| Fibrin(ogen)-induced expression of ICAM-1 and chemokines in human synovial fibroblasts. | |
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MedLine Citation:
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PMID: 11046059 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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It has long been recognized that in most inflamed arthritic joints the coagulation system is activated, leading to the local generation of fibrin, and it has long been hypothesized that the local fibrin deposition promotes inflammation and tissue destruction. However, only recently has the direct effect of fibrin on the inflammatory process been seriously investigated, and specific roles assigned to fibrin or its products as mediators of the inflammatory process. Although fibrin and/or fibrinogen (fibrin(ogen)) is abundantly present in inflamed tissues and joints rich in fibroblastic cells, no significant data on fibrin(ogen)-induced gene expression by fibroblasts have been published. We now demonstrate that coculture of human synovial fibroblasts with fibrin(ogen) results in the up-regulation of ICAM-1 as well as increased production of the chemokines IL-8 and growth-related oncogene-alpha. Increased ICAM-1 expression was fibrin(ogen) dose-dependent and was demonstrated by ELISA, flow cytometry, and functional adhesion assays. Levels of ICAM-1 induced by fibrin(ogen) were comparable to those that could be induced by cytokine stimulation. Fibrin(ogen) stimulation of ICAM-1 could be suppressed by pyrrolidinedithiocarbamate, an inhibitor of NF-kappaB activation. Chemokine production was induced by fibrin(ogen) in cell culture supernatants >100-fold as compared with controls. Thus, through its activation of synovial fibroblasts, fibrin(ogen) deposition may promote the recruitment (via chemokines) and retention (via adhesion molecules) of lymphocytes within the arthritic joint. |
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Authors:
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X Liu; T H Piela-Smith |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 165 ISSN: 0022-1767 ISO Abbreviation: J. Immunol. Publication Date: 2000 Nov |
Date Detail:
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Created Date: 2000-11-03 Completed Date: 2000-11-30 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 5255-61 Citation Subset: AIM; IM |
Affiliation:
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Division of Rheumatology, University of Connecticut Health Center, Farmington, CT 06030, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antioxidants
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pharmacology Arthritis, Rheumatoid / immunology, pathology Cell Adhesion / drug effects, immunology Cells, Cultured Chemokines / biosynthesis*, secretion Drug Synergism Female Fibrin / antagonists & inhibitors, physiology Fibrinogen / antagonists & inhibitors, physiology* Fibroblasts / drug effects, immunology, metabolism*, secretion Humans Intercellular Adhesion Molecule-1 / biosynthesis*, metabolism Male Pyrrolidines / pharmacology Synovial Membrane / drug effects, immunology, metabolism*, secretion T-Lymphocytes / drug effects, physiology Thiocarbamates / pharmacology Thrombin / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Chemokines; 0/Pyrrolidines; 0/Thiocarbamates; 126547-89-5/Intercellular Adhesion Molecule-1; 25769-03-3/pyrrolidine dithiocarbamic acid; 9001-31-4/Fibrin; 9001-32-5/Fibrinogen; EC 3.4.21.5/Thrombin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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