A novel adipocytokine visfatin protects against H2O2-induced myocardial apoptosis: A missing link between obesity and cardiovascular disease

doi:10.1002/jcp.24257

科研成果详情

题名	A novel adipocytokine visfatin protects against H2O2-induced myocardial apoptosis: A missing link between obesity and cardiovascular disease
作者	Xiao, Jing 1,2; Sun, Bing 1,2; Li, Ming 3; Wu, Ying 3; Sun, Xiao-Bo 1,2
发表日期	2013-03
发表期刊	JOURNAL OF CELLULAR PHYSIOLOGY 影响因子和分区
语种	英语
原始文献类型	Article
其他关键词	COLONY-ENHANCING FACTOR ; METABOLIC SYNDROME ; NICOTINAMIDE PHOSPHORIBOSYLTRANSFERASE ; EXPRESSION ; IMPACT ; CARDIOMYOCYTES ; OUTCOMES ; THERAPY ; PARADOX ; PATHWAY
摘要	Fat accumulation in obese individuals worsens the clinical outcomes of cardiovascular disease (CVD). Paradoxically, increased circulating adipocytokines secreted from visceral fat may confer cardioprotective effects. Visfatin, a novel adipocytokine, has anti-diabetic, anti-tumor, and pro-inflammatory properties. However, its effects on cardiomyocytes and the underlying mechanisms remain unknown. This article demonstrated that visfatin counteracted H2O2-induced apoptotic damage in H9c2 cardiomyocytes in a time-dependent manner. Qualitative immunofluorescence approaches demonstrated that visfatin pretreatment attenuated H2O2-induced DNA fragmentation (TdT-mediated dUTP-biotin nick end-labeling), phosphatidyl serine exposure (Annexin V/PI staining), and mitochondrial membrane potential (??m) depolarization (JC-1 staining). Biochemical studies on cardiomyoctes showed improved cell viability and reduced caspase-3 activation caused by visfatin pretreatment. Visfatin did not inhibit the death receptor-dependent apoptotic pathways, as characterized by its absence in both Fas and TNFR1 down-regulation. Instead, visfatin specifically suppressed the mitochondria-dependent apoptotic pathways, as characterized by changed levels of p53 and its downstream Bcl-2 family genes. Visfatin also up-regulated the protein levels of phosphorylated AMPK, and the anti-apoptotic action of visfatin was attenuated by the AMPK-specific inhibitor compound C. These results suggested that visfatin plays a critical role in cardioprotection by suppressing myocardial apoptosis via AMPK activation. These findings may be the missing link between obesity and CVD. J. Cell. Physiol. 228: 495501, 2013. (C) 2012 Wiley Periodicals, Inc.
资助项目	Major scientific and technological special project for significant new drugs formulation [2012ZX09501001]; Chinese Postdoctoral Science FoundationChina Postdoctoral Science Foundation [20110490325]
出版者	WILEY
出版地	HOBOKEN
ISSN	0021-9541
EISSN	1097-4652
卷号	228 期号:3 页码:495-501
DOI	10.1002/jcp.24257
页数	7
WOS类目	Cell Biology ; Physiology
WOS研究方向	Cell Biology ; Physiology
WOS记录号	WOS:000311912900001
收录类别	SCIE ; SCOPUS
URL	查看原文
PubMed ID	23065734
SCOPUSEID	2-s2.0-84870398212
通讯作者地址	[Sun, Xiao-Bo]Chinese Acad Med Sci, Inst Med Plant Dev IMPLAD, Res Ctr Pharmacol & Toxicol, 151 Malianwa N Rd, Beijing 100193, Peoples R China.
引用统计	被引频次：27[WOS] [WOS记录] [WOS相关记录]
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/8560
专题	第二临床医学院、附属第二医院、育英儿童医院_中医系
通讯作者	Sun, Xiao-Bo
作者单位	1.Chinese Acad Med Sci, Inst Med Plant Dev IMPLAD, Res Ctr Pharmacol & Toxicol, Beijing 100193, Peoples R China; 2.Peking Union Med Coll, Beijing 100193, Peoples R China; 3.Wenzhou Med Coll, Acad Chinese Mat Med, Wenzhou, Peoples R China
推荐引用方式 GB/T 7714	Xiao, Jing,Sun, Bing,Li, Ming,et al. A novel adipocytokine visfatin protects against H2O2-induced myocardial apoptosis: A missing link between obesity and cardiovascular disease[J]. JOURNAL OF CELLULAR PHYSIOLOGY,2013,228(3):495-501.
APA	Xiao, Jing, Sun, Bing, Li, Ming, Wu, Ying, & Sun, Xiao-Bo. (2013). A novel adipocytokine visfatin protects against H2O2-induced myocardial apoptosis: A missing link between obesity and cardiovascular disease. JOURNAL OF CELLULAR PHYSIOLOGY, 228(3), 495-501.
MLA	Xiao, Jing,et al."A novel adipocytokine visfatin protects against H2O2-induced myocardial apoptosis: A missing link between obesity and cardiovascular disease".JOURNAL OF CELLULAR PHYSIOLOGY 228.3(2013):495-501.