MicroRNA-186-5p inhibits H9c2 cells apoptosis induced by oxygen-glucose deprivation by targeting ERK1/2.

BACKGROUND

Serum miR-186-5p levels are increased in acute myocardial infarction (AMI) patients and might contribute to assessing the prognosis of AMI patients. In this study, we further investigated the underlying molecular mechanism of miR-186-5p that participated in the pathological processes of myocardial ischemia.

METHODS

The AMI models of rats and oxygen-glucose deprivation (OGD) models of H9c2 cells were established. Bioinformatics databases, luciferase reporting, and western blotting assays were performed to identify the regulatory target of miR-186-5p. Transfection and functional experiments were conducted to further define the possible molecular mechanism of miR-186-5p during the process of glucose deficiency and hypoxia.

RESULTS

The level of miR-186-5p was found to significantly decrease in H9c2 cells after OGD treatment, while it increased in the culture medium from OGD-treated H9c2 cells. Using bioinformatics databases, luciferase reporting, and western blotting assays, we identified that ERK1/2 might serve as the negative regulatory target of miR-186-5p. Combined with further transfection experiments, we indicated that miR-186-5p might inhibit the expression and activation of ERK1/2. This finding was also reflected in the reduction of their downstream cleaved caspase-3. Through functional experiments, we revealed that miR-186-5p might inhibit apoptosis and promote proliferation in OGD-treated H9c2 cells.

CONCLUSIONS

We demonstrated that miR-186-5p might suppress OGD-induced apoptosis in H9c2 cells by targeting the ERK1/2 pathway.