title: Morphological characteristics of the microvasculature in healing myocardial infarcts.
abstract: Myocardial infarction (MI) is associated with an angiogenic response, critical for healing and cardiac repair. Using a canine model of myocardial ischemia and reperfusion, we examined the structural characteristics of the evolving microvasculature in healing MI. After 7 days of reperfusion, the infarcted territory was rich in capillaries and contained enlarged, pericyte-poor "mother vessels" and endothelial bridges. During scar maturation arteriolar density in the infarct increased, and a higher percentage of microvessels acquired a pericyte coat (60.4 +/- 6.94% after 28 days of reperfusion vs 30.17 +/- 3.65% after 7 days of reperfusion; p<0.05). The microvascular endothelium in the early stages of healing showed intense CD31/PECAM-1 and CD146/Mel-CAM immunoreactivity but weak staining with the Griffonia simplicifolia lectin I (GS-I). In contrast, after 28 days of reperfusion, most infarct microvessels demonstrated significant lectin binding. Our findings suggest that the infarct microvasculature undergoes a transition from an early phase of intense angiogenic activity to a maturation stage associated with pericyte recruitment and formation of a muscular coat. In addition, in the endothelium of infarct microvessels CD31 and CD146 expression appears to precede that of the specific sugar groups that bind the GS-I lectin. Understanding of the mechanisms underlying the formation and remodeling of the microvasculature after MI may be important in designing therapeutic interventions to optimize cardiac repair.
authors.affiliation: Section of Cardiovascular Sciences, Department of Medicine, Methodist Hospital and DeBakey Heart Center, Baylor College of Medicine, Houston, Texas 77030, USA.
authors.forename: Guofeng
authors.initials: G
authors.lastname: Ren
authors.forename: Lloyd H
authors.initials: LH
authors.lastname: Michael
authors.forename: Mark L
authors.initials: ML
authors.lastname: Entman
authors.forename: Nikolaos G
authors.initials: NG
authors.lastname: Frangogiannis
mesh_terms: D000818:Animals; D015703:Antigens, CD; D000954:Antigens, Surface / Q000378:metabolism; D001160:Arterioles / Q000378:metabolism / Q000473:pathology; D051929:CD146 Antigen; D002196:Capillaries / Q000378:metabolism / Q000473:pathology; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology*; D004285:Dogs; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005260:Female; D007150:Immunohistochemistry; D037102:Lectins; D008297:Male; D008562:Membrane Glycoproteins; D009203:Myocardial Infarction / Q000473:pathology*; D018919:Neovascularization, Physiologic; D019006:Neural Cell Adhesion Molecules; D020286:Pericytes / Q000473:pathology; D037121:Plant Lectins; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000378:metabolism
chemical_list: D015703:Antigens, CD; D000954:Antigens, Surface; D051929:CD146 Antigen; C045475:Griffonia simplicifolia lectins; D037102:Lectins; D008562:Membrane Glycoproteins; D019006:Neural Cell Adhesion Molecules; D037121:Plant Lectins; D019408:Platelet Endothelial Cell Adhesion Molecule-1