This study aimed to investigate the potential role of microRNA-202-5p (miR-202-5p) in regulating myocardial ischemia-caused injury and to explore the underlying mechanisms. Rat embryonic ventricular cardiomyocyte-derived H9c2 cells were treated with hypoxia to generate an in vitro myocardial ischemia model, followed by the transfection with a miR-202-5p mimic and inhibitor. Subsequently, the effects of miR-202-5p on cell viability, apoptosis, migration, and invasion were analyzed. A luciferase reporter assay was used to identify the target gene of miR-202-5p. Besides, the regulatory relationship between miR-202-5p and the PI3K/AKT/FOXO3a pathway was investigated in hypoxia-induced H9c2 cells. Compared to normal H9c2 cells, the hypoxia treatment resulted in a significant damage to H9c2 cells, thereby decreasing the cell viability, migration, and invasion ability and inducing the cell apoptosis. miR-202-5p was significantly upregulated in hypoxia-induced H9c2 cells. After cell transfection, the suppression of miR-202-5p significantly alleviated the hypoxia-induced damage in H9c2 cells through the suppression of cell apoptosis and the promotion of cell viability, migration, and invasion ability. SRY-box 6 (SOX6) was found to be a direct target of miR-202-5p. The knockdown of SOX6 significantly aggravated the hypoxia-induced myocardial damage to H9c2 cells, which was alleviated after the inhibition of miR-202-5p expression. Besides, miR-202-5p suppression resulted in the activation of the PI3K/AKT/FOXO3a pathway in H9c2 cells. The data presented in this study revealed that miR-202-5p was upregulated in H9c2 cells during myocardial ischemia. The overexpressed miR-202-5p may aggravate the myocardial ischemia-caused injury by downregulating SOX6 to suppress the activation of the PI3K/AKT/FOXO3a pathway. Thus, miR-202-5p may serve as a potential target for the clinical treatment of myocardial ischemia.
Keywords: MicroRNA-202-5p; PI3K/AKT/FOXO3a pathway; SOX6; myocardial ischemia.
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