Global microRNA profiling of the mouse ventricles during development of severe hypertrophic cardiomyopathy and heart failure

PLoS One. 2012;7(9):e44744. doi: 10.1371/journal.pone.0044744. Epub 2012 Sep 14.

Abstract

MicroRNAs (miRNAs) regulate post-transcriptional gene expression during development and disease. We have determined the miRNA expression levels of early- and end-stage hypertrophic cardiomyopathy (HCM) in a severe, transgenic mouse model of the disease. Five miRNAs were differentially expressed at an early stage of HCM development. Time-course analysis revealed that decreased expression of miR-1 and miR-133a commences at a pre-disease stage, and precedes upregulation of target genes causal of cardiac hypertrophy and extracellular matrix remodelling, suggesting a role for miR-1 and miR-133a in early disease development. At end-stage HCM, 16 miRNA are dysregulated to form an expression profile resembling that of other forms of cardiac hypertrophy, suggesting common responses. Analysis of the mRNA transcriptome revealed that miRNAs potentially target 15.7% upregulated and 4.8% downregulated mRNAs at end-stage HCM, and regulate mRNAs associated with cardiac hypertrophy and electrophysiology, calcium signalling, fibrosis, and the TGF-β signalling pathway. Collectively, these results define the miRNA expression signatures during development and progression of severe HCM and highlight critical miRNA regulated gene networks that are involved in disease pathogenesis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiomyopathy, Hypertrophic / genetics*
  • Disease Models, Animal
  • Gene Expression Profiling*
  • Gene Expression Regulation
  • Heart Failure / genetics*
  • Heart Ventricles / metabolism*
  • Heart Ventricles / pathology
  • Male
  • Mice
  • Mice, Transgenic
  • MicroRNAs / genetics*
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reproducibility of Results
  • Transcription, Genetic

Substances

  • MicroRNAs
  • RNA, Messenger

Grants and funding

RS is the recipient of a Rotary Australia PhD scholarship (www.rotaryaustralia.org.au). WR is a recipient of a National Health and Medical Research Council (NHMRC) of Australia fellowship (No. 517756; www.nhmrc.gov.au). CS is the recipient of an NHMRC Practitioner fellowship (No. 571084). This work was supported by a research project grant from NHMRC (No. 635576). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.