The role and mechanism of miR-92a in endothelial autophagy

Abstract

Abstract Vascular endothelial cells (EC) are monolayer flat cells that form the vascular wall, and their dysfunction plays an important role in the pathogenesis of cardiovascular diseases.MicroRNA (miRNA) is a key regulatory factor that regulates multiple functions of EC, and is an ideal choice for diagnosis and treatment of various cardiovascular diseases.It is reported that miR-92a is up-regulated in the serum and cardiovascular tissues of patients with cardiovascular diseases. Elevated miR-92a leads to EC dysfunction by promoting EC inflammation, cell apoptosis and oxidative stress.However, it is not clear whether miR-92a affects EC autophagy. Therefore, the purpose of this study is to explore the effect of mir-92a on EC autophagy and the molecular mechanism of regulating EC autophagy.The autophagy inducer rapamycin (rapa) was used to treat EA. hy926 endothelial cells to construct endothelial cell autophagy model; The expression level of miR-92a was detected by qRT-PCR;The effect of miR-92a on the autophagy activity of EA. hy926 endothelial cells was studied by using liposome transfection technology to overexpress or inhibit miR-92a ;The level of autophagy was evaluated by western blot, immunofluorescence staining and transmission electron microscopy;Bioinformatics software and double luciferase experiment were used to to screen and confirm the combination of miR-92a and FOXO3;The results showed that the expression of miR-92a increased in the rapa-induced autophagy model of EA. hy926 endothelial cells;The experimental results after overexpression and inhibition of miR-92a showed that the up-regulation of miR-92a inhibited the autophagy of endothelial cells, while the inhibition of miR-92a promoted the autophagy of endothelial cells.In addition, miR-92a can directly bind to the 3 'untranslated region of the autophagy-related gene FOXO3 and reduce the expression of FOXO3.In conclusion, this study suggests that miR-92a may affect the occurrence and development of cardiovascular diseaseIn by targeting FOXO3 to inhibit the autophagy activity of EA. hy926 endothelial cells.