Critical roles of microRNA-141-3p and CHD8 in hypoxia/reoxygenation-induced cardiomyocyte apoptosis

Cell & Bioscience

Yu Zhou¹  Jia Hu²  Anna Qin²  Xinbin Zheng²  Yeshuo Ma²  Ting Zhong²  Bifeng Yao²  Deling Yin²  Xiaoya Wan² 

[1] Department of Neurology, Renmin Hospital of Wuhan University;Xiangya School of Pharmaceutical Science, Central South University;

关键词: MiR-141-3p;    CHD8;    Cardiomyocyte;    Apoptosis;    Hypoxia/reoxygenation;    P21;   

DOI  :  10.1186/s13578-020-00384-5

来源: DOAJ

【 摘 要 】

Abstract Background Cardiovascular diseases are currently the leading cause of death in humans. The high mortality of cardiac diseases is associated with myocardial ischemia and reperfusion (I/R). Recent studies have reported that microRNAs (miRNAs) play important roles in cell apoptosis. However, it is not known yet whether miR-141-3p contributes to the regulation of cardiomyocyte apoptosis. It has been well established that in vitro hypoxia/reoxygenation (H/R) model can follow in vivo myocardial I/R injury. This study aimed to investigate the effects of miR-141-3p and CHD8 on cardiomyocyte apoptosis following H/R. Results We found that H/R remarkably reduces the expression of miR-141-3p but enhances CHD8 expression both in mRNA and protein in H9c2 cardiomyocytes. We also found either overexpression of miR-141-3p by transfection of miR-141-3p mimics or inhibition of CHD8 by transfection of small interfering RNA (siRNA) significantly decrease cardiomyocyte apoptosis induced by H/R. Moreover, miR-141-3p interacts with CHD8. Furthermore, miR-141-3p and CHD8 reduce the expression of p21. Conclusion MiR-141-3p and CHD8 play critical roles in cardiomyocyte apoptosis induced by H/R. These studies suggest that miR-141-3p and CHD8 mediated cardiomyocyte apoptosis may offer a novel therapeutic strategy against myocardial I/R injury-induced cardiovascular diseases.

【 授权许可】

Unknown