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Updated: Apr 15, 2026
Induction of Myocardial Infarction and Myocardial Ischemia-Reperfusion Injury in Mice
Published on: January 19, 2022
MicroRNA-150 protects the mouse heart from ischaemic injury by regulating cell death
Yaoping Tang1, Yongchao Wang1, Kyoung-Mi Park1
1Vascular Biology Center, Medical College of Georgia, Georgia Regents University, Augusta, GA, USA.
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.
Insights
MicroRNA-150 (miR-150) plays a crucial role in protecting heart cells from injury. Deleting miR-150 in mice led to abnormal heart remodeling after myocardial infarction, highlighting its protective function.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Biomarker Discovery
Background:
- MicroRNAs (miRs) exhibit dynamic expression changes during cardiac injury.
- miR-150 is downregulated in various heart conditions and proposed as a superior heart failure biomarker.
- Previous research linked beta-arrestin-biased signaling to miR-150 processing in the heart.
Purpose of the Study:
- To investigate the role of miR-150 in cardiac ischemic injury and heart failure.
- To elucidate the mechanisms by which miR-150 influences cardiac remodeling and survival.
Main Methods:
- Genetic deletion of miR-150 in mouse models.
- Assessment of cardiac structure and function post-myocardial infarction (MI).
- Analysis of gene expression, focusing on pro-apoptotic and inflammatory pathways.
Main Results:
- Genetic absence of miR-150 resulted in adverse cardiac structural and functional remodeling following MI.
- miR-150 directly represses the expression of pro-apoptotic genes egr2 and p2x7r in cardiomyocytes.
- These findings suggest a protective role for miR-150 in mitigating ischemic damage.
Conclusions:
- miR-150 is a key regulator of cardiomyocyte survival during cardiac injury.
- The study identifies miR-150 as a critical factor in the response to ischemic heart damage.
- miR-150's role in repressing pro-apoptotic genes underscores its cardioprotective potential.
