MiR-147b inhibits cell viability and promotes apoptosis of rat H9c2 cardiomyocytes via down-regulating KLF13 expression.

Recently, microRNAs (miRNAs) have been shown to involve in the process of heart failure. This study aims to investigate the functional role of miR-147b in rat H9c2 cardiomyocytes and explore the underlying molecular mechanisms. Cell viability of H9c2 cells was detected by MTT assay. Cell apoptosis was detected by flow cytometry. Expression of miR-147b and KLF13 mRNA was detected by quantitative real-time PCR. The relationship between miR-147b and KLF13 was verified by dual-luciferase reporter assay. Protein levels were detected by western blot analysis. It was found that H2O2 inhibited cell viability and promoted cell apoptosis of H9c2 cells in a concentration-dependent manner. MiR-147b overexpression suppressed cell viability and increased apoptosis in H9c2 cells, while knock-down of miR-147b increased cell viability and reduced apoptosis in H2O2-treated H9c2 cells. Luciferase reporter assay and in vitro functional assay showed that KLF13 was a downstream target of miR-147b, and KLF13 knock-down suppressed cell viability and induced apoptosis in H9c2 cells. Enforced expression of KLF13 restored the effects of miR-147b overexpression on cell viability and apoptosis in H9c2 cells. MiR-147b modulated the expression levels of apoptosis-related proteins, and the effects of miR-147b overexpression on apoptosis-related proteins levels were prevented by enforced expression of KLF13 in H9c2 cells. The in vivo experiments showed that miR-147b was up-regulated, and KLF13 was down-regulated in the myocardial tissues from rats with chronic heart failure. Collectively, miR-147b inhibits viability and promotes cell apoptosis by targeting KLF13 in H9c2 cells, which may be associated with the pathogenesis of heart failure.