title: Platelet-derived growth factor involvement in myocardial remodeling following infarction.
abstract: Cardiac remodeling occurs in the infarcted heart (MI). The underlying regulatory mechanisms are under investigation. Platelet-derived growth factor (PDGF) is a family of growth factors that stimulates cell growth, differentiation and migration. Herein, we sought to determine whether PDGF is involved in cardiac repair/remodeling following MI. The temporal and spatial expressions of PDGF isoforms (A, B, C and D) and PDGF receptor (PDGFR)-α and β as well as cell types expressing PDGF were examined in the infarcted rat heart. Sham-operated rats served as controls. We found that the normal myocardium expressed all PDGF isoforms, and cell types expressing PDGF were primarily interstitial cells. Following MI, PDGF-A and D were significantly increased in the infarcted myocardium during 6 weeks of the observation period and cells expressing PDGF-A and D were primarily endothelial cells, macrophages and myofibroblasts (myoFb). PDGF-B and C expressions were, however, reduced in the infarcted heart. In the noninfarcted myocardium, PDGF-D expression was increased in the late stage of MI and cells expressing PDGF-D were predominantly fibroblasts. Both PDGFR-α and β were significantly increased in the infarcted myocardium in the early and late stages of MI and in the noninfarcted myocardium in the late stage of MI. Enhanced PDGF-A, PDGF-D and PDGFR are coincident with angiogenesis, and inflammatory and fibrogenic responses in the infarcted myocardium, suggesting their regulation on cardiac repair. Elevated PDGF-D in the noninfarcted myocardium suggests its involvement in the development of interstitial fibrosis that appears in the late stage of MI.
authors.affiliation: Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
authors.forename: Wenyuan
authors.initials: W
authors.lastname: Zhao
authors.forename: Tieqiang
authors.initials: T
authors.lastname: Zhao
authors.forename: Valerie
authors.initials: V
authors.lastname: Huang
authors.forename: Yuanjian
authors.initials: Y
authors.lastname: Chen
authors.forename: Robert A
authors.initials: RA
authors.lastname: Ahokas
authors.forename: Yao
authors.initials: Y
authors.lastname: Sun
mesh_terms: D000818:Animals; D001345:Autoradiography; D015153:Blotting, Western; D049109:Cell Proliferation; D004195:Disease Models, Animal; D004719:Endomyocardial Fibrosis / Q000150:complications / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D042783:Endothelial Cells / Q000166:cytology / Q000378:metabolism; D015870:Gene Expression; D008264:Macrophages / Q000166:cytology / Q000378:metabolism; D008297:Male; D009203:Myocardial Infarction / Q000150:complications / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D058628:Myofibroblasts / Q000166:cytology / Q000378:metabolism; D009928:Organ Specificity; D010982:Platelet-Derived Growth Factor / Q000235:genetics / Q000378:metabolism*; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017479:Receptors, Platelet-Derived Growth Factor / Q000235:genetics / Q000378:metabolism*; D020257:Ventricular Remodeling / Q000235:genetics*
chemical_list: D010982:Platelet-Derived Growth Factor; D020033:Protein Isoforms; D017479:Receptors, Platelet-Derived Growth Factor