title: Of mice and dogs: species-specific differences in the inflammatory response following myocardial infarction.
abstract: Large animal models have provided much of the descriptive data regarding the cellular and molecular events in myocardial infarction and repair. The availability of genetically altered mice may provide a valuable tool for specific cellular and molecular dissection of these processes. In this report we compare closed chest models of canine and mouse infarction/reperfusion qualitatively and quantitatively for temporal, cellular, and spatial differences. Much like the canine model, reperfused mouse hearts are associated with marked induction of endothelial adhesion molecules, cytokines, and chemokines. Reperfused mouse infarcts show accelerated replacement of cardiomyocytes by granulation tissue leading to a thin mature scar at 14 days, when the canine infarction is still cellular and evolving. Infarcted mouse hearts demonstrate a robust but transient postreperfusion inflammatory reaction, associated with a rapid up-regulation of interleukin-10 and transforming growth factor-beta. Unlike canine infarcts, infarcted mouse hearts show only transient macrophage infiltration and no significant mast cell accumulation. In correlation, the growth factor for macrophages, M-CSF, shows modest and transient up-regulation in the early days of reperfusion; and the obligate growth factor for mast cells, stem cell factor, SCF, is not induced. In summary, the postinfarction inflammatory response and resultant repair in the mouse heart shares many common characteristics with large mammalian species, but has distinct temporal and qualitative features. These important species-specific differences should be considered when interpreting findings derived from studies using genetically altered mice.
authors.affiliation: Section of Cardiovascular Sciences, Baylor College of Medicine, the Methodist Hospital, and the DeBakey Heart Center, Houston, Texas 77030, USA.
authors.forename: Oliver
authors.initials: O
authors.lastname: Dewald
authors.forename: Guofeng
authors.initials: G
authors.lastname: Ren
authors.forename: Georg D
authors.initials: GD
authors.lastname: Duerr
authors.forename: Martin
authors.initials: M
authors.lastname: Zoerlein
authors.forename: Christina
authors.initials: C
authors.lastname: Klemm
authors.forename: Christine
authors.initials: C
authors.lastname: Gersch
authors.forename: Sophia
authors.initials: S
authors.lastname: Tincey
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; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D016207:Cytokines / Q000096:biosynthesis; D004195:Disease Models, Animal; D004285:Dogs; D007150:Immunohistochemistry; D007249:Inflammation / Q000473:pathology*; D008297:Male; D051379:Mice; D032342:Muscle Cells / Q000473:pathology; D009203:Myocardial Infarction / Q000473:pathology*; D015425:Myocardial Reperfusion; D018919:Neovascularization, Physiologic / Q000502:physiology; D013045:Species Specificity; D013997:Time Factors
chemical_list: D015815:Cell Adhesion Molecules; D016207:Cytokines