Plasminogen activator inhibitor type‐1 deficiency attenuates murine antigen‐induced arthritis

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Abstract
Objective. To examine the role of plasminogen activator inhibitor type‐1 (PAI‐1), the major fibrinolytic inhibitor, in vivo during murine antigen‐induced arthritis (AIA). Methods. AIA was induced in PAI‐1‐deficient mice and control wild‐type mice. Arthritis severity was evaluated by technetium 99m (99mTc) uptake in the knee joints and by histological scoring. Intra‐articular fibrin deposition was examined by immunohistochemistry and synovial fibrinolysis quantitated by tissue D‐dimer measurements and zymograms. Results. Joint inflammation, quantitated by 99mTc uptake, was significantly reduced in PAI‐1−/− mice on day 7 after arthritis onset (PP−/− mice, as shown by histological grading of safranin‐O staining on day 10 after arthritis onset (P−/− mice (P−/− mice (P−/− mice, as shown by zymographic analysis. Conclusions. These results indicate that deficiency of PAI‐1 results in increased synovial fibrinolysis, leading to reduced fibrin accumulation in arthritic joints and reduced severity of AIA.