                AU  - Feng, Wenjin 
                AU  - Yang, Danlu 
                AU  - Jin, Lingting 
                AU  - Wang, Jiaojiao 
                AU  - Wang, Mianxian 
                AU  - Ting, Zhang 
                AU  - Xue, Feng 
                AU  - Zhang, Jingjing 
                AU  - Meng, Chaobo 
                AU  - Chen, Roumeng 
                AU  - Zheng, Xinru 
                AU  - Du, Leilei 
                AU  - Xuan, Lina 
                AU  - Wang, Ying 
                AU  - Xie, Tian 
                AU  - Huang, Zhihui 
                TI  - D-galactose induces senescence of glioblastoma cells through YAP-CDK6 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103819
                DO  - 10.18632/aging.103819
                SP  - 18501
                EP  - 18521
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Xu, Xingxing 
                AU  - Shen, Xiya 
                AU  - Feng, Wenjin 
                AU  - Yang, Danlu 
                AU  - Jin, Lingting 
                AU  - Wang, Jiaojiao 
                AU  - Wang, Mianxian 
                AU  - Ting, Zhang 
                AU  - Xue, Feng 
                AU  - Zhang, Jingjing 
                AU  - Meng, Chaobo 
                AU  - Chen, Roumeng 
                AU  - Zheng, Xinru 
                AU  - Du, Leilei 
                AU  - Xuan, Lina 
                AU  - Wang, Ying 
                AU  - Xie, Tian 
                AU  - Huang, Zhihui 
                TI  - D-galactose induces senescence of glioblastoma cells through YAP-CDK6 pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103819
                DO  - 10.18632/aging.103819
                SP  - 18501
                EP  - 18521
                PY  - 
                AB  - Treatment of glioblastoma using radiotherapy and chemotherapy has various outcomes, key among them being cellular senescence. However, the molecular mechanisms of this process remain unclear. In the present study, we tested the ability of D-galactose (D-gal), a reducing sugar, to induce senescence in glioblastoma cells. Following pretreatment with D-gal, glioblastoma cell lines (C6 and U87MG) showed typical characteristics of senescence. These included the reduced cell proliferation, hypertrophic morphology, increased senescence-associated &#x3B2;-galactosidase activity, downregulation of Lamin B1, and upregulation of several senescence-associated genes such as p16, p53, and NF-&#x3BA;B. Furthermore, our results showed that D-gal was more suitable than etoposide (a DNA-damage drug) in inducing senescence of glioblastoma cells. Mechanistically, D-gal inactivated the YAP-CDK6 signaling pathway, while overexpression of YAP or CDK6 could restore D-gal-induced senescence of C6 cells. Finally, metformin, an anti-aging agent, activated the YAP-CDK6 pathway and suppressed D-gal-induced senescence of C6 cells. Taken together, these findings established a new model for analyzing senescence in glioblastoma cells, which occurred through the YAP-CDK6 pathway. This is expected to provide a basis for development of novel therapies for the treatment of glioblastoma.
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GPA peptide inhibits NLRP3 inflammasome activation to ameliorate colitis through AMPK pathway

Zhao Deng, Jiangjin Ni, Xiaoyu Wu, Hongkui Wei, Jian Peng,

https://doi.org/10.18632/aging.103825 pp 18522—18544

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Deng Z, Ni J, Wu X, Wei H, Peng J, . GPA peptide inhibits NLRP3 inflammasome activation to ameliorate colitis through AMPK pathway. . 12:18522-18544. https://doi.org/10.18632/aging.103825

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                TY  - JOUR
                AU  - Deng, Zhao 
                AU  - Ni, Jiangjin 
                AU  - Wu, Xiaoyu 
                AU  - Wei, Hongkui 
                AU  - Peng, Jian 
                TI  - GPA peptide inhibits NLRP3 inflammasome activation to ameliorate colitis through AMPK pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103825
                DO  - 10.18632/aging.103825
                SP  - 18522
                EP  - 18544
                PY  - 
                AB  - Ulcerative colitis (UC) is a chronic and idiopathic inflammatory disease that affects the colon, resulting in immune dysregulation and the production of large amounts of pro-inflammatory cytokines. Pyroptosis and NLRP3 inflammasome are associated with various kinds of inflammatory diseases including colitis. The purpose of this study is to investigate the protective effects and regulatory mechanism of Gly-Pro-Ala (GPA) peptide on DSS-induced colitis. In vivo, we find GPA peptide could exert anti-inflammatory effects on DSS-induced mice colitis, and its anti-inflammatory effects are abolished in NLRP3-/- mice. In macrophage, GPA suppresses the assembly of NLRP3 inflammasome and GSDMD cleavage. Furthermore, GPA maintains mitochondrial homeostasis through inhibiting ROS, mtDNA and NLRP3 mitochondrial localization, with other signals related to NLRP3 inflammasome unaffected. Furthermore, the inhibitory effects of GPA on reactive oxygen species (ROS) are found to be achieved by increasing AMPK phosphorylation. Our results suggest that GPA inhibits NLRP3 inflammasome activation through increasing AMPK phosphorylation to suppress ROS, and can be applied in the prevention of colitis through targeting NLRP3.
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MiR-520d-5p modulates chondrogenesis and chondrocyte metabolism through targeting HDAC1

Jiajia Lu, Zhibin Zhou, Bin Sun, Bin Han, Qiang Fu, Yaguang Han, Wang Yuan, Zeng Xu, Aimin Chen,

https://doi.org/10.18632/aging.103831 pp 18545—18560

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Lu J, Zhou Z, Sun B, Han B, Fu Q, Han Y, Yuan W, Xu Z, Chen A, . MiR-520d-5p modulates chondrogenesis and chondrocyte metabolism through targeting HDAC1. . 12:18545-18560. https://doi.org/10.18632/aging.103831

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                TY  - JOUR
                AU  - Lu, Jiajia 
                AU  - Zhou, Zhibin 
                AU  - Sun, Bin 
                AU  - Han, Bin 
                AU  - Fu, Qiang 
                AU  - Han, Yaguang 
                AU  - Yuan, Wang 
                AU  - Xu, Zeng 
                AU  - Chen, Aimin 
                TI  - MiR-520d-5p modulates chondrogenesis and chondrocyte metabolism through targeting HDAC1
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103831
                DO  - 10.18632/aging.103831
                SP  - 18545
                EP  - 18560
                PY  - 
                AB  - MicroRNAs (miRNAs) play an essential role in the chondrogenesis and the progression of osteoarthritis (OA). This study aimed to determine miRNAs associated with chondrogenesis of human mesenchymal stem cells (hMSCs) and chondrocyte metabolism. MiRNAs were screened in hMSCs during chondrogenesis by RNA-seq and qRT-PCR. MiRNA expression was determined in primary human chondrocytes (PHCs), and degraded cartilage samples. MiRNA mimics and inhibitors were transfected to cells to determine the effect of miRNA. Bioinformatic analysis and luciferase reporter assays were applied to determine the target gene of miRNA. The results demonstrated that miR-520d-5p was increased in hMSCs chondrogenesis. The overexpression and knockdown of miR-520d-5p promoted and inhibited chondrogenesis, and regulated chondrocyte metabolism. Histone deacetylase 1 (HDAC1) was decreased in hMSCs chondrogenesis, and HDAC1 was a targeting gene of miR-520d-5p. CI994, HDAC1 inhibitor, elevated cartilage-specific gene expressions and promoted hMSCs chondrogenesis. In IL-1&#x3B2;-treated PHCs, CI994 promoted AGGRECAN expression and suppressed MMP-13 expression, abolishing the effect of IL-1&#x3B2; on PHCs. Taken together, these results suggest that miR-520d-5p promotes hMSCs chondrogenesis and regulates chondrocyte metabolism through targeting HDAC1. This study provides novel understanding of the molecular mechanism of OA progression.
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Chetomin rescues pathogenic phenotype of LRRK2 mutation in drosophila

Ling Ling Chua, Patrick Ho, Joanne Toh, Eng-King Tan,

https://doi.org/10.18632/aging.103843 pp 18561—18570

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Chua LL, Ho P, Toh J, Tan E, . Chetomin rescues pathogenic phenotype of LRRK2 mutation in drosophila. . 12:18561-18570. https://doi.org/10.18632/aging.103843

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                TY  - JOUR
                AU  - Chua, Ling Ling 
                AU  - Ho, Patrick 
                AU  - Toh, Joanne 
                AU  - Tan, Eng-King 
                TI  - Chetomin rescues pathogenic phenotype of LRRK2 mutation in drosophila
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103843
                DO  - 10.18632/aging.103843
                SP  - 18561
                EP  - 18570
                PY  - 
                AB  - Leucine-rich repeat kinase 2 (LRRK2) is a complex protein kinase involved in a diverse set of functions. Mutations in LRRK2 are a common cause of autosomal dominant familial Parkinson&#x2019;s disease. Peroxiredoxin 2 (PRDX2) belongs to a family of anti-oxidants that protect cells from oxidative stress. Importantly, PRDX2 is a cytoplasmic protein, similar to Leucine-rich repeat kinase 2, which localizes predominantly in the cytosol. Here, we demonstrated that Leurice-rich repeat kinase 2 phosphorylates PRDX2 in Drosophila, leading to a loss of dopaminergic neurons, climbing ability and shortened lifespan. These pathogenic phenotypes in the LRRK2 Drosophila were rescued with transgenic expression of PRDX2. Chetomin, a PRDX2 mimic, belongs to a class of epidithio-diketopiperazine fungal secondary metabolites (containing a dithiol group that has hydrogen peroxide-reducing activity). As proof of principle, we demonstrated that Chetomin recapitulated the rescue in these mutant Drosophila. Our findings suggest that Chetomin can be a potential therapeutic compound in LRRK2 linked Parkinson&#x2019;s disease.
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Characterization of LncRNA SNHG22 as a protector of NKIRAS2 through miR-4492 binding in osteosarcoma

Huo-Liang Zheng, Run-Ze Yang, Wen-Ning Xu, Tao Liu, Peng-Bo Chen, Xin-Feng Zheng, Bo Li, Lei-Sheng Jiang, Sheng-Dan Jiang,

https://doi.org/10.18632/aging.103849 pp 18571—18587

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Zheng H, Yang R, Xu W, Liu T, Chen P, Zheng X, Li B, Jiang L, Jiang S, . Characterization of LncRNA SNHG22 as a protector of NKIRAS2 through miR-4492 binding in osteosarcoma. . 12:18571-18587. https://doi.org/10.18632/aging.103849

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                TY  - JOUR
                AU  - Zheng, Huo-Liang 
                AU  - Yang, Run-Ze 
                AU  - Xu, Wen-Ning 
                AU  - Liu, Tao 
                AU  - Chen, Peng-Bo 
                AU  - Zheng, Xin-Feng 
                AU  - Li, Bo 
                AU  - Jiang, Lei-Sheng 
                AU  - Jiang, Sheng-Dan 
                TI  - Characterization of LncRNA SNHG22 as a protector of NKIRAS2 through miR-4492 binding in osteosarcoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103849
                DO  - 10.18632/aging.103849
                SP  - 18571
                EP  - 18587
                PY  - 
                AB  - Many studies have revealed the function of long noncoding RNA (LncRNA) in regulating tumorigenesis of osteosarcoma (OS). As a subgroup of LncRNA, small nucleolar RNA host genes (SNHGs) have emerged as potentially important in OS. According to our recent findings, small nucleolar RNA host gene 22 (SNHG22) plays an important role in inhibiting the growth and metastasis of OS. However, the underlying mechanism of SNHG22 in regulating OS progression remains unknown. In this study, we confirmed that SNHG22 was downregulated in OS, and the overexpression of SNHG22 significantly inhibited OS progression in vivo and in vitro. Meanwhile, overexpression of SNHG22 also inhibited the migration and proliferation of human umbilical vein endothelial cells (HUVECs) and prevented the epithelial-to-mesenchymal transition (EMT) in OS. Furthermore, the interaction between miR-4492 and SNHG22 we previously predicted was validated by RNA pull-down assays and RNA immunoprecipitation assays. Dual-luciferase reporter assays showed that SNHG22 could directly interact with miR-4492 and upregulate the expression of NK-&#x3BA;B inhibitor-interacting Ras-like 2 (NKIRAS2) by its competing endogenous RNA (ceRNA) activity on miR-4492. In conclusion, our study has clarified the function of SNHG22 in OS progression and suggests a novel therapeutic target for OS.
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Lipopolysaccharide upregulates miR-132/212 in Hirschsprung-associated enterocolitis, facilitating pyroptosis by activating NLRP3 inflammasome via targeting Sirtuin 1 (SIRT1)

Hongxing Li, Lingling Zhou, Zhengke Zhi, Xiurui Lv, Zhonghong Wei, Xin Zhang, Weibing Tang, Meiling Tong,

https://doi.org/10.18632/aging.103852 pp 18588—18602

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Li H, Zhou L, Zhi Z, Lv X, Wei Z, Zhang X, Tang W, Tong M, . Lipopolysaccharide upregulates miR-132/212 in Hirschsprung-associated enterocolitis, facilitating pyroptosis by activating NLRP3 inflammasome via targeting Sirtuin 1 (SIRT1). . 12:18588-18602. https://doi.org/10.18632/aging.103852

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                TY  - JOUR
                AU  - Li, Hongxing 
                AU  - Zhou, Lingling 
                AU  - Zhi, Zhengke 
                AU  - Lv, Xiurui 
                AU  - Wei, Zhonghong 
                AU  - Zhang, Xin 
                AU  - Tang, Weibing 
                AU  - Tong, Meiling 
                TI  - Lipopolysaccharide upregulates miR-132/212 in Hirschsprung-associated enterocolitis, facilitating pyroptosis by activating NLRP3 inflammasome via targeting Sirtuin 1 (SIRT1)
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103852
                DO  - 10.18632/aging.103852
                SP  - 18588
                EP  - 18602
                PY  - 
                AB  - Hirschsprung disease (HSCR) is a congenital disorder attributed to the failure of the neural crest derivatives migrating and/or differentiating along the hindgut. The most frequent complication in Hirschsprung disease patients is Hirschsprung-associated enterocolitis (HAEC). However, its pathogenesis has not been fully understood. This study investigated miRNAs influenced by Lipopolysaccharide (LPS) in postoperative HAEC patients, their effect on enterocolitis and the underlying mechanism. MiR-132 and miR-212 were up-regulated in HAEC dilated tissues and LPS-treated mice enteritis samples. LPS-stimulated HT29 cells showed a high expression of miR-132 and miR-212. QRT-PCR analysis, western blotting, luciferase reporter assay, and flow cytometric analysis were carried out in vitro, showing that miR-132 and miR-212 could directly inhibit Sirtuin 1 (SIRT1) expression. Consequently, SIRT1 deficiency in LPS-stimulated HT29 cell line and LPS-treated mice activated NLRP3 inflammasome and Caspase-1-mediated pyroptosis. Furthermore, the above inflammation activation was reversed by miR-132/212 inhibitor or SIRT1 overexpression plasmid transfection.In conclusion, LPS upregulated miR-132 and miR-212 expression in HAEC, suppressing SIRT1 and facilitating NLRP3 inflammasome activation, which induced pyroptosis. Our findings illustrated the role of LPS/miR-132/-212/SIRT1/NLRP3 regulatory network in the occurrence and progression of HAEC and proposed a new molecular pathway for LPS-mediated cell pyroptosis.
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Muscle defects due to perturbed somite segmentation contribute to late adult scoliosis

Laura Lleras-Forero, Elis Newham, Stefan Teufel, Koichi Kawakami, Christine Hartmann, Chrissy L. Hammond, Robert D. Knight, Stefan Schulte-Merker,

https://doi.org/10.18632/aging.103856 pp 18603—18621

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Lleras-Forero L, Newham E, Teufel S, Kawakami K, Hartmann C, Hammond CL, Knight RD, Schulte-Merker S, . Muscle defects due to perturbed somite segmentation contribute to late adult scoliosis. . 12:18603-18621. https://doi.org/10.18632/aging.103856

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                TY  - JOUR
                AU  - Lleras-Forero, Laura 
                AU  - Newham, Elis 
                AU  - Teufel, Stefan 
                AU  - Kawakami, Koichi 
                AU  - Hartmann, Christine 
                AU  - Hammond, Chrissy L. 
                AU  - Knight, Robert D. 
                AU  - Schulte-Merker, Stefan 
                TI  - Muscle defects due to perturbed somite segmentation contribute to late adult scoliosis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103856
                DO  - 10.18632/aging.103856
                SP  - 18603
                EP  - 18621
                PY  - 
                AB  - Scoliosis is an abnormal bending of the body axis. Truncated vertebrae or a debilitated ability to control the musculature in the back can cause this condition, but in most cases the causative reason for scoliosis is unknown (idiopathic). Using mutants for somite clock genes with mild defects in the vertebral column, we here show that early defects in somitogenesis are not overcome during development and have long lasting and profound consequences for muscle fiber organization, structure and whole muscle volume. These mutants present only mild alterations in the vertebral column, and muscle shortcomings are uncoupled from skeletal defects. None of the mutants presents an overt musculoskeletal phenotype at larval or early adult stages, presumably due to compensatory growth mechanisms. Scoliosis becomes only apparent during aging. We conclude that adult degenerative scoliosis is due to disturbed crosstalk between vertebrae and muscles during early development, resulting in subsequent adult muscle weakness and bending of the body axis.
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Asymmetrical nigral iron accumulation in Parkinson’s disease with motor asymmetry: an explorative, longitudinal and test-retest study

Xiaojun Guan, Tao Guo, Cheng Zhou, Jingjing Wu, Ting Gao, Xueqin Bai, Hongjiang Wei, Yuyao Zhang, Min Xuan, Quanquan Gu, Peiyu Huang, Chunlei Liu, Baorong Zhang, Jiali Pu, Zhe Song, Yaping Yan, Feng Cui, Minming Zhang, Xiaojun Xu,

https://doi.org/10.18632/aging.103870 pp 18622—18634

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Guan X, Guo T, Zhou C, Wu J, Gao T, Bai X, Wei H, Zhang Y, Xuan M, Gu Q, Huang P, Liu C, Zhang B, et al, . Asymmetrical nigral iron accumulation in Parkinson’s disease with motor asymmetry: an explorative, longitudinal and test-retest study. . 12:18622-18634. https://doi.org/10.18632/aging.103870

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                TY  - JOUR
                AU  - Guan, Xiaojun 
                AU  - Guo, Tao 
                AU  - Zhou, Cheng 
                AU  - Wu, Jingjing 
                AU  - Gao, Ting 
                AU  - Bai, Xueqin 
                AU  - Wei, Hongjiang 
                AU  - Zhang, Yuyao 
                AU  - Xuan, Min 
                AU  - Gu, Quanquan 
                AU  - Huang, Peiyu 
                AU  - Liu, Chunlei 
                AU  - Zhang, Baorong 
                AU  - Pu, Jiali 
                AU  - Song, Zhe 
                AU  - Yan, Yaping 
                AU  - Cui, Feng 
                AU  - Zhang, Minming 
                AU  - Xu, Xiaojun 
                TI  - Asymmetrical nigral iron accumulation in Parkinson’s disease with motor asymmetry: an explorative, longitudinal and test-retest study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103870
                DO  - 10.18632/aging.103870
                SP  - 18622
                EP  - 18634
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Guan, Xiaojun 
                AU  - Guo, Tao 
                AU  - Zhou, Cheng 
                AU  - Wu, Jingjing 
                AU  - Gao, Ting 
                AU  - Bai, Xueqin 
                AU  - Wei, Hongjiang 
                AU  - Zhang, Yuyao 
                AU  - Xuan, Min 
                AU  - Gu, Quanquan 
                AU  - Huang, Peiyu 
                AU  - Liu, Chunlei 
                AU  - Zhang, Baorong 
                AU  - Pu, Jiali 
                AU  - Song, Zhe 
                AU  - Yan, Yaping 
                AU  - Cui, Feng 
                AU  - Zhang, Minming 
                AU  - Xu, Xiaojun 
                TI  - Asymmetrical nigral iron accumulation in Parkinson’s disease with motor asymmetry: an explorative, longitudinal and test-retest study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103870
                DO  - 10.18632/aging.103870
                SP  - 18622
                EP  - 18634
                PY  - 
                AB  - Parkinson&#x2019;s disease (PD) is commonly characterized by asymmetrical motor impairment. This study aimed to clarify the iron distributions in PD patients with significant motor asymmetry and their longitudinal alterations. This study included 123 PD patients and 121 normal controls. Thirty-eight PD patients were revisited. PD patients with significant motor asymmetry were identified by using an objective criterion. Inter-group, inter-hemisphere and inter-visit differences of regional tissue susceptibility were analyzed. Iron accumulation in dominantly and non-dominantly affected substantia nigra (SN) were observed in PD patients with motor asymmetry compared with normal controls (p &lt; 0.005, Bonferroni corrected). Iron accumulation in the dominantly affected SN was significantly higher than that in the non-dominantly affected SN (p &lt; 0.01, Bonferroni corrected). After follow-up, time effect on the iron content in SN was observed, directing to decrease in PD patients with motor asymmetry without hemispherical difference (p &lt; 0.05). In conclusion, asymmetrical iron accumulation in SN was associated with the motor asymmetry in PD at baseline, while along the disease evolution iron content in SN became longitudinally decreased. All these findings provide new evidence for PD pathogenesis that the abnormal iron metabolism in SN is complicated and not always unidirectional.
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Visfatin increases ICAM-1 expression and monocyte adhesion in human osteoarthritis synovial fibroblasts by reducing miR-320a expression

Yat-Yin Law, Yu-Min Lin, Shan-Chi Liu, Min-Huan Wu, Wen-Hui Chung, Chun-Hao Tsai, Yi-Chin Fong, Chih-Hsin Tang, Chin-Kun Wang,

https://doi.org/10.18632/aging.103889 pp 18635—18648

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Law Y, Lin Y, Liu S, Wu M, Chung W, Tsai C, Fong Y, Tang C, Wang C, . Visfatin increases ICAM-1 expression and monocyte adhesion in human osteoarthritis synovial fibroblasts by reducing miR-320a expression. . 12:18635-18648. https://doi.org/10.18632/aging.103889

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                TY  - JOUR
                AU  - Law, Yat-Yin 
                AU  - Lin, Yu-Min 
                AU  - Liu, Shan-Chi 
                AU  - Wu, Min-Huan 
                AU  - Chung, Wen-Hui 
                AU  - Tsai, Chun-Hao 
                AU  - Fong, Yi-Chin 
                AU  - Tang, Chih-Hsin 
                AU  - Wang, Chin-Kun 
                TI  - Visfatin increases ICAM-1 expression and monocyte adhesion in human osteoarthritis synovial fibroblasts by reducing miR-320a expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103889
                DO  - 10.18632/aging.103889
                SP  - 18635
                EP  - 18648
                PY  - 
                AB  - Pathophysiological events that modulate the progression of structural changes in osteoarthritis (OA) include monocyte adhesion and infiltration, and synovial inflammation. In particular, the adhesion protein intercellular adhesion molecule type 1 (ICAM-1) promotes monocyte recruitment into the synovial tissue. Visfatin is an adipocyte hormone that promotes the release of inflammatory cytokines during OA progression. We report that visfatin enhances ICAM-1 expression in human OA synovial fibroblasts (OASFs) and facilitates the adhesion of monocytes with OASFs. AMPK and p38 inhibitors, as well as their respective siRNAs, attenuated the effects of visfatin upon ICAM-1 synthesis and monocyte adhesion. We also describe how miR-320a negatively regulates visfatin-induced promotion of ICAM-1 expression and monocyte adhesion. We detail how visfatin affects ICAM-1 expression and monocyte adhesion with OASFs by inhibiting miR-320a synthesis via the AMPK and p38 signaling pathways.
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Knockdown of TXNDC9 induces apoptosis and autophagy in glioma and mediates cell differentiation by p53 activation

Tingting Zheng, Keke Chen, Xue Zhang, Huanhuan Feng, Yu Shi, Li Liu, Jun Zhang, Yun Chen,

https://doi.org/10.18632/aging.103915 pp 18649—18659

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Zheng T, Chen K, Zhang X, Feng H, Shi Y, Liu L, Zhang J, Chen Y, . Knockdown of TXNDC9 induces apoptosis and autophagy in glioma and mediates cell differentiation by p53 activation. . 12:18649-18659. https://doi.org/10.18632/aging.103915

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                TY  - JOUR
                AU  - Zheng, Tingting 
                AU  - Chen, Keke 
                AU  - Zhang, Xue 
                AU  - Feng, Huanhuan 
                AU  - Shi, Yu 
                AU  - Liu, Li 
                AU  - Zhang, Jun 
                AU  - Chen, Yun 
                TI  - Knockdown of TXNDC9 induces apoptosis and autophagy in glioma and mediates cell differentiation by p53 activation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103915
                DO  - 10.18632/aging.103915
                SP  - 18649
                EP  - 18659
                PY  - 
                AB  - Glioma is the most common malignant brain tumor. Because of its high degree of malignancy, the effect of surgical treatment, radiotherapy, chemotherapy, or immunotherapy is not ideal. TXNDC9 belongs to thioredoxin domain-containing proteins, which is involved in tumor progression. However, no research associated with TXNDC9 has been reported in glioma. In this study, we found that TXNDC9 was upregulated in glioma. Knockdown of TXNDC9 would prevent proliferation and metastasis, induce the apoptosis rate of glioma cells, and promote the expression Cleaved-caspase3, Cleaved-caspase8, Cleaved-caspase9. Meanwhile, knockdown of TXNDC9 induced autophagy by increasing the level of LC3 and Beclin-1. Cell morphology and expression analysis of GFAP, Vimentin, verified that TXNDC9 could regulate glioma cell differentiation. During this program, the expression of p53 changes dramatically. The apoptosis, autophagy, and cell differentiation program were blocked by p53 inhibitor treatment. In conclusion, the silencing of TXNDC9 induces apoptosis and autophagy in glioma and promotes cell differentiation by controlling p53 and may function as a new mechanism in glioma.
                ER  -

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β-lactolin increases cerebral blood flow in dorsolateral prefrontal cortex in healthy adults: a randomized controlled trial

Yasuhisa Ano, Keiko Kobayashi, Mamoru Hanyuda, Ryuta Kawashima,

https://doi.org/10.18632/aging.103951 pp 18660—18675

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Ano Y, Kobayashi K, Hanyuda M, Kawashima R, . β-lactolin increases cerebral blood flow in dorsolateral prefrontal cortex in healthy adults: a randomized controlled trial. . 12:18660-18675. https://doi.org/10.18632/aging.103951

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                TY  - JOUR
                AU  - Ano, Yasuhisa 
                AU  - Kobayashi, Keiko 
                AU  - Hanyuda, Mamoru 
                AU  - Kawashima, Ryuta 
                TI  - β-lactolin increases cerebral blood flow in dorsolateral prefrontal cortex in healthy adults: a randomized controlled trial
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103951
                DO  - 10.18632/aging.103951
                SP  - 18660
                EP  - 18675
                PY  - 
                AB  - The number of elderly individuals with age-related cognitive decline or dementia is rapidly increasing. Dairy product consumption, including &#x3B2;-lactolin, is beneficial for their cognitive function. The underlying mechanism of &#x3B2;-lactolin&#x2019;s effects on human brain activity is yet to be investigated. We examined the &#x3B2;-lactolin effects on human cerebral blood flow (CBF) using near-infrared spectroscopy (NIRS) in a placebo-controlled randomized double-blind study, which reported according to the CONSORT guidelines. Fifty healthy participants (aged 45&#x2013;60 years) were randomly allocated into the &#x3B2;-lactolin or the placebo group (n = 25 each) and supplemented for 6 weeks. During the 6th week, oxy-hemoglobin during the working memory tasks was measured using 34-channels (CHs) NIRS. The changes of oxy-hemoglobin, which represents the CBF, in CH 23 located at the left dorsolateral prefrontal cortex (DLPFC) during the spatial working memory task showed higher statistical significance (false discovery rate (q) = 0.045) in the &#x3B2;-lactolin than in the placebo group. The oxy-Hb changes in CH23 have a co-relationship with the working memory task reaction time. This clinical trial showed an increase in the CBF in the left DLPFC area during the 6-week &#x3B2;-lactolin supplementation. This study contributes to elucidating the underlying mechanisms of &#x3B2;-lactolin on cognitive performance.
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Identification of genomic alterations and associated transcriptomic profiling reveal the prognostic significance of MMP14 and PKM2 in patients with pancreatic cancer

Haiwei Wang, Xinrui Wang, Liangpu Xu, Yingying Lin, Ji Zhang, Hua Cao,

https://doi.org/10.18632/aging.103958 pp 18676—18692

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Wang H, Wang X, Xu L, Lin Y, Zhang J, Cao H, . Identification of genomic alterations and associated transcriptomic profiling reveal the prognostic significance of MMP14 and PKM2 in patients with pancreatic cancer. . 12:18676-18692. https://doi.org/10.18632/aging.103958

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                TY  - JOUR
                AU  - Wang, Haiwei 
                AU  - Wang, Xinrui 
                AU  - Xu, Liangpu 
                AU  - Lin, Yingying 
                AU  - Zhang, Ji 
                AU  - Cao, Hua 
                TI  - Identification of genomic alterations and associated transcriptomic profiling reveal the prognostic significance of MMP14 and PKM2 in patients with pancreatic cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103958
                DO  - 10.18632/aging.103958
                SP  - 18676
                EP  - 18692
                PY  - 
                AB  - Pancreatic cancer is characterized by multiple genomic
                alterations, including KRAS mutations, TP53 mutations and CDKN2A deletion.
                However, the prognostic relevance of those genomic alterations and associated
                transcriptomic profiling in pancreatic cancer are unclear. Integrated analysis
                of The Cancer Genome Atlas (TCGA) datasets revealed that KRAS mutation, TP53
                mutation and CDKN2A deletion were all bad prognostic factors in pancreatic
                cancer. And KRAS mutation, TP53 mutation and CDKN2A deletion were coordinated
                and co-occurred in pancreatic cancer. Transcriptomic analysis showed that MMP14
                and PKM2 were both up-regulated by KRAS mutation, TP53 mutation or CDKN2A
                deletion. Also, MMP14 and PKM2 were both associated with unfavorable outcomes
                in pancreatic cancer. Compared with normal tissues, MMP14 and PKM2 were
                up-regulated in pancreatic cancer tissues. Moreover, MMP14 and PKM2 were highly
                expressed in high grade of pancreatic cancer. Furthermore, MMP14 and PKM2 were
                correlated with each other, and the combination of MMP14 and PKM2 could be used
                as better prognostic markers than MMP14 or PKM2 alone. At last, the high
                expression and bad prognostic effects of MMP14 and PKM2 in pancreatic cancer
                were validated using tissue microarray. Overall, the genomic alterations and
                associated transcriptomic profiling analysis suggested new prognostic makers of
                MMP14 and PKM2 in pancreatic cancer.
                ER  -

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Resemblance and differences in dietary restriction nephroprotective mechanisms in young and old rats

Nadezda V. Andrianova, Ljubava D. Zorova, Irina B. Pevzner, Vasily A. Popkov, Valery P. Chernikov, Denis N. Silachev, Egor Y. Plotnikov, Dmitry B. Zorov,

https://doi.org/10.18632/aging.103960 pp 18693—18715

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Andrianova NV, Zorova LD, Pevzner IB, Popkov VA, Chernikov VP, Silachev DN, Plotnikov EY, Zorov DB, . Resemblance and differences in dietary restriction nephroprotective mechanisms in young and old rats. . 12:18693-18715. https://doi.org/10.18632/aging.103960

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                TY  - JOUR
                AU  - Andrianova, Nadezda V. 
                AU  - Zorova, Ljubava D. 
                AU  - Pevzner, Irina B. 
                AU  - Popkov, Vasily A. 
                AU  - Chernikov, Valery P. 
                AU  - Silachev, Denis N. 
                AU  - Plotnikov, Egor Y. 
                AU  - Zorov, Dmitry B. 
                TI  - Resemblance and differences in dietary restriction nephroprotective mechanisms in young and old rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103960
                DO  - 10.18632/aging.103960
                SP  - 18693
                EP  - 18715
                PY  - 
                AB  - Dietary restriction (DR) is the strategy ameliorating the morbidity of various pathologies, including age-associated diseases. Acute kidney injury (AKI) remains a problem for the elderly with DR being a promising approach for diminishing its consequences. We evaluated the possible nephroprotective potential of short-term DR in young and old rats. DR in young rats resulted in pronounced beneficial effects normalizing lipid metabolism (triglycerides concentration, adiponectin level) activating autophagic-lysosomal system evaluated by LC3II/LC3I ratio, LAMP1, p62/SQSTM1 levels, and LysoTracker Green staining. DR had a remarkable recovering effect on mitochondrial structure and functions including regaining of mitochondrial membrane potential, the elevation of SIRT-3, PGC-1&#x3B1;, Bcl-XL levels and partial restoration of ultrastructure. The beneficial effects of DR resulted in the mitigation of oxidative stress including a decrease in levels of protein carbonylation and lipid peroxidation. Aging led to decreased activity of autophagy, elevated oxidative stress and impaired kidney regenerative capacity. Eventually, in old rats, even 8-week DR was not able to ameliorate AKI, but it caused some rejuvenating effects including elevation of mitochondrial membrane potential and Bcl-XL levels, as well as lowered severity of the oxidative stress. Thus, the age-associated decline of protective signaling demands extended DR to achieve nephroprotective potential in old animals.
                ER  -

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Identification of robust genetic signatures associated with lipopolysaccharide-induced acute lung injury onset and astaxanthin therapeutic effects by integrative analysis of RNA sequencing data and GEO datasets

Kaimin Mao, Wei Geng, Yuhan Liao, Ping Luo, Hua Zhong, Pei Ma, Juanjuan Xu, Shuai Zhang, Qi Tan, Yang Jin,

https://doi.org/10.18632/aging.104042 pp 18716—18740

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Mao K, Geng W, Liao Y, Luo P, Zhong H, Ma P, Xu J, Zhang S, Tan Q, Jin Y, . Identification of robust genetic signatures associated with lipopolysaccharide-induced acute lung injury onset and astaxanthin therapeutic effects by integrative analysis of RNA sequencing data and GEO datasets. . 12:18716-18740. https://doi.org/10.18632/aging.104042

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                TY  - JOUR
                AU  - Mao, Kaimin 
                AU  - Geng, Wei 
                AU  - Liao, Yuhan 
                AU  - Luo, Ping 
                AU  - Zhong, Hua 
                AU  - Ma, Pei 
                AU  - Xu, Juanjuan 
                AU  - Zhang, Shuai 
                AU  - Tan, Qi 
                AU  - Jin, Yang 
                TI  - Identification of robust genetic signatures associated with lipopolysaccharide-induced acute lung injury onset and astaxanthin therapeutic effects by integrative analysis of RNA sequencing data and GEO datasets
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104042
                DO  - 10.18632/aging.104042
                SP  - 18716
                EP  - 18740
                PY  - 
                AB  - Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are life-threatening clinical conditions predominantly arising from uncontrolled inflammatory reactions. It has been found that the administration of astaxanthin (AST) can exert protective effects against lipopolysaccharide (LPS)-induced ALI; however, the robust genetic signatures underlying LPS induction and AST treatment remain obscure. Here we performed a statistical meta-analysis of five publicly available gene expression datasets from LPS-induced ALI mouse models, conducted RNA-sequencing (RNA-seq) to screen differentially expressed genes (DEGs) in response to LPS administration and AST treatment, and integrative analysis to determine robust genetic signatures associated with LPS-induced ALI onset and AST administration. Both the meta-analyses and our experimental data identified a total of 198 DEGs in response to LPS administration, and 11 core DEGs (Timp1, Ly6i, Cxcl13, Irf7, Cxcl5, Ccl7, Isg15, Saa3, Saa1, Tgtp1, and Gbp11) were identified to be associated with AST therapeutic effects. Further, the 11 core DEGs were verified by quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC), and functional enrichment analysis revealed that these genes are primarily associated with neutrophils and chemokines. Collectively, these findings unearthed the robust genetic signatures underlying LPS administration and the molecular targets of AST for ameliorating ALI/ARDS which provide directions for further research.
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A comprehensive analysis of the fatal toxic effects associated with CD19 CAR-T cell therapy

Changjing Cai, Diya Tang, Ying Han, Edward Shen, Omar Abdihamid Ahmed, Cao Guo, Hong Shen, Shan Zeng,

https://doi.org/10.18632/aging.104058 pp 18741—18753

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Cai C, Tang D, Han Y, Shen E, Ahmed OA, Guo C, Shen H, Zeng S, . A comprehensive analysis of the fatal toxic effects associated with CD19 CAR-T cell therapy. . 12:18741-18753. https://doi.org/10.18632/aging.104058

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                TY  - JOUR
                AU  - Cai, Changjing 
                AU  - Tang, Diya 
                AU  - Han, Ying 
                AU  - Shen, Edward 
                AU  - Ahmed, Omar Abdihamid 
                AU  - Guo, Cao 
                AU  - Shen, Hong 
                AU  - Zeng, Shan 
                TI  - A comprehensive analysis of the fatal toxic effects associated with CD19 CAR-T cell therapy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104058
                DO  - 10.18632/aging.104058
                SP  - 18741
                EP  - 18753
                PY  - 
                AB  - To determine the incidence, spectrum, timing, and clinical features of CD19 Chimeric antigen receptor (CAR-T) cell therapy-associated fatal toxic effects. We initiated a comprehensive analysis. First, we retrospectively queried the real-world data from a World Health Organization (WHO) pharmacovigilance database (Vigilyze). Furthermore, we performed a meta-analysis of published trials of CD19 CAR-T cell therapy. From screening the WHO database, we identified 1200 patients: 499 received Kymriah therapy, and 701 received Yescarta therapy. We compared the adverse reactions of the two drugs. We evaluated all published clinical trials, comprising 19 trials and 890 patients. Our meta-analysis showed that the incidence of fatal toxic effects associated with death was 5.4%. Infections and infestations appeared to present the highest risk of death. The toxic effect specific median time to death was 30, 30, and 68 days for total, cytokine release syndrome (CRS), and nervous system disorders (NSD), respectively. We observed a high mortality rate for some toxic effects and an early onset of death with varied causes, indicating the need for clinicians to pay more attention to the monitoring and treatment of these fatal toxic effects when using CD19 CAR-T cell therapy, especially for infections and infestations.
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COVID-19
Neurological manifestations in COVID-19 and its possible mechanism

Xiaojia Tang, Yuhan Luo, Yuxia Song, Hongyang Fan, Sisi Dong, Peipei Liu, Yingzhu Chen,

https://doi.org/10.18632/aging.103732 pp 18754—18764

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Tang X, Luo Y, Song Y, Fan H, Dong S, Liu P, Chen Y, . Neurological manifestations in COVID-19 and its possible mechanism. . 12:18754-18764. https://doi.org/10.18632/aging.103732

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                TY  - JOUR
                AU  - Tang, Xiaojia 
                AU  - Luo, Yuhan 
                AU  - Song, Yuxia 
                AU  - Fan, Hongyang 
                AU  - Dong, Sisi 
                AU  - Liu, Peipei 
                AU  - Chen, Yingzhu 
                TI  - Neurological manifestations in COVID-19 and its possible mechanism
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103732
                DO  - 10.18632/aging.103732
                SP  - 18754
                EP  - 18764
                PY  - 
                AB  - In December 2019, the first cases of the acute respiratory illness now known as Corona Virus Disease 2019 (COVID-19) occurred in Wuhan, Hubei Province, China. The main clinical manifestations of COVID-19 are a fever, dry cough and general weakness, although in some patients, a headache, tight chest, diarrhea, etc. are the first clinical manifestations. Neurological practice is involved in all aspects of medicine, from primary care for patients with migraines to consultations with patients in the intensive care unit. Few disorders spare the nervous system, and newly emerging infections are no exception. As neurologists, we are concerned about the effects of SARS-CoV-2 infections on the nervous system. Multiple neuropathy, rhabdomyolysis, cerebrovascular disease, central nervous system infections and other common neurological diseases require attention during this outbreak.
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Psychological aging, depression, and well-being

Maria Mitina, Sergey Young, Alex Zhavoronkov,

https://doi.org/10.18632/aging.103880 pp 18765—18777

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Mitina M, Young S, Zhavoronkov A, . Psychological aging, depression, and well-being. . 12:18765-18777. https://doi.org/10.18632/aging.103880

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                TY  - JOUR
                AU  - Mitina, Maria 
                AU  - Young, Sergey 
                AU  - Zhavoronkov, Alex 
                TI  - Psychological aging, depression, and well-being
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103880
                DO  - 10.18632/aging.103880
                SP  - 18765
                EP  - 18777
                PY  - 
                AB  - Aging is a multifactorial process, which affects the human body on every level and results in both biological and psychological changes. Multiple studies have demonstrated that a lower subjective age is associated with better mental and physical health, cognitive functions, well-being and satisfaction with life. In this work we propose a list of non-modifiable and modifiable factors that may possibly be influenced by subjective age and its changes across an individual&#x2019;s lifespan. These factors can be used for a future development of individual psychological aging clocks, which may be utilized as a sensitive measure for health status and overall life satisfaction. Furthermore, recent progress in artificial intelligence and biomarkers of biological aging have enabled scientists to discover and evaluate the efficacy of potential aging- and disease-modifying drugs and interventions. We propose that biomarkers of psychological age, which are just as important as those for biological age, may likewise be used for these purposes. Indeed, these two types of markers complement one another. We foresee the development of a broad range of parametric and deep psychological and biopsychological aging clocks, which may have implications for drug development and therapeutic interventions, and thus healthcare and other industries.
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COVID-19
SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime

Renato Domingues, Alice Lippi, Cristian Setz, Tiago F. Outeiro, Anita Krisko,

https://doi.org/10.18632/aging.103989 pp 18778—18789

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Domingues R, Lippi A, Setz C, Outeiro TF, Krisko A, . SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime. . 12:18778-18789. https://doi.org/10.18632/aging.103989

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                TY  - JOUR
                AU  - Domingues, Renato 
                AU  - Lippi, Alice 
                AU  - Setz, Cristian 
                AU  - Outeiro, Tiago F. 
                AU  - Krisko, Anita 
                TI  - SARS-CoV-2, immunosenescence and inflammaging: partners in the COVID-19 crime
                JO  - 
                JA  - 
                VL  - 12
                IS  - 18
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103989
                DO  - 10.18632/aging.103989
                SP  - 18778
                EP  - 18789
                PY  - 
                AB  - Pneumonia outbreak in the city of Wuhan, China, prompted the finding of a novel strain of severe acute respiratory syndrome virus (SARS-CoV-2). Here, we discuss potential long-term consequences of SARS-CoV-2 infection, and its possibility to cause permanent damage to the immune system and the central nervous system. Advanced chronological age is one of the main risk factors for the adverse outcomes of COVID-19, presumably due to immunosenescence and chronic low-grade inflammation, both characteristic of the elderly. The combination of viral infection and chronic inflammation in advanced chronological age might cause multiple detrimental unforeseen consequences for the predisposition and severity of neurodegenerative diseases and needs to be considered so that we can be prepared to deal with future outcomes of the ongoing pandemic.
                ER  -

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Correction for: hsa_circRNA6448-14 promotes carcinogenesis in esophageal squamous cell carcinoma

Yaowen Zhang, Xiang Yuan, Ning Yue, Lidong Wang, Junqi Liu, Ningtao Dai, Haijun Yang, Ruitai Fan, Fuyou Zhou,

https://doi.org/10.18632/aging.104164 pp 18790

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Zhang Y, Yuan X, Yue N, Wang L, Liu J, Dai N, Yang H, Fan R, Zhou F, . Correction for: hsa_circRNA6448-14 promotes carcinogenesis in esophageal squamous cell carcinoma. . 12:18790-18790. https://doi.org/10.18632/aging.104164

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Volume 12, Issue 18

About the Cover

Editorials

Anubhuti Dixit, Varsha Singh,

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Alejandro Mata-Cabana, Francisco Javier Romero-Expósito, María Olmedo,

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Mario D. Cordero, Jesús Ruiz-Cabello,

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Priority Research Papers

Jun Tan, Xiangyu Wang, Bor-Jang Hwang, Rex Gonzales, Olivia Konen, Li Lan, A-Lien Lu,

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Zhigang Zhang, He N. Xu, Siyu Li, Antonio Davila Jr, Karthikeyani Chellappa, James G. Davis, Yuxia Guan, David W. Frederick, Weiqing Chu, Huaqing Zhao, Lin Z. Li, Joseph A. Baur,

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Divya Venkatesh, Brent R. Stockwell, Carol Prives,

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Research Papers

Alexei Kurakin, Dale E. Bredesen,

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Xiaoqi Zhu, Junyan Shen, Shengyu Feng, Ce Huang, Zhongmin Liu, Yi Eve Sun, Hailiang Liu,

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Qi Yan, Kimberly C. Paul, Ake T. Lu, Cynthia Kusters, Alexandra M. Binder, Steve Horvath, Beate Ritz,

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Sabela Da Silva-Álvarez, Jorge Guerra-Varela, Daniel Sobrido-Cameán, Ana Quelle, Antón Barreiro-Iglesias, Laura Sánchez, Manuel Collado,

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Qi Chen, Sheng Min Guo, Hou Qiang Huang, Guo Ping Huang, Yi Li, Zi Hui Li, Run Huang, Lu Xiao, Chun Rong Fan, Qing Yuan, Si Lin Zheng,

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Shunliang Sheng, Yi Hu, Furong Yu, Wenjuan Tong, Shufen Wang, Yanlin Cai, Jiayu Zhu,

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Chun-Hao Chan, Chia-Yu Wu, Navneet Kumar Dubey, Hong-Jian Wei, Jui-Hua Lu, Samantha Mao, Joy Liang, Yu-Hsuan Liang, Hsin-Chung Cheng, Win-Ping Deng,

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Jianlong Bu, Pinyi Zhang, Kaibin Zhu, Yubo Yan, Bowen Shi, Junfeng Wang, Shidong Xu,

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Shichao Zhang, Zhu Zeng, Yongfen Liu, Jiangtao Huang, Jinhua Long, Yun Wang, Xiaoyan Peng, Zuquan Hu, Yan Ouyang,

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Xiaoyu Cheng, Tian Liu, Lidan Ma, Zhen Liu, Ying Xin, Zhaotong Jia, Ying Chen, Changgui Li, Ruixia Sun,

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Ling-Hsuan Wu, Bor-Ren Huang, Sheng-Wei Lai, Chingju Lin, Hsiao-Yun Lin, Liang-Yo Yang, Dah-Yuu Lu,

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Zongying Li, Shuyi Cao,

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Liang Shao, Wei Sun, Hao Zhang, Ping Zhang, Zhihong Wang, Wenwu Dong, Liang He, Ting Zhang, Yuan Qin,

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