MicroRNA-497 Inhibits Cardiac Hypertrophy by Targeting Sirt4

Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to overload pressure of heart. From abundant studies, a conclusion is drawn that many microRNAs (miRNAs) are associated with cardiac hypertrophy and heart failure. To investigate the role of microRNA-497 (miR-497) in myocar...

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Bibliographic Details
Published in:PloS one 2016-12, Vol.11 (12), p.e0168078-e0168078
Main Authors: Xiao, Yimin, Zhang, Xiaofei, Fan, Shihao, Cui, Guanghao, Shen, Zhenya
Format: Article
Language:English
Subjects:
Analysis
Angiotensin
Animals
Animals, Newborn
Aorta
Apoptosis
Biology and life sciences
Bone cancer
Breast cancer
Cardiology
Cardiomegaly - genetics
Cardiomyocytes
Cardiovascular disease
Cells, Cultured
Disease Models, Animal
Enlargement
Fibroblasts
Gene expression
Gene Expression Regulation, Enzymologic
Health aspects
Heart
Heart diseases
Heart failure
Heart function
Heart hypertrophy
Heart surgery
Hypertrophy
Laboratory animals
Medicine and Health Sciences
Metabolism
Mice
Mice, Inbred C57BL
MicroRNA
MicroRNAs
MicroRNAs - physiology
miRNA
Mitochondrial Proteins - genetics
Mitochondrial Proteins - metabolism
Myocardium
Myocardium - metabolism
Myocardium - pathology
Myocytes, Cardiac - metabolism
Research and Analysis Methods
Ribonucleic acid
RNA
Science
Sirtuins - genetics
Sirtuins - metabolism
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Summary:Cardiac hypertrophy is an adaptive enlargement of the myocardium in response to overload pressure of heart. From abundant studies, a conclusion is drawn that many microRNAs (miRNAs) are associated with cardiac hypertrophy and heart failure. To investigate the role of microRNA-497 (miR-497) in myocardial hypertrophy, two models were established in this study from cell level to integral level. Cardiac hypertrophy was induced by using angiotensin Ⅱ (Ang Ⅱ) in vitro and was created by transverse abdominal aortic constriction (TAC) in vivo. There was a significant decrease expression of miR-497 in cardiac hypertrophy models. Moreover, overexpression of miR-497 inhibited myocardial hypertrophy both in vitro and in vivo without heart function variation. In addition, luciferase reporter assays demonstrated that Sirt4 was a direct target gene of miR-497. Taking together, our study indicates that miR-497 modulates cardiac hypertrophy by targeting Sirt4 and may serve as a potential therapeutic substance in the course.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0168078