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Cardiovasc Res. 2015 Jun 1;106(3):387-97. doi: 10.1093/cvr/cvv121. Epub 2015 Mar 30.

MicroRNA-150 protects the mouse heart from ischaemic injury by regulating cell death.

Author information

  • 1Vascular Biology Center, Medical College of Georgia, Georgia Regents University, Augusta, GA, USA.
  • 2Vascular Biology Center, Medical College of Georgia, Georgia Regents University, Augusta, GA, USA Department of Biochemistry and Molecular Biology, Medical College of Georgia, Georgia Regents University CB-3717, 1459 Laney Walker Blvd, Augusta, GA, USA ilkim@gru.edu.

Abstract

AIMS:

Cardiac injury is accompanied by dynamic changes in the expression of microRNAs (miRs). For example, miR-150 is down-regulated in patients with acute myocardial infarction, atrial fibrillation, dilated and ischaemic cardiomyopathy as well as in various mouse heart failure (HF) models. Circulating miR-150 has been recently proposed as a better biomarker of HF than traditional clinical markers such as brain natriuretic peptide. We recently showed using the β-arrestin-biased β-blocker, carvedilol that β-arrestin1-biased β1-adrenergic receptor cardioprotective signalling stimulates the processing of miR-150 in the heart. However, the potential role of miR-150 in ischaemic injury and HF is unknown.

METHODS AND RESULTS:

Here, we show that genetic deletion of miR-150 in mice causes abnormalities in cardiac structural and functional remodelling after MI. The cardioprotective roles of miR-150 during ischaemic injury were in part attributed to direct repression of the pro-apoptotic genes egr2 (zinc-binding transcription factor induced by ischaemia) and p2x7r (pro-inflammatory ATP receptor) in cardiomyocytes.

CONCLUSION:

These findings reveal a pivotal role for miR-150 as a regulator of cardiomyocyte survival during cardiac injury.

KEYWORDS:

Apoptotic genes; Biased G protein-coupled receptor signalling; Cardioprotection; β-arrestin

PMID:
25824147
PMCID:
PMC4447807
DOI:
10.1093/cvr/cvv121
[PubMed - indexed for MEDLINE]
Free PMC Article
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