MicroRNA-93 inhibits ischemia-reperfusion induced cardiomyocyte apoptosis by targeting PTEN

被引:93
作者
Ke, Zun-Ping [1 ]
Xu, Peng [1 ]
Shi, Yan [2 ,3 ]
Gao, Ai-Mei [4 ]
机构
[1] Fudan Univ, Peoples Hosp Shanghai 5, Dept Cardiol, Shanghai 200433, Peoples R China
[2] Xuzhou Med Coll, Affiliated Huaian Hosp, Dept Emergency, Huaian, Peoples R China
[3] Second Peoples Hosp Huaian, Huaian, Peoples R China
[4] Fudan Univ, Peoples Hosp Shanghai 5, Dept Pharm, Shanghai 200433, Peoples R China
关键词
microRNA-93; ischemia/reperfusion; PTEN; AKT; apoptosis; Pathology Section; INJURY; PROLIFERATION; PHOSPHATASE; EXPRESSION; REDUCTION; PROTECTS;
D O I
10.18632/oncotarget.8941
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNAs have been implicated in some biological and pathological processes, including the myocardial ischemia/reperfusion (I/R) injury. Recent findings demonstrated that miR-93 might provide a potential cardioprotective effect on ischemic heart disease. This study was to investigate the role of miR-93 in I/Rinduced cardiomyocyte injury and the potential mechanism. In this study, we found that hypoxia/reoxygenation (H/R) dramatically increased LDH release, MDA contents, ROS generation, and endoplasmic reticulum stress (ERS)-mediated cardiomyocyte apoptosis, which were attenuated by co-transfection with miR-93 mimic. Phosphatase and tensin homolog (PTEN) was identified as the target gene of miR-93. Furthermore, miR-93 mimic significantly increased p-Akt levels under H/R, which was partially released by LY294002. In addtion, Ad-miR-93 also attenuated myocardial I/R injury in vivo, manifested by reduced LDH and CK levels, infarct area and cell apoptosis. Taken together, our findings indicates that miR-93 could protect against I/R-induced cardiomyocyte apoptosis by inhibiting PI3K/AKT/PTEN signaling.
引用
收藏
页码:28796 / 28805
页数:10
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