MicroRNA-151 Attenuates Apoptosis of Endothelial Cells Induced by Oxidized Low-density Lipoprotein by Targeting Interleukin-17A (IL-17A)

Apoptosis of endothelial cells plays an important role in atherosclerosis (AS). MicroRNAs (miRNAs) have been confirmed to participate in the process of endothelial cell apoptosis. The main purpose of this study was to investigate the mechanism of miR-151 and interleukin-17A (IL-17A) in apoptosis of atherosclerotic endothelial cells. The expression levels of miR-151 in human aortic endothelial cells (HAEC) after Ox-LDL treatment were detected by qRT-PCR. The expression levels of IL-17A were detected by qRT-PCR and Western blot. The effects of miR-151 and IL-17A on the apoptosis rate were detected by flow cytometry. The relationship between miR-151 and IL-17A was assessed by bioinformatics analysis and luciferase assay. The expression levels of miR-151 in HAEC after Ox-LDL treatment were reduced, and the expression of IL-17A was upregulated. MiR-151 and si-IL-17A inhibited the apoptosis rate of aortic endothelial cells treated by Ox-LDL. MiR-151 and si-IL-17A reduced the expression levels of c-caspase-9, c-caspase-3, and BAX proteins in Ox-LDL-treated HAEC and increased the expression levels of Bcl-2. MiR-151 inhibited the apoptosis of endothelial cells in AS, and IL-17A was a new target for miR-151. Our findings provided a potential treatment for atherosclerosis in the treatment of AS.

Automated summary

This study investigated the mechanism of miR-151 and IL-17A in apoptosis of atherosclerotic endothelial cells. The results showed that miR-151 and si-IL-17A inhibited the apoptosis rate of aortic endothelial cells treated by Ox-LDL by reducing the expression levels of apoptotic proteins and increasing the expression levels of anti-apoptotic protein Bcl-2. MiR-151 was found to inhibit endothelial cell apoptosis in AS, and IL-17A was identified as a new target for miR-151.