MicroRNA-497 Inhibits Cardiac Hypertrophy by Targeting Sirt4

• Published in: PloS one Vol. 11; no. 12; p. e0168078
• Main Authors: Xiao, Yimin, Zhang, Xiaofei, Fan, Shihao, Cui, Guanghao, Shen, Zhenya
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 16.12.2016; Public Library of Science (PLoS)
• 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; China
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0168078

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.