microRNA-30a attenuates TGF-β1-induced activation of pulmonary fibroblast cell by targeting FAP-α

J Cell Mol Med. 2020 Mar;24(6):3745-3750. doi: 10.1111/jcmm.15020. Epub 2020 Jan 28.

Abstract

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.

Keywords: FAP-α; MRC5; TGF-β1; miR-30a; pulmonary fibrosis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Cell Line
  • Endopeptidases / genetics
  • Endopeptidases / metabolism*
  • Fibroblasts / drug effects
  • Fibroblasts / metabolism*
  • Humans
  • Lung / cytology*
  • Membrane Proteins / genetics
  • Membrane Proteins / metabolism*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism
  • Transforming Growth Factor beta1 / pharmacology*

Substances

  • MIRN30a microRNA, human
  • Membrane Proteins
  • MicroRNAs
  • Transforming Growth Factor beta1
  • Endopeptidases
  • fibroblast activation protein alpha