Alzheimer's Amyloid-beta Accelerates Human Neuronal Cell Senescence Which Could Be Rescued by Sirtuin-1 and Aspirin
2022-06-17
发表期刊FRONTIERS IN CELLULAR NEUROSCIENCE (IF:4.2[JCR-2023],5.1[5-Year])
EISSN1662-5102
卷号16
发表状态已发表
DOI10.3389/fncel.2022.906270
摘要Cellular senescence is a major biological process related to aging. Neuronal cell senescence contributes to the pathogenesis of many aging-related neurodegenerative diseases including Alzheimer's disease (AD). In this study, we showed that amyloid-beta(42) oligomers (A beta), one of the core pathological players of AD, significantly upregulated the expression of senescence markers, p21, plasminogen activator inhibitor-1 (PAI-1), and SA-beta-gal (senescence-associated beta-galactosidase) in multiple human neuronal cells, including SK-N-SH cells, SH-SY5Y cells, and neural stem cell (NSC)-derived neuronal cells. Moreover, it was consistently observed among the cells that A beta promoted senescence-associated DNA damage as the levels of 8-OHdG staining, histone variant H2AX phosphorylation (gamma-H2AX), and genomic DNA lesion increased. Mechanism study revealed that the exposure of A beta markedly suppressed the expression of sirtuin-1 (SIRT1), a critical regulator of aging, and the exogenous expression of SIRT1 alleviated A beta-induced cell senescence phenotypes. To our surprise, a widely used cardiovascular drug aspirin considerably rescued A beta-induced cellular senescence at least partially through its regulation of SIRT1. In conclusion, our findings clearly demonstrate that exposure of A beta alone is sufficient to accelerate the senescence of human neuronal cells through the downregulation of SIRT1.
关键词A beta cell senescence human neuronal cells SIRT1 DNA damage
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收录类别SCI ; SCIE
语种英语
资助项目National Key Research and Development Program of China[2018YFA0108003] ; "Strategic Priority Research Program" of the Chinese Academy of Sciences[XDA16010309] ; National Science Foundation for Young Scientists of China[81901094]
WOS研究方向Neurosciences & Neurology
WOS类目Neurosciences
WOS记录号WOS:000885442500001
出版者FRONTIERS MEDIA SA
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文献类型期刊论文
条目标识符https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/251690
专题生命科学与技术学院_特聘教授组_裴钢组
生命科学与技术学院_博士生
通讯作者Huang, Shichao; Pei, Gang
作者单位
1.ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai, Peoples R China
2.Chinese Acad Sci, State Key Lab Cell Biol, CAS Ctr Excellence Mol Cell Sci, Shanghai Inst Biochem & Cell Biol,Univ Chinese Ac, Shanghai, Peoples R China
3.Tongji Univ, Shanghai Key Lab Signaling & Dis Res, Inst Regenerat Med, Shanghai East Hosp,Sch Life Sci & Technol, Shanghai, Peoples R China
4.Tongji Univ, Shanghai Key Lab Signaling & Dis Res, Sch Life Sci & Technol, Collaborat Innovat Ctr Brain Sci, Shanghai, Peoples R China
5.Chinese Acad Sci, Inst Stem Cell & Regenerat, Beijing, Peoples R China
第一作者单位生命科学与技术学院
通讯作者单位生命科学与技术学院
第一作者的第一单位生命科学与技术学院
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GB/T 7714
Li, Yi,Lu, Juan,Hou, Yujun,et al. Alzheimer's Amyloid-beta Accelerates Human Neuronal Cell Senescence Which Could Be Rescued by Sirtuin-1 and Aspirin[J]. FRONTIERS IN CELLULAR NEUROSCIENCE,2022,16.
APA Li, Yi,Lu, Juan,Hou, Yujun,Huang, Shichao,&Pei, Gang.(2022).Alzheimer's Amyloid-beta Accelerates Human Neuronal Cell Senescence Which Could Be Rescued by Sirtuin-1 and Aspirin.FRONTIERS IN CELLULAR NEUROSCIENCE,16.
MLA Li, Yi,et al."Alzheimer's Amyloid-beta Accelerates Human Neuronal Cell Senescence Which Could Be Rescued by Sirtuin-1 and Aspirin".FRONTIERS IN CELLULAR NEUROSCIENCE 16(2022).
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