Journal
CARDIOVASCULAR RESEARCH
Volume 106, Issue 3, Pages 387-397Publisher
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvv121
Keywords
beta-arrestin; Apoptotic genes; Biased G protein-coupled receptor signalling; Cardioprotection
Categories
Funding
- American Heart Association (AHA) [13POST16840074]
- National Institutes of Health (NIH) [R01 DK083379, R01 HL124251]
- AHA [12GRNT12100048, 14SDG18970040]
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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 beta-arrestin-biased beta-blocker, carvedilol that beta-arrestin1-biased beta(1)-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.
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