Abstract
MicroRNAs play essential roles in the regulation and pathophysiology of acute myocardial infarction (AMI). The purpose of the present study was to assess the expression signature of miR-206 in rat heart with AMI and the corresponding molecular mechanism. The expression of miR-206 significantly decreased in the infarcted myocardial areas and in hypoxia-induced cardiomyocytes, compared with that in the noninfarcted areas. Overexpression of miR-206 decreased cardiomyocytes apoptosis and the down-regulation of miR-206 increased cardiomyocytes apoptosis in vitro. In addition, overexpression of miR-206 in rat heart in vivo remarkably reduced myocardial infarct size and cardiomyocytes apoptosis. We identified that miR-206 had a protective effect on cardiomyocytes apoptosis with the association of its target protein tyrosine phosphatase 1B (PTP1B). Gain-of-function of miR-206 inhibited PTP1B expression and loss-of-function of miR-206 up-regulated PTP1B expression. Furthermore, overexpression of PTP1B significantly increased cardiomyocytes apoptosis. These results together suggest the protective effect of miR-206 against cardiomyocytes apoptosis induced by AMI by targeting PTP1B.
Highlights
Acute myocardial infarction (AMI) is one of the common but life-threatening cardiovascular conditions that the blood flow is abruptly blocked in the coronary arteries causing myocardial tissue damage [1]
We found that miR-206 has protective effects against AMI-induced apoptosis of cardiomyocytes by directly targeting protein tyrosine phosphatase 1B (PTP1B), which would be beneficial in elucidating the mechanisms underlying AMI
The expression levels of miR-206 in cultured neonatal rat cardiomyocytes that were exposed to hypoxia were assessed by qRT-PCR
Summary
Acute myocardial infarction (AMI) is one of the common but life-threatening cardiovascular conditions that the blood flow is abruptly blocked in the coronary arteries causing myocardial tissue damage [1]. There is an estimated 3–4 million people in the world affected by AMI and the case fatality is extremely high. MicroRNAs (miRNAs) are endogenous small non-coding RNA sequences that can bind to a complementary mRNA in the 3 UTR region and functions post-transcriptionally to negatively regulate target gene expression by degrading the targeted RNAs or inhibiting their translation [2]. There is an estimated 1000 miRNA genes in the human genome and they might regulate ∼60% of protein-coding genes [3,4,5], which suggest the fundamental roles of miRNAs in major cellular functions in humans. Dysregulation of miRNAs has been identified to be involved in the pathogenesis of many different diseases such as tumorigenesis, neurological and myocardial diseases [6,7,8]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
