MicroRNA-19b-1 reverses ischaemia-induced heart failure by inhibiting cardiomyocyte apoptosis and targeting Bcl2 l11/BIM.
Wenbo YangYanxin HanChendie YangYanjia ChenWeilin ZhaoXiuxiu SuKe YangWei JinPublished in: Heart and vessels (2019)
Ischaemia induces cardiac apoptosis and leads to a loss of cardiac function and heart failure after myocardial infarction. MicroRNA-19b-1 (miR-19b-1), a key member of the miR-17/92 cluster, plays crucial roles in inhibiting apoptosis. However, the role of miR-19b-1 in ischaemia-induced heart failure remains unknown. In this study, ischaemia resulted in cardiac apoptosis and the suppression of miR-19b-1 expression, whereas miR-19b-1 overexpression inhibited ischaemia-induced cardiac apoptosis in vivo and in vitro. Moreover, miR-19b-1 not only attenuated the infarct size but also ameliorated heart failure after myocardial infarction, including the changes in the left ventricular ejection fraction and volume load. Mechanically, miR-19-1 targeted and downregulated the mRNA and protein expression of Bcl2l11/BIM, a pro-apoptotic gene of the Bcl-2 family. Together, these results revealed an essential role of miR-19b-1 in ischaemia-induced heart failure.
Keyphrases
- heart failure
- left ventricular
- oxidative stress
- diabetic rats
- cell death
- cell cycle arrest
- high glucose
- endoplasmic reticulum stress
- cardiac resynchronization therapy
- cell proliferation
- ejection fraction
- aortic stenosis
- acute myocardial infarction
- long non coding rna
- poor prognosis
- drug induced
- acute heart failure
- signaling pathway
- hypertrophic cardiomyopathy
- long noncoding rna
- dna methylation
- coronary artery disease
- angiotensin ii
- percutaneous coronary intervention
- single cell
- left atrial
- mitral valve
- genome wide
- anti inflammatory
- cancer therapy