MicroRNA-204 protects H9C2 cells against hypoxia/reoxygenation-induced injury through regulating SIRT1-mediated autophagy

被引:43
|
作者
Qiu, Ruixia [1 ]
Li, Wen [2 ]
Liu, Yunhai [2 ]
机构
[1] 1 Peoples Hosp Jining City, Dept Med Affairs, Jining, Shandong, Peoples R China
[2] 1 Peoples Hosp Jining City, Dept Emergency, 6 Jiankang Rd, Jining 272011, Shandong, Peoples R China
关键词
microRNA-204; H9C2; cells; Hypoxia/reoxygenation injury; Apoptosis; Autophagy; SIRT1; ISCHEMIA/REPERFUSION INJURY; MYOCARDIAL-INFARCTION; APOPTOSIS; CARDIOMYOCYTES; EXPRESSION; TARGET; SIRT1;
D O I
10.1016/j.biopha.2018.01.165
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Ischemia/reperfusion (I/R) injury is a main cause of acute myocardial infarction, and the pathogenesis of I/R injury is still not definitely confirmed. In the present study, we aimed to explore the roles of miR-204 in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury in vitro. The H9C2 cells were subjected to hypoxia for 12 h followed by reoxygenation for another 24 h, and we found that miR-204 was significantly down-regulated after H/R treatment. Transfection of miR-204 mimics attenuated the H/R-induced impaired cell viability and increased apoptosis rates. Furthermore, SIRT1 was identified as a direct target of miR-204, and its expression is negatively regulated by miR-204. Forced expression of SIRT1 could partly rescue the effects of miR-204 on H/Rinduced apoptosis and autophagy. Taken together, our study first revealed that overexpression of miR-204 has a protective effect against myocardial I/R injury.
引用
收藏
页码:15 / 19
页数:5
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