title: Dermatopontin promotes adhesion, spreading and migration of cardiac fibroblasts in vitro.
abstract: Dermatopontin (DPT), an extracellular matrix (ECM) protein, has been previously shown to be upregulated in the infarct zone of experimentally induced myocardial infarction (MI) rats. However, the accurate role that DPT exerts in the ventricular remodeling process after MI remains poorly understood. In this study, we evaluated the expression pattern of DPT mRNA and protein as well as its secretion in cultured neonatal rat cardiomyocytes (CMs) and cardiac fibroblasts (CFs) under conditions of hypoxia and serum deprivation (hypoxia/SD). Further, we tested the possible roles of DPT in CFs adhesion, spreading, migration and proliferation, which greatly promote the ventricular remodeling process after MI. Results showed that hypoxia/SD stimulated DPT expression and secretion in CMs and CFs and that DPT promoted adhesion, spreading and migration of CFs whereas had no effect on CFs proliferation. In addition, functional blocking antibodies specific for integrin α3 and β1 significantly reduced CFs adhesion and migration that DPT induced, suggesting that integrin α3β1 is at least one receptor for CFs adhesion and migration to DPT. These results implicated that DPT participates in the ventricular remodeling process after MI and may act as a potential therapeutic target for ventricular remodeling.
authors.affiliation: State Key Laboratory of Cardiovascular Disease, National Center for Cardiovascular Disease and Fuwai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, PR China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Liu
authors.forename: Liukun
authors.initials: L
authors.lastname: Meng
authors.forename: Qiang
authors.initials: Q
authors.lastname: Shi
authors.forename: Shenghua
authors.initials: S
authors.lastname: Liu
authors.forename: Chuanjue
authors.initials: C
authors.lastname: Cui
authors.forename: Shengshou
authors.initials: S
authors.lastname: Hu
authors.forename: Yingjie
authors.initials: Y
authors.lastname: Wei
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D019138:Antibodies, Blocking / Q000378:metabolism; D015153:Blotting, Western; D002448:Cell Adhesion / Q000502:physiology*; D015687:Cell Hypoxia / Q000502:physiology; D002465:Cell Movement / Q000502:physiology*; D049109:Cell Proliferation; D002478:Cells, Cultured; D011508:Chondroitin Sulfate Proteoglycans / Q000378:metabolism*; D017931:DNA Primers / Q000235:genetics; D004797:Enzyme-Linked Immunosorbent Assay; D016326:Extracellular Matrix Proteins / Q000378:metabolism*; D005347:Fibroblasts / Q000378:metabolism; D005455:Fluorescent Antibody Technique; D005786:Gene Expression Regulation / Q000502:physiology*; D066298:In Vitro Techniques; D039201:Integrin alpha3beta1 / Q000276:immunology; D009203:Myocardial Infarction / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D019138:Antibodies, Blocking; D011508:Chondroitin Sulfate Proteoglycans; D017931:DNA Primers; C582422:Dpt protein, rat; D016326:Extracellular Matrix Proteins; D039201:Integrin alpha3beta1