Other
12 Authors
- Kim IM,
- Su H,
- Broskova Z,
- Tang Y,
- Ramesh G,
- Teoh JP,
- Wang Y,
- Hu Q,
- Ranganathan P,
- Li J,
- Jayakumar C,
- Park KM
| First Author | Tang Y | Year | 2015 |
| Journal | Cardiovasc Res | Volume | 106 |
| Issue | 3 | Pages | 387-97 |
| PubMed ID | 25824147 | Mgi Jnum | J:251061 |
| Mgi Id | MGI:6106332 | Doi | 10.1093/cvr/cvv121 |
| Citation | Tang Y, et al. (2015) MicroRNA-150 protects the mouse heart from ischaemic injury by regulating cell death. Cardiovasc Res 106(3):387-97 |
| abstractText | 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 beta1-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. |
