Sestrin2 attenuates cellular senescence by inhibiting NADPH oxidase 4 expression

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dc.contributor.authorChae Young Hwang-
dc.contributor.authorYing Hao Han-
dc.contributor.authorSeung-Min Lee-
dc.contributor.authorSang Mi Cho-
dc.contributor.authorDae Yeul Yu-
dc.contributor.authorKi-Sun Kwon-
dc.date.accessioned2021-01-12T03:30:39Z-
dc.date.available2021-01-12T03:30:39Z-
dc.date.issued2020-
dc.identifier.issn25084798-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/23991-
dc.description.abstractBackground: Sestrin2 (Sesn2) is involved in the maintenance of metabolic homeostasis and aging via modulation of the 5' AMP-activated protein kinase-mammalian target of rapamycin (AMPK-mTOR) pathway. Methods: Wild-type and Sesn2 knockout (KO) mice of the 129/SvJ background were maintained in a pathogen-free authorized facility under a 12-hour dark/light cycle at 20°C-22°C and 50%-60% humidity. Mouse embryonic fibroblasts (MEFs) were prepared from 13.5-day-old embryos derived from Sesn2-KO mice mated with each other. Results: The MEFs from Sesn2-KO mice showed enlarged and flattened morphologies and senescence-associated β-galactosidase activity, accompanied by an elevated level of reactive oxygen species. These senescence phenotypes recovered following treatment with N-acetyl-cysteine. Notably, the mRNA levels of NADPH oxidase 4 (NOX4) and transforming growth factor (TGF)-β were markedly increased in Sesn2-KO MEFs. Treatment of Sesn2-KO MEFs with the NOX inhibitor diphenyleneiodonium and the TGF-β inhibitor SB431542 restored cell growth inhibited by Sesn2-KO. Conclusion: Sesn2 attenuates cellular senescence via suppression of TGF-β- and NOX4-induced reactive oxygen species generation and subsequent inhibition of AMPK.-
dc.publisherKorea Soc-Assoc-Inst-
dc.titleSestrin2 attenuates cellular senescence by inhibiting NADPH oxidase 4 expression-
dc.title.alternativeSestrin2 attenuates cellular senescence by inhibiting NADPH oxidase 4 expression-
dc.typeArticle-
dc.citation.titleAnnals of Geriatric Medicine and Research-
dc.citation.number4-
dc.citation.endPage304-
dc.citation.startPage297-
dc.citation.volume24-
dc.contributor.affiliatedAuthorChae Young Hwang-
dc.contributor.affiliatedAuthorYing Hao Han-
dc.contributor.affiliatedAuthorSeung-Min Lee-
dc.contributor.affiliatedAuthorSang Mi Cho-
dc.contributor.affiliatedAuthorDae Yeul Yu-
dc.contributor.affiliatedAuthorKi-Sun Kwon-
dc.contributor.alternativeName황채영-
dc.contributor.alternativeName한영호-
dc.contributor.alternativeName이승민-
dc.contributor.alternativeName조상미-
dc.contributor.alternativeName유대열-
dc.contributor.alternativeName권기선-
dc.identifier.bibliographicCitationAnnals of Geriatric Medicine and Research, vol. 24, no. 4, pp. 297-304-
dc.identifier.doi10.4235/agmr.20.0051-
dc.subject.keywordNOX4-
dc.subject.keywordReactive oxygen species-
dc.subject.keywordSenescence-
dc.subject.keywordSestrin2-
dc.subject.localNOX4-
dc.subject.localReactive oxygen species-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localSenescence-
dc.subject.localSestrin2-
dc.description.journalClassN-
Appears in Collections:
Division of Research on National Challenges > Aging Research Center > 1. Journal Articles
Ochang Branch Institute > Division of Bioinfrastructure > Laboratory Animal Resource Center > 1. Journal Articles
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