MicroRNA-155 promotes ox-LDL-induced autophagy in human umbilical vein endothelial cells by targeting the PI3K/Akt/mTOR pathway

Abstract

Endothelial cell autophagy has a protective role in inhibiting inflammation and preventing the development of atherosclerosis, which may be regulated by microRNA (miR)-155. The present study aimed to investigate the mechanisms of autophagy in the development of atherosclerosis. Human umbilical vein endothelial cells model in vitro and using oxidized low-density lipoprotein (ox-LDL) stimulated cells to simulate the atherosclerosis. MiR-155 mimics, miR-155 inhibitors, and a negative control were respectively transfected in human umbilical vein endothelial cells to analyzed alterations in the expression of miR-155. It was demonstrated that overexpression of miR-155 promoted autophagic activity in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells, whereas inhibition of the expression of miR-155 reduced autophagic activity. Overexpression of miR-155 revealed that it regulated autophagy via the phosphatidylinositol-3 kinase (PI3K)/RAC-a serine/threonine-protein kinase (Akt)/mechanistic target of rapamycin pathway (mTOR) signaling pathway. A luciferase reporter assay demonstrated that miR-155 directly bound to the PI3K catalytic subunit a and Ras homolog enriched in brain 3'-untranslated region and inhibited its luciferase activity. Therefore, the results of the present study suggested that miR-155 promoted autophagy in vascular endothelial cells and that this may have occurred via targeting of the PI3K/Akt/mTOR pathway. Thus, miR-155 may be considered as a potential therapeutic target for the treatment of atherosclerosis.