[No authors listed]
Myocardial ischemia/reperfusion (I/R) injury is a major pathological process in coronary heart disease and cardiac surgery, and is associated with aberrant microRNA (miR) expression. Previous studies have demonstrated that inhibition of miR-15a expression may ameliorate I/Râinduced myocardial injury. In the present study, the potential role and underlying mechanism of miRâ15a in hypoxia/reoxygenationâinduced apoptosis of cardiomyocytes was investigated. Myocardial I/R was simulated in cultured H9c2 cells by 24 h hypoxia followed by 24 h reoxygenation. Using recombinant lentivirus vectors, the inhibition of miRâ15a was indicated to significantly reduce cardiomyocyte apoptosis and release of lactate dehydrogenase and malondialdehyde. Conversely, upregulated miRâ15a expression was proâapoptotic. Mothers against decapentaplegic homolog 7 (SMAD7) was identified by bioinformatics analysis as a potential target of miRâ15a. Luciferase reporter assays and western blotting for endogenous SMAD7 protein indicated that miRâ15a inhibited SMAD7 expression via its 3'âuntranslated region. Nuclear levels of nuclear factorâκB (NFâκB) p65 were increased by miRâ15a expression and decreased by miRâ15a inhibition, which is consistent with the possibility that the inhibition of SMAD7 by miR-15a results in NFâκB activation. These findings suggested that the therapeutic effects of miRâ15a inhibition on I/R injury may potentially be explained by its ability to release SMADâ7âdependent NFâκB inhibition. This may provide evidence for miRâ15a as a potential therapeutic target for the treatment of cardiac I/R injury.
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