Hypoxia plays an important role in many heart diseases. MicroRNA-9 (miR-9) has been reported to beinvolved in hypoxia-induced cell proliferation, injury and apoptosis in cardiomyocytes. However, the underlyingmechanism still remains poorly understood. The expression levels of miR-9 and cyclin-dependent kinase8 (CDK8) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The relative proteinexpression was measured by Western blot. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide(MTT), lactate dehydrogenase (LDH) measurement, flow cytometry assays were conducted to detect cellproliferation, the release of LDH and cell apoptosis, respectively. The potential relationship between miR-9 andCDK8 was predicted by online database, and confirmed by dual-luciferase reporter assay. We found that miR-9was increased, while CDK8 was decreased in hypoxia-treated H9c2 cells. miR-9 down-regulation or CDK8up-regulation promoted cell proliferation, while repressed cell damage and apoptosis in hypoxia-induced H9c2cells. Moreover, CDK8 was identified to be target of miR-9, and CDK8 knockdown could reverse the effects ofmiR-9 inhibitor on cell proliferation, damage and apoptosis in hypoxia-treated H9c2 cells. Besides, miR-9could regulate the Wnt/b-catenin pathway by targeting CDK8 in hypoxic-induced H9c2 cells. In conclusion,miR-9 repressed cell proliferation and promoted cell damage and apoptosis by binding to CDK8 through theWnt/beta-catenin pathway in hypoxic-induced H9c2 cells, which provided a new direction for further studying thetreatment of hypoxia-aroused heart diseases.
Volume 46, 2021
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