miR-19b controls cardiac fibroblast proliferation and migration

J Cell Mol Med. 2016 Jun;20(6):1191-7. doi: 10.1111/jcmm.12858. Epub 2016 Apr 6.

Abstract

Cardiac fibrosis is a fundamental constituent of a variety of cardiac dysfunction, making it a leading cause of death worldwide. However, no effective treatment for cardiac fibrosis is available. Therefore, novel therapeutics for cardiac fibrosis are highly needed. Recently, miR-19b has been found to be able to protect hydrogen peroxide (H2 O2 )-induced apoptosis and improve cell survival in H9C2 cardiomyocytes, while down-regulation of miR-19b had opposite effects, indicating that increasing miR-19b may be a new therapeutic strategy for attenuating cellular apoptosis during myocardial ischaemia-reperfusion injury. However, considering the fact that microRNAs might exert a cell-specific role, it is highly interesting to determine the role of miR-19b in cardiac fibroblasts. Here, we found that miR-19b was able to promote cardiac fibroblast proliferation and migration. However, miR-19b mimics and inhibitors did not modulate the expression level of collagen I. Pten was identified as a target gene of miR-19b, which was responsible for the effect of miR-19b in controlling cardiac fibroblast proliferation and migration. Our data suggest that the role of miR-19b is cell specific, and systemic miR-19b targeting in cardiac remodelling might be problematic. Therefore, it is highly needed and also urgent to investigate the role of miR-19b in cardiac remodelling in vivo.

Keywords: Pten; cardiac fibrosis; miR-19b.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Cell Movement* / genetics
  • Cell Proliferation
  • Fibroblasts / cytology*
  • Fibroblasts / metabolism*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Myocardium / cytology*
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / metabolism
  • Rats, Sprague-Dawley

Substances

  • MIRN19 microRNA, rat
  • MicroRNAs
  • PTEN Phosphohydrolase