Long Non-Coding RNA-ROR Mediates the Reprogramming in Cardiac Hypertrophy

PLoS One. 2016 Apr 15;11(4):e0152767. doi: 10.1371/journal.pone.0152767. eCollection 2016.

Abstract

Background: Cardiac hypertrophy associated with various cardiovascular diseases results in heart failure and sudden death. A clear understanding of the mechanisms of hypertrophy will benefit the development of novel therapies. Long non-coding RNAs (lncRNAs) have been shown to play essential roles in many biological process, however, whether lncRNA-ROR plays functional roles in the reprogramming of cardiomyocyte remains unclear.

Methodology/principal findings: Here we show that lncRNA-ROR plays important roles in the pathogenesis of cardiac hypertrophy. In hypertrophic heart and cardiomyocytes, the expression of lncRNA-ROR is dramatically increased, downregulation of which attenuates the hypertrophic responses. Furthermore, the expression of lncRNA-ROR negatively correlates with miR-133, whose expression is increased when lncRNA-ROR is knocked down. In line with this, overexpression of miR-133 prevents the elevation of lncRNA-ROR and re-expression of ANP and BNP in cardiomyocytes subject to phenylephrine treatment.

Conclusions/significance: Taken together, our study demonstrates that lncRNA-ROR promotes cardiac hypertrophy via interacting with miR-133, indicating that lncRNA-ROR could be targeted for developing novel antihypertrophic therapeutics.

MeSH terms

  • Animals
  • Cardiomegaly / genetics*
  • Cardiomegaly / pathology
  • Gene Expression Regulation / drug effects
  • Gene Knockdown Techniques
  • Male
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs / genetics
  • Myocytes, Cardiac / drug effects
  • Myocytes, Cardiac / pathology
  • Phenylephrine / pharmacology
  • RNA, Long Noncoding / genetics*
  • RNA, Long Noncoding / metabolism

Substances

  • MicroRNAs
  • Mirn133 microRNA, mouse
  • RNA, Long Noncoding
  • Phenylephrine

Grants and funding

The authors received no specific funding for this work.