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American Journal of Pathology, Vol 149, 1427-1433, Copyright © 1996 by American Society for Investigative Pathology
REGULAR ARTICLES |
ST Nikkari, M Hoyhtya, J Isola and T Nikkari
Department of Medical Biochemistry, University of Tampere Medical School, Finland.
Inflammation precedes erosion and rupture of atherosclerotic atheromas and aneurysms. Inflammatory infiltrates of macrophages have been shown to secrete proteolytic enzymes, including matrix metalloproteinases (MMPs), that weaken the arterial wall. The effect of inflammation on arterial structure and remodeling can be studied in primary vascular inflammatory diseases such as in temporal arteritis. We examined the 72- kd gelatinase (MMP-2) and the 92-kd gelatinase (MMP-9) in inflamed and uninvolved temporal arteries from 10 patients with temporal arteritis and 5 controls by immunohistochemistry. The substrates of these enzymes, type IV collagen and elastin, were detected by immunohistochemistry and histochemical staining, respectively. Both diseased and normal artery specimens had moderate staining for immunoreactive MMP-2. Temporal arteritis specimens had clearly enhanced immunostaining for MMP-9 compared with normal arteries. MMP-9 was specifically localized to macrophages in regions of internal elastic lamina disruption, which may thus be of pathological significance.
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