MicroRNA-1185 Induces Endothelial Cell Apoptosis by Targeting UVRAG and KRIT1

MicroRNA-1185 Induces Endothelial Cell Apoptosis by Targeting UVRAG and KRIT1

Blog Article

Background/Aims: Atherosclerosis is a multifactorial chronic disease and is the main cause of death and impairment in the world.Endothelial injury and apoptosis play a crucial role in the onset and development of atherosclerosis.MicroRNAs (miRNAs) have been proven to be involved in the pathogenesis of atherosclerosis.

However, studies of the functional role of apoptosis-related miRNAs in the endothelium during atherogenesis are limited.Methods: Cell injury and apoptosis were measured here in five types of cells transfected with miR-1185 or co-transfected with miR-1185 and its inhibitor.Bioinformatics analysis and a luciferase reporter assay were used to confirm the targets of miR-1185.

The effects of the targets of miR-1185 on endothelial apoptosis were determined using small-interfering RNA.Results: In this study, we first report that miR-1185 significantly promoted apoptosis in endothelial cells but not in vascular smooth muscle cells and sequal eclipse 5 battery macrophages.A mechanistic analysis showed that ultraviolet irradiation resistance-associated gene (UVRAG) and krev1 interaction trapped gene 1 (KRIT1), targets of miR-1185, mediated miR-1185-induced endothelial cell apoptosis.

Conclusion: The results revealed the impact of miR-1185 on endothelial apoptosis, suggesting that miR-1185 may be a potential target for the prevention and treatment of atherosclerosis.