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miR-139-5p inhibits isoproterenol-induced cardiac hypertrophy by targetting c-Jun
- Source :
- Bioscience Reports
- Publication Year :
- 2018
- Publisher :
- Portland Press Ltd., 2018.
-
Abstract
- Hypertrophic cardiomyopathy (HCM) is a serious monogenic disease characterized by cardiac hypertrophy, fibrosis, sudden cardiac death, and heart failure. Previously, we identified that miR-139-5p was down-regulated in HCM patients. However, the regulatory effects of miR-139-5p remain unclear. Thus, we investigated the role of miR-139-5p in the regulation of cardiac hypertrophy. The expression of miR-139-5p in left ventricular tissues in HCM patients and mice subjected to transverse aortic constriction (TAC) was significantly down-regulated. Knockdown of miR-139-5p expression in neonatal rat cardiomyocytes (NRCMs) induced cardiomyocyte enlargement and increased atrial natriuretic polypeptide (ANP) expression. Overexpression of miR-139-5p antagonized isoproterenol (ISO)-induced cardiomyocyte enlargement and ANP/brain natriuretic peptide (BNP) up-regulation. More importantly, we found that c-Jun expression was inhibited by miR-139-5p in NRCMs. Knockdown of c-Jun expression significantly attenuated cardiac hypertrophy induced by miR-139-5p deprivation. Our data indicated that miR-139-5p was down-regulated in the hearts of HCM patients and that it inhibited cardiac hypertrophy by targetting c-Jun expression.
- Subjects :
- 0301 basic medicine
medicine.medical_specialty
Biophysics
Biochemistry
Sudden cardiac death
03 medical and health sciences
Fibrosis
Internal medicine
medicine
cardiovascular diseases
Molecular Biology
Research Articles
miR-139-5p
Gene knockdown
isoproterenol
business.industry
c-Jun
c-jun
Hypertrophic cardiomyopathy
Cell Biology
hypertrophic cardiomyopathy
medicine.disease
Brain natriuretic peptide
030104 developmental biology
Endocrinology
Heart failure
Cardiac hypertrophy
cardiovascular system
business
Research Article
Subjects
Details
- ISSN :
- 15734935 and 01448463
- Volume :
- 38
- Database :
- OpenAIRE
- Journal :
- Bioscience Reports
- Accession number :
- edsair.doi.dedup.....c526c317bbeb9853a8b61d4d5fdbc2e1