Roles of miR‑4463 in H2O2‑induced oxidative stress in human umbilical vein endothelial cells.

Oxidative stress is implicated in the pathophysiology of vascular diseases, including atherosclerosis, aneurysm and arteriovenous fistula. A previous study from our lab suggested that microRNA (miR)‑4463 may be involved in the pathogenesis of vascular disease; however, the roles of oxidative stress in the molecular mechanisms underlying the actions of miR‑4463 in vascular disease have yet to be elucidated. The aim of the present study was to investigate the role of miR‑4463 in hydrogen peroxide (H2O2)‑induced oxidative stress in human umbilical vein endothelial cells (HUVECs). Reverse transcription‑quantitative polymerase chain reaction was used to assess the expression levels of miR‑4463 in HUVECs treated with various concentrations of H2O2. Flow cytometry was used to evaluate the percentage of apoptotic cells, and the protein expression levels of the apoptotic markers cleaved (C)‑caspase3, poly (adenosine diphosphate‑ribose) polymerase 1 (PARP1), B cell lymphoma‑2 (Bcl‑2), Bcl‑2‑associated X protein (Bax) and X‑linked inhibitor of apoptosis protein (XIAP) were determined using western blot analysis. The results demonstrated that the apoptotic rate of HUVECs was increased following treatment with H2O2 in a concentration‑dependent manner, and the expression of miR‑4463 was also upregulated in a dose‑dependent manner. Following transfection with miR‑4463 mimics, the levels of malondialdehyde and reactive oxygen species were increased in HUVECs, with a corresponding increase in the apoptotic rate. Furthermore, western blot analysis revealed that the protein expression levels of C‑caspase3, PARP1 and Bax were upregulated, whereas the levels of Bcl‑2 and XIAP were downregulated. In conclusion, the present findings suggested that the upregulation of miR‑4463 may enhance H2O2‑induced oxidative stress and promote apoptosis in HUVECs in vitro.