Role of microRNA‑130a in myocardial hypoxia/reoxygenation injury

The aim of this study was to investigate the role of microRNA (miR)-130a in the pathogenesis of myocardial hypoxia/reoxygenation (H/R) injury. Primary rat cardiomyocytes were cultured and subjected to H/R treatment. Reverse transcription‑quantitative polymerase chain reaction was performed to detect the levels of miR‑130a, western blot analysis was used to determine the expression of various proteins, and CCK‑8 assay was performed to determine cell viability. In addition, flow cytometry was used to assess apoptosis. The cell viability was significantly decreased and the apoptosis rate was significantly increased in H/R‑treated primary cardiomyocytes, and the expression level of miR‑130a was also elevated in these model cells. Transfection with miR‑130a inhibitor significantly elevated the cell viability and reduced the apoptosis rate in H/R‑treated cardiomyocytes. Bioinformatics analysis indicated that autophagy‑related gene 14 (ATG14) is the target for miR‑130a, which was confirmed by dual‑luciferase reporter assay and western blot analysis. When the H/R model cells were co‑transfected with miR‑130a inhibitor and small interfering RNA against ATG14, the cell viability was significantly reduced and the apoptosis rate was significantly elevated, compared with that of cells transfected with miR‑130a inhibitor alone. miR‑130a inhibitor transfection significantly elevated the levels of ATG14 and phosphorylated (p‑)Beclin 1, increased the LC3II/LC3I ratio, and decreased the expression levels of P62 and cleaved caspase‑3, while the co‑transfection of miR‑130a inhibitor and siR‑ATG14 attenuated these effects in H/R‑induced primary cardiomyocytes. These results indicate that miR‑130a is involved in H/R‑induced injuries in primary cardiomyocytes, and that the inhibition of miR‑130a increases the levels of ATG14 and p‑Beclin 1, thereby increasing autophagy and inhibiting apoptosis in these cells.