Open AccessmicroRNA‐30a attenuates TGF‐β1–induced activation of pulmonary fibroblast cell by targeting FAP‐α
Author(s) -
Wu Geting,
Xie Bin,
Lu Can,
Chen Chen,
Zhou Jianhua,
Deng Zhenghao
Publication year - 2020
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.15020
Subject(s) - fibroblast , pulmonary fibrosis , bronchoalveolar lavage , idiopathic pulmonary fibrosis , fibroblast activation protein, alpha , microrna , transforming growth factor , cancer research , medicine , interstitial lung disease , pathological , lung , cell , fibrosis , immunology , pathology , chemistry , biology , cell culture , cancer , gene , biochemistry , genetics
Idiopathic interstitial pulmonary fibrosis is a common diffuse interstitial lung disease and has poor prognosis. And one of the pathological features of it is persistent fibroblast activation. It was reported that microRNA‐30a was down‐regulated in bronchoalveolar lavage fluid from idiopathic pulmonary fibrosis patients. But whether miR‐30a is involved in fibroblast activation and its specific mechanism is unclear. In this study, we aimed to investigate the role of miR‐30a in fibroblast activation induced by TGF‐β1. We found miR‐30a could targetedly suppress FAP‐α expression. In MRC5 cells, miR‐30a was not only involved in regulating the expression of FAP‐α, col1a and α‐SMA induced by TGF‐β1 but also had a role in cell proliferation with or without TGF‐β1 treatment via regulating FAP‐α expression. Thus, the results indicated that miR‐30a alleviated fibroblast activation by regulating the expression of FAP‐α.