title: Complement receptors in atherosclerotic lesions.
abstract: Accumulation of cholesterol in the tunica intima of arteries is a feature of atherosclerotic development. Recently, the demonstration of oxidized LDL in atherosclerotic lesions considerably strengthened the possibility of its role in the atherogenesis in vivo. However, the mechanism of lipid accumulation in monocyte-derived macrophages has not yet been clarified. It has been reported that the complement system may be related to atherosclerosis. In this report, complement receptors in the atherosclerotic lesions obtained from autopsy sample were investigated. Initially C3b receptors were detected using sheep erythrocytes bearing human C3b (EAC1423b cells). EAC1423b cells adherent to only aortic sections showing intimal thickening, but not to intact artery. Second, immunostaining of consecutive aortic sections was performed. Apo B and C5b-9 complex were stained using the indirect immunoperoxidase method, and macrophage, C3b receptor (CR1) and C3bi receptor (CR3) were stained using monoclonal antibody in the alkaliphosphatase anti-alkaliphosphatase method. In the intact artery of 3 month old patient, antigen- specific staining were not observed. In intimal thickening and atheroma of older patients, consecutive sections suggested that complement receptor-expressing cells were macrophages. Staining for apo B antigen existed at extracellular site in the intima, and C5b-9 complex was observed in intima and partially in the media. The above data showed that macrophage complement receptors were expressed in the atherosclerotic lesions when the complement system was activated. We conclude that these data suggest that the complement system and complement receptors may be related to the uptake of LDL by macrophages.
authors.affiliation: 2nd Department of Internal Medicine, Nihon University School of Medicine, Tokyo, Japan.
authors.forename: E
authors.initials: E
authors.lastname: Saito
authors.forename: T
authors.initials: T
authors.lastname: Fujioka
authors.forename: H
authors.initials: H
authors.lastname: Kanno
authors.forename: E
authors.initials: E
authors.lastname: Hata
authors.forename: T
authors.initials: T
authors.lastname: Ueno
authors.forename: T
authors.initials: T
authors.lastname: Matsumoto
authors.forename: Y
authors.initials: Y
authors.lastname: Takahashi
authors.forename: T
authors.initials: T
authors.lastname: Tochihara
authors.forename: T
authors.initials: T
authors.lastname: Yasugi
mesh_terms: D000293:Adolescent; D000328:Adult; D001013:Aorta, Thoracic / Q000378:metabolism* / Q000473:pathology; D001161:Arteriosclerosis / Q000378:metabolism* / Q000473:pathology; D003179:Complement C3b / Q000378:metabolism; D015938:Complement Membrane Attack Complex / Q000378:metabolism*; D006801:Humans; D007223:Infant; D008264:Macrophages / Q000473:pathology; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D011951:Receptors, Complement / Q000378:metabolism; D017463:Receptors, Complement 3b
chemical_list: D015938:Complement Membrane Attack Complex; D011951:Receptors, Complement; D017463:Receptors, Complement 3b; D003179:Complement C3b