title: MiR-155 Knockout in Fibroblasts Improves Cardiac Remodeling by Targeting Tumor Protein p53-Inducible Nuclear Protein 1.
abstract: Cardiac remodeling caused by acute myocardial infarction (AMI) represents a major challenge for heart failure research. MiR-155 has been identified as a key mediator of cardiac inflammation and hypertrophy. In this study, we investigate the role of miR-155 in cardiac remodeling induced by AMI. We demonstrate that miR-155 expressed in cardiac fibroblasts is a potent contributor to cardiac remodeling. We reveal that in vivo, miR-155 knockout improves left ventricular function, reduces infarct size, and attenuates collagen deposition, whereas overexpression of miR-155 produces the opposite effects. MiR-155 knockout also inhibits cardiac fibroblast proliferation and differentiation into myofibroblasts. In addition, downregulation of tumor protein p53-inducible nuclear protein 1 (TP53INP1) by small interfering RNA reverses the effects of miR-155 knockout on cardiac fibroblasts. Our data reveal that knockout of miR-155 in cardiac fibroblasts improves cardiac remodeling by targeting TP53INP1, which may be a novel treatment strategy for cardiac remodeling.
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.
authors.forename: Wangwei
authors.initials: W
authors.lastname: He
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China huanghedoctorwhu@163.com.
authors.forename: He
authors.initials: H
authors.lastname: Huang
authors.affiliation: Department of Cardiology, The First Affiliated Hospital of Xiamen University, Xiamen, PR China.
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xie
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.
authors.forename: Zhiqiang
authors.initials: Z
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Fan
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.
authors.forename: Bin
authors.initials: B
authors.lastname: Kong
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.
authors.forename: Dan
authors.initials: D
authors.lastname: Huang
authors.affiliation: Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, PR China.
authors.forename: Yali
authors.initials: Y
authors.lastname: Xiao
mesh_terms: D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D002478:Cells, Cultured; D003094:Collagen / Q000378:metabolism; D004195:Disease Models, Animal; D005347:Fibroblasts / Q000378:metabolism* / Q000473:pathology; D005786:Gene Expression Regulation; D005838:Genotype; D008297:Male; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D009203:Myocardial Infarction / Q000235:genetics / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D058628:Myofibroblasts / Q000378:metabolism / Q000473:pathology; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D010641:Phenotype; D034622:RNA Interference; D015398:Signal Transduction; D013997:Time Factors; D014162:Transfection; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; D009687:Nuclear Proteins; C518507:tumor protein 53-induced nuclear protein 1, mouse; D003094:Collagen
keywords: acute myocardial infarction; cardiac remodeling; fibroblast; microRNA; tumor protein p53-inducible nuclear protein 1