MiR-129-5p attenuates hypoxia-induced apoptosis in rat H9c2 cardiomyocytes by activating autophagy.

Abstract

Autophagy is closely associated with apoptosis in H9c2 cardiomyocytes as a result of hypoxia. The present study aimed to determine whether microRNAs (miRs) mediated apoptosis and autophagy in hypoxia-stimulated H9c2 cardiomyocytes. miR microarrays and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) assays were used to detect differentially expressed miRs in H9c2 cardiomyocytes following hypoxia stimulation. Annexin V-fluorescein isothiocyanate double staining was performed to evaluate hypoxia-induced cell apoptosis, and the protein expression levels of autophagy-associated genes were detected using western blotting. miR microarrays and qRT-PCR assays showed that the expression of miR-129-5p is significantly decreased in hypoxia-exposed H9c2 cardiomyocytes. Under hypoxic stimulation, miR-129-5p mimics alleviated hypoxia-induced cell apoptosis and also restored autophagy in H9c2 cardiomyocytes. However, transfection with miR-129-5p inhibitors accelerated hypoxia-induced cell apoptosis and autophagy deficiency in H9c2 cardiomyocytes. Furthermore, overexpression of miR-129-5p enhanced cell viability and reduced the release of lactate dehydrogenase in hypoxia-stimulated H9c2 cardiomyocytes. These findings highlight the protective effect of miR-129-5p against hypoxia-induced apoptosis in H9c2 cardiomyocytes through the activation of autophagy.