标题:SIRT5 prevents cigarette smoke extract-induced apoptosis in lung epithelial cells via deacetylation of FOXO3
作者:Wang, Yongfeng; Zhu, Yuanbin; Xing, Shigang; Ma, Ping; Lin, Dianjie
作者机构:[Wang, Yongfeng; Lin, Dianjie] Shandong Univ, Sch Med, Jinan 250012, Shandong, Peoples R China.; [Wang, Yongfeng; Zhu, Yuanbin; Xing, Shigang; Ma, P 更多
通讯作者:Lin, DJ
通讯作者地址:[Lin, DJ]Shandong Univ, Sch Med, 44 Wenhua West Rd, Jinan 250012, Shandong, Peoples R China.
来源:CELL STRESS & CHAPERONES
出版年:2015
卷:20
期:5
页码:805-810
DOI:10.1007/s12192-015-0599-7
关键词:Chronic obstructive pulmonary disease; Cigarette smoking; SIRT5; FOXO3;; Apoptosis
摘要:Cigarette smoking plays an important role in increased incidence of chronic obstructive pulmonary disease (COPD). The underlying mechanism in which cigarette smoking induced impairment of lung epithelial cells is still unknown. SIRT5 is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase, which has been implicated in the regulation of metabolism, stress responses, and aging. Forkhead box O-3 (FOXO3) belongs to the O subclass of the forkhead family of transcription factors. It is also involved in protection from oxidative stress by upregulating antioxidants in epithelial cells. Here, we show that cigarette smoke extract (CSE) induces SIRT5 to deacetylate FOXO3 at K271 and K290. Deacetylation of FOXO3 promotes its nuclear localization. Notably, transfection with FOXO3 K271R- or K290R-attenuated CSE-induced apoptosis in SIRT5 knocked down cells, suggesting the protective effects of SIRT5, is mediated by FOXO3. In contrast, CSE stress upregulates SIRT5, which activates FOXO3 alpha leading to rescuing apoptosis. Thus, SIRT5 constitutes a determinant of apoptosis by CSE in lung epithelial cells.
收录类别:SCOPUS;SCIE
WOS核心被引频次:11
Scopus被引频次:14
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84938751485&doi=10.1007%2fs12192-015-0599-7&partnerID=40&md5=95ed0e38f454d626be583e1c433f7d80
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