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Deep venous thrombosis (DVT) constitutes a great threat to health worldwide. Endothelial cell injury and dysfunction comprise the critical contributor for the development of DVT. However, the mechanism behind it remains poorly elucidated. The study is aimed at investigating the role of microRNA-122 (miR-122) and oxidative stress on DVT. The results showed that miR-122 overexpression dampened H 2 O 2 -evoked cytotoxic injury in human umbilical vein endothelial cells (HUVECs) by increasing cell viability, suppressing cell apoptosis and oxidative stress injury. Notably, miR-122 overexpression attenuated provasoconstriction factor endothelin-1 (ET-1) expression in HUVECs exposed to H 2 O 2  but enhanced the productions of vasodilatation factor Prostaglandin F1 α  (PGF1 α ). Moreover, inhibition of miR-122 had the opposite results. miR-122 could inhibit the expression of p53. Low expression of p53 could enhance the protection of miR-122 on HUVEC injury. This study highlights that miR-122 overexpression may restore H 2 O 2 -induced HUVEC injury by regulating the expression of p53.

Overexpression of MicroRNA-122 Resists Oxidative Stress-Induced Human Umbilical Vascular Endothelial Cell Injury by Inhibition of p53