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Apelin protects against cardiomyocyte apoptosis induced by glucose deprivation
Alternative TitleApelin protects against cardiomyocyte apoptosis induced by glucose deprivation
Zhang Zhi1; Yu Bo1; Tao Guizhou2
2009
Source PublicationCHINESE MEDICAL JOURNAL
ISSN0366-6999
Volume122Issue:19Pages:2360-2365
AbstractBackground 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.
Other AbstractBackground 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.
KeywordISCHEMIC-HEART FAILURE REPERFUSION INJURY APJ RECEPTOR CONTRACTILITY LOCALIZATION EXPRESSION AUTOPHAGY SURVIVAL SALVAGE SYSTEM apelin apoptosis cardiomyocyte phosphatidylinositol 3-OH kinase (PI3K)/Akt
Indexed ByCSCD
Language英语
CSCD IDCSCD:3681779
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Document Type期刊论文
Identifierhttp://ir.imr.ac.cn/handle/321006/151908
Collection中国科学院金属研究所
Affiliation1.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
Recommended Citation
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.
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