Abstract
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 H2O2-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 H2O2 but enhanced the productions of vasodilatation factor Prostaglandin F1α (PGF1α). 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 H2O2-induced HUVEC injury by regulating the expression of p53.
Highlights
Deep vein thrombosis (DVT) affects 1-2 per 1000 people each year
We identified the role of miR-122 in DVT and revealed its regulatory functions and molecular mechanisms in human umbilical vein endothelial cells (HUVECs) injury
The results demonstrated that the expression of miR-122 was significantly lower in the DVT patients compared to the normal controls
Summary
Deep vein thrombosis (DVT) affects 1-2 per 1000 people each year. And its prevalence increases with age [1,2,3]. Endothelial cell injury and dysfunction are major factors contributed to DVT. Previous studies reported that excessive oxidative stress is a common cause of vascular endothelial cell injury [6,7,8]. Intracellular reactive oxygen species (ROS) can aggravate apoptosis in vascular endothelial cells and decrease antiapoptotic molecule expression [9]. The molecular mechanism of oxidation stressinduced endothelial cell injury is unclear. A previous study demonstrated that miR-122 was induced by ROS in human endothelial cells and its expression is associated with endothelial cell apoptosis [10]. The regulatory relationship among miR-122, p53, and oxidation stress-induced vascular. The present study was conducted to study the role of miR-122 in vascular endothelial cell injury. We investigate whether miR-122 regulates p53 participating in oxidation stress-induced vascular endothelial cell apoptosis
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