Influence of microRNA-30a on cardiomyocyte apoptosis under hypoxia condition and mechanism study

Wang Ke; Shi Jihong; Wei Zhenheng

doi:10.3969/j.issn.1674-4055.2019.07.29

Abstract：Objective To discuss the influence of microRNA-30a (miR-30a) on cardiomyocyte apoptosis under hypoxia condition and mechanism. Methods H9C2 cells were randomly divided into control group (without treatment), hypoxia group (hypoxia treatment for 24 h), hypoxia+negative control group (hypoxia+NC group, transfected with negative control of miR-30a followed by hypoxia treatment for 24 h), and hypoxia+miR-30a group (transfected with miR-30a mimics followed by hypoxia treatment for 24 h). The expression of miR-30a was detected by using real-time fluorescence quantitative polymerase chain reaction (RT-PCR) in all groups, and content of superoxide dismutase (SOD), malondialdehyde (MDA) and lactic dehydrogenase (LDH) in supernatant were detected by using chromatoptometry. The survival rate was detected by using methyl thiazolyl tetrazolium test (MTT), and apoptosis was detected by using flow cytometer. The expressions of STAT3, p-STAT3 and cleaved caspase-3 were detected by using Western blotting assay. Results Compared with control group, the expressions of miR-30a, cleaved caspase-3 and p-STAT3 increased significantly, SOD content decreased, content of MDA and LDH increased, survival rate decreased and apoptosis increased in hypoxia group, hypoxia+NC group and hypoxia+miR-30a group (P＜0.05). After transfected with miR-30a mimics followed by miR-30a up-regulation, all above indexes were improved under hypoxia condition. Conclusion MiR-30a can enhance oxidative stress injury and promote hypoxia-induced apoptosis through activating STAT3 signaling pathway.