LAB/IN VITRO RESEARCH e-ISSN 1643-3750 © Med Sci Monit, 2016; 22: 1808-1816 DOI: 10.12659/MSM.896428
MicroRNA-208b Alleviates Post-Infarction Myocardial Fibrosis in a Rat Model by Inhibiting GATA4
Received: 2015.10.26 Accepted: 2015.11.17 Published: 2016.05.29
Authors’ BCEF Contribution: Chaoyuan Zhou Study Design A BCF Qintao Cui Data Collection B BDF Guobao Su Statistical Analysis C Data Interpretation BF D Xiaoliang Guo Manuscript Preparation E DF Xiaochen Liu Literature Search F A Jie Zhang Funds Collection G
Corresponding Author: Source of support:
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Department of Cardiovascular Surgery, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan, P.R. China
Jie Zhang, e-mail: [email protected] Departmental sources
Myocardial infarction affects the health of many people. Post-infarction myocardial fibrosis has attracted much attention, but details of the mechanism remain elusive. In this study, the role of microRNA-208b (miR-208b) in modulating post-infarction myocardial fibrosis and the related mechanism were investigated. A rat model of myocardial infarction induced by ligating the left anterior descending artery was used to analyze the expression and roles of miR-208b by overexpression with the lentivirus vector of pre-miR-208b. Myocardial function was assessed and the expression of fibrosis-related factors type I collagen (COL1) and ACTA2 (alias aSMA) was detected. Myocardial fibroblasts isolated from newborn rats were transfected with luciferase reporter vectors containing wild-type or mutant Gata4 3’ UTR to verify the relationship between Gata4 and miR208b. We then transfected the specific small interference RNA of Gata4 to detect changes in COL1 and ACTA2. miR-208b was down-regulated in hearts of model rats (P
MicroRNA-208b Alleviates Post-Infarction Myocardial Fibrosis in a Rat Model by Inhibiting GATA4
Received: 2015.10.26 Accepted: 2015.11.17 Published: 2016.05.29
Authors’ BCEF Contribution: Chaoyuan Zhou Study Design A BCF Qintao Cui Data Collection B BDF Guobao Su Statistical Analysis C Data Interpretation BF D Xiaoliang Guo Manuscript Preparation E DF Xiaochen Liu Literature Search F A Jie Zhang Funds Collection G
Corresponding Author: Source of support:
Background:
Material/Methods:
Results:
Conclusions:
MeSH Keywords:
Full-text PDF:
Department of Cardiovascular Surgery, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan, P.R. China
Jie Zhang, e-mail: [email protected] Departmental sources
Myocardial infarction affects the health of many people. Post-infarction myocardial fibrosis has attracted much attention, but details of the mechanism remain elusive. In this study, the role of microRNA-208b (miR-208b) in modulating post-infarction myocardial fibrosis and the related mechanism were investigated. A rat model of myocardial infarction induced by ligating the left anterior descending artery was used to analyze the expression and roles of miR-208b by overexpression with the lentivirus vector of pre-miR-208b. Myocardial function was assessed and the expression of fibrosis-related factors type I collagen (COL1) and ACTA2 (alias aSMA) was detected. Myocardial fibroblasts isolated from newborn rats were transfected with luciferase reporter vectors containing wild-type or mutant Gata4 3’ UTR to verify the relationship between Gata4 and miR208b. We then transfected the specific small interference RNA of Gata4 to detect changes in COL1 and ACTA2. miR-208b was down-regulated in hearts of model rats (P
