title: Expression of pentraxin 3 (PTX3) in human atherosclerotic lesions.
abstract: Pentraxin 3 (PTX3) and C-reactive protein (CRP) are members of the pentraxin superfamily. PTX3 expression is induced in response to inflammatory signals, and is produced at sites of inflammation by several types of cell, primarily monocytes/macrophages, dendritic cells (DCs), endothelial cells, smooth muscle cells (SMCs), and fibroblasts, but is not produced by hepatocytes, which are a major source of CRP. The aim of our study was to investigate the expression pattern of PTX3 in human atherosclerotic lesions using a novel monoclonal antibody against PTX3. We examined coronary arterial thrombi containing an atherosclerotic plaque component removed from patients with acute myocardial infarction and human aortic tissues with various degrees of atherosclerosis sampled from autopsy cases. Immunohistochemical study of paraffin and frozen sections indicated that macrophages, mainly foam cells, expressed PTX3 in advanced atherosclerotic lesions. Interestingly, we also clearly observed PTX3-positive neutrophils infiltrating into atherosclerotic plaques, suggesting that PTX3 derived from neutrophils as well as macrophages plays an important role in atherogenesis.
authors.affiliation: Department of Cellular Function, Division of Cellular and Molecular Pathology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
authors.forename: As
authors.initials: A
authors.lastname: Savchenko
authors.forename: M
authors.initials: M
authors.lastname: Imamura
authors.forename: R
authors.initials: R
authors.lastname: Ohashi
authors.forename: S
authors.initials: S
authors.lastname: Jiang
authors.forename: T
authors.initials: T
authors.lastname: Kawasaki
authors.forename: G
authors.initials: G
authors.lastname: Hasegawa
authors.forename: I
authors.initials: I
authors.lastname: Emura
authors.forename: H
authors.initials: H
authors.lastname: Iwanari
authors.forename: M
authors.initials: M
authors.lastname: Sagara
authors.forename: T
authors.initials: T
authors.lastname: Tanaka
authors.forename: T
authors.initials: T
authors.lastname: Hamakubo
authors.forename: T
authors.initials: T
authors.lastname: Kodama
authors.forename: M
authors.initials: M
authors.lastname: Naito
mesh_terms: D000368:Aged; D000818:Animals; D000911:Antibodies, Monoclonal / Q000096:biosynthesis / Q000276:immunology; D001011:Aorta / Q000276:immunology / Q000473:pathology; D050197:Atherosclerosis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D002097:C-Reactive Protein / Q000032:analysis* / Q000276:immunology; D005260:Female; D005487:Foam Cells / Q000737:chemistry; D006801:Humans; D015151:Immunoblotting / Q000379:methods; D007150:Immunohistochemistry; D007249:Inflammation; D008297:Male; D051379:Mice; D018345:Mice, Knockout; D008875:Middle Aged; D009203:Myocardial Infarction / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D009504:Neutrophils / Q000737:chemistry; D000683:Serum Amyloid P-Component / Q000032:analysis* / Q000276:immunology; D000099153:Pentraxins
chemical_list: D000911:Antibodies, Monoclonal; D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins