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The plasminogen act...
The plasminogen activator/plasmin system is essential for development of the joint inflammatory phase of collagen type II-induced arthritis.
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- Li, Jinan (författare)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik,Umeå University, Umeå, Sweden
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- Ny, Annelii (författare)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik,Umeå University, Umeå, Sweden; Flanders Interuniversity Institute for Biotechnology, KU Leuven, Leuven, Belgium
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- Leonardsson, Göran (författare)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik,Umeå University, Umeå, Sweden
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- Nandakumar, Kutty Selva, 1965- (författare)
- Lund University, Lund, Sweden
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- Holmdahl, Rikard (författare)
- Lund University,Lunds universitet,Immunologi,Forskargrupper vid Lunds universitet,Immunology,Lund University Research Groups,Lund University, Lund, Sweden
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- Ny, Tor (författare)
- Umeå universitet,Institutionen för medicinsk kemi och biofysik,Umeå University, Umeå, Sweden
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(creator_code:org_t)
- New York : Elsevier, 2005
- 2005
- Engelska.
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Ingår i: American Journal of Pathology. - New York : Elsevier. - 0002-9440 .- 1525-2191. ; 166:3, s. 783-792
- Relaterad länk:
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http://www.ncbi.nlm....
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http://ajp.amjpathol... (free)
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https://doi.org/10.1...
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https://urn.kb.se/re...
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https://lup.lub.lu.s...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- The plasminogen activator (PA) system has been proposed to have important roles in rheumatoid arthritis. Here we have used the autoimmune collagen type II (CII)-induced arthritis (CIA) model and mice deficient for urokinase-type PA (uPA) or plasminogen to investigate the role of the PA system for development of arthritis. Our data revealed that uPA-deficient mice have a lower severity and incidence of CIA than wild-type mice. Furthermore, although >80% of wild-type control mice developed CIA, we found that none of the 50 plasminogen-deficient littermates that were tested developed CIA within a 40-day period. Antibody generation after CII immunization as well as the binding of labeled anti-CII antibodies to the surface of cartilage were similar in wild-type and plasminogen-deficient mice. No sign of inflammation was seen when plasminogen-deficient mice were injected with a mixture of monoclonal antibodies against CII. However, after daily injections of human plasminogen, these mice developed arthritis within 5 days. Our finding that infiltration of inflammatory cells into the synovial joints was impaired in plasminogen-deficient mice suggests that uPA and plasminogen are important mediators of joint inflammation. Active plasmin is therefore essential for the induction of pathological inflammatory joint destruction in CIA.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)
Nyckelord
- Animals
- Antibodies; Monoclonal/chemistry
- Arthritis/*immunology/pathology
- Arthritis; Experimental/*immunology/pathology
- Collagen Type II/*metabolism
- Enzyme-Linked Immunosorbent Assay
- Epitopes
- Immunohistochemistry
- Inflammation/*metabolism
- Joints/*immunology
- Mice
- Mice; Inbred C57BL
- Plasmin/*metabolism
- Plasminogen/*metabolism/*physiology
- Plasminogen Activators/*metabolism
- Time Factors
- Urinary Plasminogen Activator/*physiology
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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