MicroRNA-30e regulates TGF-β-mediated NADPH oxidase 4-dependent oxidative stress by Snai1 in atherosclerosis.

MicroRNAs (miRNAs) are small non‑coding RNA molecules that regulate gene expression at a post‑transcription level in living organisms. Great attention has been paid to the role of miRNAs in the pathogenesis of atherosclerosis (AS). The present study was designed to investigate the function of miRNA‑30e in atherosclerosis and to explore potential mechanisms. The expression of miRNA‑30e was decreased in an AS model, compared with the normal group. The downregulation of miRNA‑30e increased oxidative stress and reactive oxygen species levels in vitro. Then, overexpression of miRNA‑30e led to decreased oxidative stress and levels in vitro. The downregulation of miRNA‑30e induced the protein expression of Snai1, transforming growth factor (TGF)‑β and mothers against decapentaplegic homolog 2 (Smad2) and suppressed that of NADPH oxidase 4 (Nox4) in vitro. The activation of Snai1 or TGF‑β attenuated the effects of miRNA‑30e on oxidative stress in vitro. Consistently, the inhibition of Nox4 attenuated the effects of miRNA‑30e on oxidative stress in vitro. These findings demonstrated for the first time that miRNA‑30e regulated AS by TGF‑β‑mediated NADPH oxidase 4‑dependent oxidative stress via Snai1.

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