Rapamycin‑induced miR‑30a downregulation inhibits senescence of VSMCs by targeting Beclin1.

Vascular senescence is considered to be an independent risk factor for cardiovascular diseases. The present study aimed to investigate the effects of rapamycin on miR‑30a and its relationship with autophagy and senescence in vascular smooth muscle cells (VSMCs). Young and aging VSMCs were treated with rapamycin or transfected with miR‑30a mimics. Measurement of cellular senescence was conducted using senescence‑associated (SA)‑β‑Galactosidase (gal) staining. Dual luciferase reporter assay was used to confirm binding for miR‑30a and Beclin1. The expression levels of miR‑30a and Beclin1 were determined with reverse transcription‑quantitative polymerase chain reaction analysis. Autophagy‑related protein levels were determined using immunofluorescence or western blot assays. The results demonstrated that rapamycin treatment significantly decreased miR‑30a expression and increased Beclin1 expression in both young and aging cells, as well as promoted autophagy in VSMCs. In addition, rapamycin inhibited senescence in VSMCs and could also alleviate the aging VSMC cycle arrest. Dual luciferase reporter assay confirmed that miR‑30a could directly bind the 3'untranslated region of Beclin1 and inhibit its expression. Furthermore, miR‑30a inhibited autophagy and promoted senescence of VSMCs. In conclusion, the present results indicated that rapamycin could inhibit the senescence of VSMCs by downregulating miR‑30a, which resulted in upregulation of Beclin1 and activation of autophagy. The current study is the first to demonstrate an inhibitory role of rapamycin on VSMC senescence and might provide novel insights and potential new molecular targets in senescence treatment.