MiR-486 regulates cardiomyocyte apoptosis by p53-mediated BCL-2 associated mitochondrial apoptotic pathway

BMC Cardiovascular Disorders

Research Article

Qiang Su¹  Jiabao Liang¹  Yuanxi Lu¹  Lang Li¹  Yuhan Sun¹  Xiantao Wang¹ 

[1] Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, 530021, Nanning, China;

关键词: Cardiomyocyte;    Apoptosis;    miR-486;    P53;    BCL-2 pathway;   

DOI  :  10.1186/s12872-017-0549-7

 received in 2016-12-19, accepted in 2017-05-02,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundCardiomyocyte apoptosis is a common pathological manifestation that occurs in several heart diseases. This study aimed to explore the mechanism of microRNA-486 (miR-486) in cardiomyocyte apoptosis by interfering with the p53-activated BCL-2 associated mitochondrial pathway.MethodsmiR-486 mimics and inhibitors were transfected into the primary cardiomyocytes of suckling Sprague-Dawley rat pups, and H2O2 was used to induce apoptosis. Flow cytometry and TUNEL were both used to detect cardiomyocyte apoptosis, while the relative mRNA transcript and protein levels of miR-486, p53, Bbc3, BCL-2, and cleaved caspase-3 were detected using RT-PCR and western blot analysis, respectively.ResultsmiR-486 overexpression significantly decreased the expressions of p53, Bbc3 and cleaved caspase-3 (P < 0.05), and BCL-2 expression was significantly increased (P < 0.05), which in turn caused a significant decrease in the rate of cardiomyocyte apoptosis (P < 0.05). In contrast, miR-486 silencing resulted in an elevated rate of cardiomyocyte apoptosis (P < 0.05).ConclusionmiR-486 may regulate cardiomyocyte apoptosis via p53-mediated BCL-2 associated mitochondrial apoptotic pathway. Therefore, up-regulating miR-486 expression in cardiomyocytes can effectively reduce the activation of the BCL-2 associated mitochondrial apoptotic pathway, consequently protecting cardiomyocytes.

【 授权许可】

CC BY   
© The Author(s). 2017

【 图 表 】

Fig. 1