MicroRNA-150 protects the mouse heart from ischaemic injury by regulating cell death
Cardiovascular research, 2015•academic.oup.com
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 …
(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 …
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.
Oxford University Press