Linked Life Data

8548035

Source:http://linkedlifedata.com/resource/pubmed/id/8548035

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1996-2-20
pubmed:abstractText
One-step fluorescein-conjugated polyclonal antibody technique has shown that C-reactive protein (CRP) was located only extracellularly in human atherosclerotic lesions. In this report a more sensitive streptavidin-biotin technique was applied to detect the localization of CRP in human atherosclerotic lesions. Immunohistochemical staining with polyclonal and monoclonal anti-human CRP antibodies both produced a brown color extracellularly in the necrotic lesions, and intracellularly in CD68+ foam cells. The latter suggests an uptake of CRP-lipid complexes by macrophages. The staining is human CRP-specific because it was eliminated by preabsorption of the monoclonal antibody with pure human CRP, or by substitution of the primary antibody with non-immune rabbit serum. By overlaid CRP-binding study, a positive stain was observed on intimal smooth muscle cells and foam cells, suggesting that they have CRP-binding sites unless the CRP-binding activity was generated de novo through the fixation procedure. Accordingly, it is hypothesized that CRP may facilitate the uptake of lipids by macrophages accumulating in atherosclerotic lesions. Further, CRP might participate in cytolysis, which enlarges the necrotic area, and/or in phagocytosis that scavenges the necrotic tissue.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1320-5463
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
635-41
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Immunohistochemical localization of C-reactive protein-binding sites in human atherosclerotic aortic lesions by a modified streptavidin-biotin-staining method.
pubmed:affiliation
Department of Etiology/Pathophysiology, Shionogi & Co. Ltd, Osaka, Japan.
pubmed:publicationType
Journal Article, Comparative Study