The role of miR-145 in promoting the fibrosis of pulmonary fibroblasts

J Biol Regul Homeost Agents. 2019 Sep-Oct;33(5):1337-1345. doi: 10.23812/19-27-A.

Abstract

The effects of miR-145 (microRNA 145) on M. pneumoniae (MP)-infected MRC-5 (Medical Research Council cell strain 5) cell TGF-β/Smad (transforming growth factor beta/Smad) fibrosis pathway were explored through constructing MP-infected MRC-5 cell models. In addition, the qPCR (quantitative real-time polymerase chain reaction) and Western blot were applied to detect the mRNA and protein expressions of miR-145, TGF-β1 (transforming growth factor beta 1), Smad3, Smad4, MMP2 (matrix metalloproteinase 2), FN1 (fibronectin 1), ELN (elastin) and COLI α1 (collagen type I alpha 1) signaling molecules in TGF-β/Smad fibrosis pathway. The results showed that the expression of miR-145 in MRC-5 cells was significantly increased after MP infection. In addition, miR-145 inhibited the fibrosis promoting TGF-β/Smad pathway by targeting Smad3, a key factor in the TGF-β/Smad pathway. It can be concluded that, in the process of MP infection, the expression of miR-145 is stimulated to negatively regulate the fibrosis-promoting pathway of TGF-β/Smad.

Keywords: MRC-5 cells; TGF-β/Smad pathway; miR-145.

MeSH terms

  • Cell Line
  • Collagen Type I, alpha 1 Chain
  • Fibroblasts / microbiology
  • Fibroblasts / pathology*
  • Fibrosis
  • Humans
  • Matrix Metalloproteinase 2 / metabolism
  • MicroRNAs / metabolism*
  • Mycoplasma pneumoniae*
  • Smad Proteins / metabolism*
  • Transforming Growth Factor beta1 / metabolism

Substances

  • COL1A1 protein, human
  • Collagen Type I, alpha 1 Chain
  • MIRN145 microRNA, human
  • MicroRNAs
  • Smad Proteins
  • TGFB1 protein, human
  • Transforming Growth Factor beta1
  • Matrix Metalloproteinase 2