IMR OpenIR
Apelin protects against cardiomyocyte apoptosis induced by glucose deprivation
其他题名Apelin protects against cardiomyocyte apoptosis induced by glucose deprivation
Zhang Zhi1; Yu Bo1; Tao Guizhou2
2009
发表期刊CHINESE MEDICAL JOURNAL
ISSN0366-6999
卷号122期号:19页码:2360-2365
摘要Background Apoptosis is a major cause of ischemic heart dysfunction. Apelin, the endogenous ligand for the G-protein-coupled AN receptor, has been reported to exert cardioprotective effects during myocardial injury. The aim of this study was to investigate the effects of apelin on apoptosis of rat cardiomyocytes induced by glucose deprivation (GD) and study the related signaling pathway.
其他摘要Background Apoptosis is a major cause of ischemic heart dysfunction. Apelin, the endogenous ligand for the G-protein-coupled APJ receptor, has been reported to exert cardioprotective effects during myocardial injury. The aim of this study was to investigate the effects of apelin on apoptosis of rat cardiomyocytes induced by glucose deprivation (GD) and study the related signaling pathway.Methods Apelin and APJ mRNA expression were determined by RT-PCR in neonatal rat cardiomyocytes during different durations of GD. Cardiomyocyte apoptosis was detected by annexin V-FITC/propidium iodide (PI) staining after GD for 12 hours with or without apelin-13 (10 and 100 nmol/L) pretreatment. Protein levels of Akt and the mammalian target of rapamycin (mTOR) as well as cell apoptosis were detected in the presence or absence of LY294002 (a phosphatidylinositol 3-kinases (PI3K) inhibitor) or rapamycin (a mTOR inhibitor).Results Apelin mRNA expression was up-regulated when cardiomyocytes were exposed to GD for 6, 12, 18, and 24 hours compared with the base level (P >0.05, P <0.01, P <0.01, P <0.01). However, when cardiomyocytes were exposed to GD for up to 36 hours, apelin mRNA expression was 17% lower than the base level (P <0.05). APJ mRNA expression paralleled that of apelin. Apelin-13 pretreatment at 100 nmol/L significantly inhibited GD-induced cardiomyocyte apoptosis (P <0.05) and increased Akt and mTOR phosphorylation (P <0.01, P <0.01). At the same time apelin-13 (100 nmol/L) up-regulated Bcl-2 protein expression and down-regulated Bax and cleaved caspase-3 expression (P <0.01, P <0.05, P <0.05). The anti-apoptotic effect of apelin-13 was blocked by LY294002 (P <0.01) but not by rapamycin. Conclusions The endogenous apelin-APJ system is compensatorily up-regulated and ultimately down-regulated following sustained myocardial ischemia. Apelin protects against ischemic cardiomyocyte apoptosis via activation of the PI3K/Akt pathway.
关键词ISCHEMIC-HEART FAILURE REPERFUSION INJURY APJ RECEPTOR CONTRACTILITY LOCALIZATION EXPRESSION AUTOPHAGY SURVIVAL SALVAGE SYSTEM apelin apoptosis cardiomyocyte phosphatidylinositol 3-OH kinase (PI3K)/Akt
收录类别CSCD
语种英语
CSCD记录号CSCD:3681779
引用统计
文献类型期刊论文
条目标识符http://ir.imr.ac.cn/handle/321006/151908
专题中国科学院金属研究所
作者单位1.中国科学院金属研究所
2.Liaoning Med University, Affiliated Hosp 1, Dept Cardiol, Jinzhou 121001, Liaoning, Peoples R China
推荐引用方式
GB/T 7714
Zhang Zhi,Yu Bo,Tao Guizhou. Apelin protects against cardiomyocyte apoptosis induced by glucose deprivation[J]. CHINESE MEDICAL JOURNAL,2009,122(19):2360-2365.
APA Zhang Zhi,Yu Bo,&Tao Guizhou.(2009).Apelin protects against cardiomyocyte apoptosis induced by glucose deprivation.CHINESE MEDICAL JOURNAL,122(19),2360-2365.
MLA Zhang Zhi,et al."Apelin protects against cardiomyocyte apoptosis induced by glucose deprivation".CHINESE MEDICAL JOURNAL 122.19(2009):2360-2365.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Zhang Zhi]的文章
[Yu Bo]的文章
[Tao Guizhou]的文章
百度学术
百度学术中相似的文章
[Zhang Zhi]的文章
[Yu Bo]的文章
[Tao Guizhou]的文章
必应学术
必应学术中相似的文章
[Zhang Zhi]的文章
[Yu Bo]的文章
[Tao Guizhou]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。