Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:e10-e14
Published online before print March 14, 2002, doi: 10.1161/01.ATV.0000015595.95497.2F
Published online before print March 14, 2002, doi: 10.1161/01.ATV.0000015595.95497.2F
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© 2002 American Heart Association, Inc.
Atherosclerosis and Lipoproteins |
Production of the Long Pentraxin PTX3 in Advanced Atherosclerotic Plaques
From the Heart Research Institute (M.S.R., S.Z.), Camperdown, New South Wales, Australia; Instituto di Recerche Farmacologiche Mario Negri (B.B., C.G, A.M.), Milan, Italy; and Center for Molecular Medicine (G.K.H.), Karolinska Institute, Stockholm, Sweden.
Manuscript handled by Jeremy Pearson, London, UK.Correspondence to Dr Michael Rolph, Garvan Institute of Medical Research, 384 Victoria St, Darlinghurst, Sydney, NSW, 2010, Australia. E-mail m.rolph{at}garvan.org.au
Elevated plasma levels of the pentraxin protein family member C-reactive protein (CRP) are associated with increased risk of cardiovascular disease in both healthy and high-risk subjects. The long pentraxin family member, pentraxin 3 (PTX3), was recently described. Like CRP, PTX3 is induced by acute inflammatory stimuli and is increased in the blood of patients with acute myocardial infarction. Unlike CRP, it is expressed in a wide range of cell types, but not in hepatocytes. In this study, we have investigated the expression of PTX3 in atherosclerosis. Immunohistochemical staining of advanced atherosclerotic lesions revealed strong expression of PTX3. In contrast, no PTX3 expression was observed in nonatherosclerotic internal mammary arteries. By staining serial sections with cell type– and PTX3-specific antibodies, we observed that PTX3 was produced principally by macrophages and endothelial cells. Infrequent expression by smooth muscle cells was also observed. Our results suggest that PTX3 may contribute to the pathogenesis of atherosclerosis.
Key Words: pentraxin 3 • atherosclerosis • macrophage • immunohistochemistry • C-reactive protein
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