title: Ramipril attenuates left ventricular remodeling by regulating the expression of activin A-follistatin in a rat model of heart failure.
abstract: Prior studies have shown that overexpression of ACT A can lead to ventricular remodeling in rat models of heart failure. Furthermore, recently work studying demonstrated that stimulation of activin An expression in rat aortic smooth muscle (RASM) cells by angiotensin II (Ang II). Ramipril is a recently developed angiotensin converting enzyme (ACE) inhibitor. To investigate the effects of Ramipril on expression of ACT A-FS, we established the rat model of heart failure after myocardial infarction (MI), and divided into either a sham operation (SO), MI, or MI-Ramipril group. We found that Ramipril significantly attenuates collagen-I and III deposition (col-I and III). Notably, we determined that expression of ACT A and II activin receptor (ActRII) were significantly down-regulated in the non-infarcted area of the left ventricle in the Ramipril group, whereas the mRNA and protein levels of FS were markedly up-regulated. Our data suggested that Ramipril benefited left ventricular remodeling by reducing fibrosis and collagen accumulation in the left ventricle of rats after myocardial infarction. This observation was also associated with down-regulation of ACT A expression. This study elucidated a new protective mechanism of Ramipril and suggests a novel strategy for treatment of post-infarct remodeling and subsequent heart failure.
authors.affiliation: Department of cardiology, China-Japan Union Hospital, Jilin University, Changchun, China.|Department of Cardiology, Tianjin Fourth Central Hospital, Tianjin, China.
authors.forename: Qun
authors.initials: Q
authors.lastname: Wei
authors.affiliation: Department of Anatomy, College of Basic Medical Sciences, Jilin University, Changchun, China.
authors.forename: Haiyan
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of cardiology, China-Japan Union Hospital, Jilin University, Changchun, China.
authors.forename: Miao
authors.initials: M
authors.lastname: Liu
authors.affiliation: Department of cardiology, China-Japan Union Hospital, Jilin University, Changchun, China.
authors.forename: Chunyan
authors.initials: C
authors.lastname: Yang
authors.affiliation: Department of cardiology, China-Japan Union Hospital, Jilin University, Changchun, China.
authors.forename: Jie
authors.initials: J
authors.lastname: Yang
authors.affiliation: Department of cardiology, China-Japan Union Hospital, Jilin University, Changchun, China.|Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, China.
authors.forename: Zhonghui
authors.initials: Z
authors.lastname: Liu
authors.affiliation: Department of cardiology, China-Japan Union Hospital, Jilin University, Changchun, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Yang
mesh_terms: D028341:Activins / Q000235:genetics*; D000818:Animals; D015415:Biomarkers; D001706:Biopsy; D004195:Disease Models, Animal; D005260:Female; D005355:Fibrosis; D038681:Follistatin / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects*; D006333:Heart Failure / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D006334:Heart Function Tests; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics; D007150:Immunohistochemistry; D009203:Myocardial Infarction / Q000188:drug therapy / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D017257:Ramipril / Q000494:pharmacology*; D051381:Rats; D020257:Ventricular Remodeling / Q000187:drug effects*
chemical_list: D015415:Biomarkers; D038681:Follistatin; C422405:activin A; D028341:Activins; D017257:Ramipril