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DOI: 10.1369/jhc.3A6210.2004
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Journal of Histochemistry and Cytochemistry
Volume 52 (8): 1019-1029, 2004
Copyright ©The Histochemical Society, Inc.

Vascular Mural Cells in Healing Canine Myocardial Infarcts

Marcin Dobaczewski, Spyridon Akrivakis, Kamal Nasser, Lloyd H. Michael, Mark L. Entman and Nikolaos G. Frangogiannis

Section of Cardiovascular Sciences, the DeBakey Heart Center, Baylor College of Medicine, and the Methodist Hospital, Houston, Texas

Correspondence to: Nikolaos Frangogiannis, MD, Section of Cardiovascular Sciences, One Baylor Plaza M/S F-602, Baylor College of Medicine, Houston, TX 77030. E-mail: ngf{at}bcm.tmc.edu

Angiogenesis is a critical process in healing of myocardial infarcts, leading to the formation of highly vascular granulation tissue. However, effective cardiac repair depends on mechanisms that inhibit the angiogenic process after a mature scar is formed, preventing inappropriate expansion of the fibrotic process. Using a canine model of reperfused myocardial infarction, we demonstrated that maturation of the infarct leads to the formation of neovessels, with a thick muscular coat, that demonstrate distinct morphological characteristics. Many of these "neoarterioles" lack a defined internal elastic lamina and demonstrate irregular deposits of extracellular matrix in the media. Vascular mural cells in healing infarcts undergo phenotypic changes, showing minimal expression of desmin during the proliferative phase (1 hr occlusion/7 days reperfusion) but in the mature scar (8 weeks reperfusion) acquire a phenotype similar to that of vascular smooth muscle cells in control areas. Non-muscle myosin heavy chains A and B are induced in infarct endothelial cells and myofibroblasts, respectively, but are not expressed in neovascular mural cells. Recruitment of a muscular coat and formation of neoarterioles in mature scars may inhibit endothelial cell proliferation and vascular sprouting, stabilizing the infarct vasculature.

(J Histochem Cytochem 52:1019–1029, 2004)

Key Words: myocardial infarction • smooth muscle cell • myofibroblast • pericyte • arteriole • angiogenesis • desmin • smoothelin • {alpha}-smooth muscle actin • non-muscle myosin heavy chain


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