Cardiac shock wave therapy protects cardiomyocytes from hypoxia‑induced injury by modulating miR‑210

Cardiac shock wave therapy (SWT) has been described as a novel therapeutic strategy that is able to alleviate myocardial ischemic injury. microRNA (miRNA/miR)210 plays a cytoprotective role in cardiomyocytes in response to hypoxia by regulating cell apoptosis. The aim of the present study was to investigate whether cardiac SWT could protect cardiomyocytes from hypoxiainduced injury by regulating miR210 expression. The murine adult cardiomyocyte cell line HL1 was incubated for 5 h in hypoxic conditions, followed by reoxygenation for 12 h and treatment with SWT immediately following hypoxia in the present study. The cell viability was determined using an MTS assay. Western blot analyses were performed in order to detect cell signaling changes. Reactive oxygen species production was detected using dihydroethidium staining, and malondialdehyde levels were measured using the thiobarbituric acid method. miRNA and mRNA expression levels were confirmed via reverse transcriptionquantitative PCR. Apoptosis was evaluated by means of flow cytometry. HL1 cells were then transfected with miR210 mimics or inhibitors in order to alter miR210 expression levels, and the effects on HL1 cells were determined. Hypoxia led to elevated oxidative stress, enhanced cell apoptosis and upregulated miR210 expression levels in HL1 cells, while SWT could alleviate hypoxiainduced cell injury and further promote miR210 expression. miR210 overexpression decreased apoptosis and oxidative stress during hypoxic stress in HL1 cells, whereas inhibition of miR210 increased cell apoptosis and promoted oxidative stress. Furthermore, miR210 inhibition could reverse the effects of SWT on HL1 cells. Finally, the mRNA analysis revealed that SWT significantly attenuated apoptosisinducing factor mitochondrionassociated 3 and caspase 8 associated protein 2 mRNA expression levels in cardiomyocytes exposed to hypoxia, which were two targets of miR210. SWT could exert cardioprotective effects against hypoxiainduced cardiac injury by modulating miR210.