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

Although microRNAs (miRNAs/miRs) serve a significant role in the autophagy of vascular endothelial cells (ECs), the effect of miR-92a on the autophagy of ECs is currently unclear. Therefore, the present study aimed to investigate the impact of miR-92a on autophagy in ECs and the underlying molecular processes that control this biological activity. Firstly, an autophagy model of EA.hy926 cells was generated via treatment with the autophagy inducer rapamycin (rapa-EA.hy926 cells). The expression levels of miR-92a were then detected by reverse transcription-quantitative PCR, and the effect of miR-92a expression on the autophagic activity of rapa-EA.hy926 cells was studied by overexpressing or inhibiting miR-92a. The level of autophagy was evaluated by western blot analysis, immunofluorescence staining and transmission electron microscopy. Dual-luciferase reporter assays were used to confirm the interaction between miR-92a and FOXO3. The results demonstrated that the expression levels of miR-92a were decreased in the rapa-EA.hy926 cell autophagy model. Furthermore, overexpression and inhibition of miR-92a revealed that upregulation of miR-92a in these cells inhibited autophagy, whereas miR-92a knockdown promoted it. It was also confirmed that miR-92a directly bound to the 3 '-untranslated region of the autophagy-related gene FOXO3 and reduced its expression. In conclusion, the present study suggested that miR-92a inhibits autophagy activity in EA.hy926 cells by targeting FOXO3.