|Cardiac Hypertrophy is Positively Regulated by MicroRNA-24 in Rats|
|Gao, Juan1,2,3,4,5; Zhu, Min1,2,3,4,5; Liu, Rui-Feng1,2,3,4,5; Zhang, Jian-Shu1,2,3,4,5; Xu, Ming1,2,3,4,5|
|关键词||Cardiac Hypertrophy Cell Cycle Microrna Microrna-24|
|刊名||CHINESE MEDICAL JOURNAL|
|WOS标题词||Science & Technology|
|类目[WOS]||Medicine, General & Internal|
|研究领域[WOS]||General & Internal Medicine|
|关键词[WOS]||Cell-cycle ; Heart-failure ; Expression ; Inhibition ; Suppression ; Transition ; P27(Kip1) ; Prevents ; Fibrosis ; Therapy|
Background: Micro RNA-24 (miR-24) plays art important role in heart failure by reducing the efficiency of myocardial excitation-contraction coupling. Prolonged cardiac hypertrophy may lead to heart failure, but little is known about the role of miR-24 in cardiac hypertrophy. This study aimed to preliminarily investigate the function of miR-24 and its mechanisms in cardiac hypertrophy.
Methods: Twelve Sprague-Dawley rats with a body weight of 50 +/- 5 g were recruited and randomly divided into two groups: a transverse aortic constriction (TAC) group and a sham surgery group. Hypertrophy index was measured and calculated by echocardiography and hematoxylin and eosin staining. TargetScans algorithm-based prediction was used to search for the targets of miR-24, which was subsequently confirmed by a real-time polymerase chain reaction and luciferase assay. Immunofluorescence labeling was used to measure the cell surface area, and H-3-leucine incorporation was used to detect the synthesis of total protein in neonatal rat cardiac myocytes (NRCMs) with the overexpression of miR-24. In addition, flow cytometry was performed to observe the alteration in the cell cycle. Statistical analysis was carried out with GraphPad Prism v5.0 and SPSS 19.0. A two-sided P < 0.05 was considered as the threshold for significance.
Results: The expression of miR-24 was abnormally increased in TAC rat cardiac tissue (t = -2.938, P < 0.05), TargetScans algorithm-based prediction demonstrated that CDKN1B (p27, Kipl), a cell cycle regulator, was a putative target of miR-24, and was confirmed by luciferase assay. The expression of p27 was decreased in TAC rat cardiac tissue (t = 2.896, P < 0.05). The overexpression of miR-24 in NRCMs led to Ute decreased expression of p27 (t = 4.400, P < 0.01), and decreased G0/G1 arrest in cell cycle and cardiomyocyte hypertrophy.
Conclusion: MiR-24 promotes cardiac hypertrophy partly by affecting the cell cycle through down-regulation of p27 expression.
|作者单位||1.Peking Univ, Hosp 3, Dept Cardiol, Beijing 100191, Peoples R China;|
2.Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100191, Peoples R China;
3.Minist Hlth, Key Lab Cardiovasc Mol Biol & Regulatory Peptides, Beijing 100191, Peoples R China;
4.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing 100191, Peoples R China;
5.Beijing Key Lab Cardiovasc Receptors Res, Beijing 100191, Peoples R China
|Gao, Juan,Zhu, Min,Liu, Rui-Feng,et al. Cardiac Hypertrophy is Positively Regulated by MicroRNA-24 in Rats[J]. CHINESE MEDICAL JOURNAL,2018,131(11):1333-1341.|
|APA||Gao, Juan,Zhu, Min,Liu, Rui-Feng,Zhang, Jian-Shu,&Xu, Ming.(2018).Cardiac Hypertrophy is Positively Regulated by MicroRNA-24 in Rats.CHINESE MEDICAL JOURNAL,131(11),1333-1341.|
|MLA||Gao, Juan,et al."Cardiac Hypertrophy is Positively Regulated by MicroRNA-24 in Rats".CHINESE MEDICAL JOURNAL 131.11(2018):1333-1341.|