MiR-483-3p is involved in the pathogenesis of acute myocardial infarctions, but its association with myocardial ischemia reperfusion (IR) remains mostly unknown. In this study, an in vitro model of myocardial IR injury was established by putting H9c2 cells into hypoxia reoxygenation (HR) treatment to explore the effects and possible mechanisms of miR-483-3p in myocardial IR injury. HR exposure resulted in increased miR-483-3p levels in H9c2 cells. MiR-483-3p was overexpressed or downregulated in H9c2 cells by transfection of miR-483-3p mimic or miR-483-3p inhibitor. In HR-treated H9c2 cells, MiR-483-3p mimics inhibited cell viability, promoted lactate dehydrogenase release, and increased apoptosis, but miR-483-3p inhibitors caused the opposite effects. MDM4 was verified to be the target mRNA of miR-483-3p and negatively modulated by miR-483-3p. MiR-483-3p inhibitor upregulated MDM4 and Bcl-2, but downregulated p53 and Bax in HR-treated H9c2 cells, whereas miR-483-3p overexpression produced the opposite effects.. Moreover, MDM4 siRNA transfection partially reversed the role of miR-483-3p inhibition in HR injury and p53 pathway inactivation of H9c2 cells. In summary, by targeting the MDM4/p53 pathway, miR-483-3p inhibition may alleviate myocardial HR injury. MiR-483-3p may be a potential therapeutic target of myocardial IR injury.
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References

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