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

Yaoping Tang, Yongchao Wang, Kyoung Mi Park, Qiuping Hu, Jian Peng Teoh, Zuzana Broskova, Punithavathi Ranganathan, Calpurnia Jayakumar, Jie Li, Huabo Su, Yao Liang Tang, Ganesan Ramesh, Il-man Kim

Research output: Contribution to journalArticlepeer-review

95 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)387-397
Number of pages11
JournalCardiovascular Research
Issue number3
StatePublished - Jun 1 2015


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

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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