ArticleThe American journal of pathology2002
Differing roles for urokinase and tissue-type plasminogen activator in collagen-induced arthritis.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- The Coagulation Factors Fibrinogen, Thrombin, and Factor XII in Inflammatory Disorders-A Systematic Review.Frontiers in immunology · 2018Pooled it
- Pathogenic and Regulatory Roles of Fibrinolytic Factors in Autoimmune Diseases.Current issues in molecular biology · 2025Review
- Identification and preclinical development of an anti-proteolytic uPA antibody for rheumatoid arthritis.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Therapeutics targeting the fibrinolytic system.Experimental & molecular medicine · 2020Review
- Review
- The Urokinase Plasminogen Activation System in Rheumatoid Arthritis: Pathophysiological Roles and Prospective Therapeutic Targets.Current drug targets · 2019Review
- Absence of functional compensation between coagulation factor VIII and plasminogen in double-knockout mice.Blood advances · 2018Article
- Urokinase plasminogen activator and receptor promote collagen-induced arthritis through expression in hematopoietic cells.Blood advances · 2017Article
- A New Explanation of Inflammation in Rheumatoid Arthritis Patients With Respect to Claudin-5, Matrix Metalloproteinase-9, and Neuroserpin.Archives of rheumatology · 2016Article
- Deficiency of hyaluronan synthase 1 (Has1) results in chronic joint inflammation and widespread intra-articular fibrosis in a murine model of knee joint cartilage damage.Osteoarthritis and cartilage · 2015Article
- GM-CSF and uPA are required for Porphyromonas gingivalis-induced alveolar bone loss in a mouse periodontitis model.Immunology and cell biology · 2015Article
- Porphyromonas gingivalis-derived RgpA-Kgp Complex Activates the Macrophage Urokinase Plasminogen Activator System: IMPLICATIONS FOR PERIODONTITIS.The Journal of biological chemistry · 2015Article
- Plasminogen is a joint-specific positive or negative determinant of arthritis pathogenesis in mice.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Fibrinolysis is down-regulated in mouse collagen-induced arthritis, but its normalization does not alleviate the course of disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2011Article
- Urokinase-type plasminogen activator and arthritis progression: role in systemic disease with immune complex involvement.Arthritis research & therapy · 2010Article
- Urokinase-type plasminogen activator and arthritis progression: contrasting roles in systemic and monoarticular arthritis models.Arthritis research & therapy · 2010Article
- Fibrin(ogen) exacerbates inflammatory joint disease through a mechanism linked to the integrin alphaMbeta2 binding motif.The Journal of clinical investigation · 2007Article
- Regulatory polymorphisms in extracellular matrix protease genes and susceptibility to rheumatoid arthritis: a case-control study.Arthritis research & therapy · 2006Article
- The plasminogen activator/plasmin system is essential for development of the joint inflammatory phase of collagen type II-induced arthritis.The American journal of pathology · 2005Article
- Plasminogen activation/plasmin in rheumatoid arthritis: matrix degradation and more.The American journal of pathology · 2005Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The plasminogen activators, urokinase PA (u-PA) and tissue-type PA (t-PA), are believed to play important roles in inflammatory cell infiltration, fibrin deposition, and joint destruction associated with rheumatoid arthritis; however, their precise roles in such processes, particularly u-PA, have yet to be defined. Using gene-deficient mice we examined the relative contribution of the PAs to the chronic systemic collagen-induced arthritis model. Based on clinical and histological assessments, u-PA-/- mice developed significantly milder disease and t-PA-/- mice more severe disease compared with the relevant wild-type mice. Fibrin deposition within joints paralleled disease severity and was particularly pronounced in t-PA-/- mice. Likewise, cytokine levels in the synovium reflected the severity of disease, with interleukin-1beta levels in particular being lower in u-PA-/- mice and increased in t-PA-/- mice. The antibody response to type II collagen was normal in both knockouts; however, T cells from u-PA-/- mice had a reduced proliferative response and produced less interferon-gamma on antigen stimulation in vitro. These results indicate that the major effect of u-PA in the collagen-induced arthritis model is deleterious, whereas that of t-PA is protective. Our data highlight the complexities of PA function, and suggest that approaches either to target u-PA or to enhance local t-PA activity in joints may be of therapeutic benefit in rheumatoid arthritis.
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