miR‐34a‐5p Attenuates EMT through targeting SMAD4 in silica‐induced pulmonary fibrosis

DOI Web Site Web Site Web Site 被引用文献1件
  • Yuanmeng Qi
    School of public health Zhengzhou University Henan China
  • Ahui Zhao
    School of public health Zhengzhou University Henan China
  • Peiyan Yang
    School of public health Zhengzhou University Henan China
  • Luheng Jin
    School of public health Zhengzhou University Henan China
  • Changfu Hao
    School of public health Zhengzhou University Henan China

説明

<jats:title>Abstract</jats:title><jats:p>Silicosis is an incurable occupational disease, and its pathological feature is diffuse pulmonary fibrosis. Pulmonary epithelial‐mesenchymal transition (EMT) is one of the important events in the pathogenesis of silicosis. Previous studies found that abnormal expression of various microRNAs (miRNAs) involved in the development of lung fibrosis. However, their roles in silicosis have not been elucidated. To research the biological effects of miR‐34a in EMT process in silica‐induced lung fibrosis, we established the silicosis model in mouse and miR‐34a intervention in a cell model of TGF‐β1 stimulated lung epithelial cells (A549). The results showed that miR‐34a expression was down‐regulated in the fibrotic lung tissue after silica treatment, and it was similarly expressed in A549 cells stimulated by TGF‐β1. Meanwhile, silica‐induced EMT process can increase expression of two mesenchymal markers, α‐SMA and vimentin. Furthermore, overexpression miR‐34a markedly inhibited EMT stimulated by TGF‐β1. Mechanistically, SMAD4 was identified as the target of miR‐34a. SMAD4 levels decreased in mRNA and protein levels in A549 cells upon miR‐34a overexpression. In addition, the knockdown of SMAD4 blocked the EMT process. Taken together, miR‐34a regulated EMT, which might be partially realized by targeting SMAD4. Our data might provide new insight into treatment targets for silica‐induced pulmonary fibrosis.</jats:p>

収録刊行物

被引用文献 (1)*注記

もっと見る

問題の指摘

ページトップへ