Key result
PTX3 selectively localizes to advanced atherosclerotic lesions and is absent in nonatherosclerotic arteries.
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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.
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Rolph et al. (2002) studied Atherosclerosis. PTX3 expression vs. Nonatherosclerotic internal mammary arteries was evaluated on PTX3 expression in tissues. PTX3 is strongly expressed in advanced atherosclerotic lesions, primarily by macrophages and endothelial cells, whereas no expression was observed in nonatherosclerotic internal mammary arteries.
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