MicroRNA-29a-3p attenuates ET-1-induced hypertrophic responses in H9c2 cardiomyocytes

Gene. 2016 Jul 1;585(1):44-50. doi: 10.1016/j.gene.2016.03.015. Epub 2016 Mar 15.

Abstract

Transcription factor nuclear factor of activated T cells c4 (NFATc4) is the best-characterized target for the development of cardiac hypertrophy. Aberrant microRNA-29 (miR-29) expression is involved in the development of cardiac fibrosis and congestive heart failure. However, whether miR-29 regulates hypertrophic processes is still not clear. In this study, we investigated the potential functions of miR-29a-3p in endothelin-1 (ET-1)-induced cardiomyocyte hypertrophy. We showed that miR-29a-3p was down-regulated in ET-1-treated H9c2 cardiomyocytes. Overexpression of miR-29a-3p significantly reduced ET-1-induced hypertrophic responses in H9c2 cardiomyocytes, which was accompanied by a decrease in NFATc4 expression. miR-29a-3p targeted directly to the 3'-UTR of NFATc4 mRNA and silenced NFATc4 expression. Our results indicate that miR-29a-3p inhibits ET-1-induced cardiomyocyte hypertrophy via inhibiting NFATc4 expression.

Keywords: Cardiomyocyte hypertrophy; NFATc4; miR-29a-3p.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3' Untranslated Regions / genetics
  • Animals
  • Cardiomegaly / genetics*
  • Cell Line
  • Down-Regulation / genetics
  • Endothelin-1 / metabolism*
  • Fibrosis / genetics
  • Heart Failure / genetics*
  • MicroRNAs / biosynthesis
  • MicroRNAs / genetics*
  • Myocytes, Cardiac / pathology*
  • NFATC Transcription Factors / biosynthesis
  • NFATC Transcription Factors / genetics*
  • Nerve Tissue Proteins / biosynthesis
  • Nerve Tissue Proteins / genetics*
  • RNA, Messenger / genetics
  • Rats

Substances

  • 3' Untranslated Regions
  • Endothelin-1
  • MIRN29 microRNA, rat
  • MicroRNAs
  • NFATC Transcription Factors
  • Nerve Tissue Proteins
  • Nfatc4 protein, rat
  • RNA, Messenger