MiR-182 alleviates the development of cyanotic congenital heart disease by suppressing HES1.

miRNAs have been pointed to play critical roles in the protection and development of cyanotic congenital heart disease (CHD). MiR-182 is found to be associated with multiple heart diseases. However, little is known about the function and underlying mechanisms of miR-182 on cyanotic CHD. Here, H9c2 cells were exposed to hypoxia to construct the model of cyanotic CHD in vitro. qRT-PCR assay revealed that miR-182 expression was downregulated in serum samples from patients with cyanotic CHD and hypoxia-induced cardiomyocytes. Gain- and loss-of-function demonstrated that miR-182 overexpression promoted cell proliferation and suppressed apoptosis in hypoxia-induced H9c2 cells, while miR-182 knockdown repressed cell proliferation and promoted apoptosis. Dual-luciferase reporter assay verified that HES1 was a direct target of miR-182, and miR-182 repressed HES1 expression by binding to its 3'-UTR. Moreover, miR-182-mediated regulatory effect on cell proliferation and apoptosis was reversed by the restoration of HES1 expression. In conclusion, our study demonstrated that miR-182 exerted protection effect through suppressing HES1 in hypoxia-induced cardiomyocytes, highlighting its role as a potential therapeutic strategy for cyanotic CHD.

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