Enhanced expression of genes involved in coagulation and fibrinolysis in murine arthritis

Rheumatoid arthritis (RA) is a common autoimmune disease of unknown etiology, characterized by chronic synovial inflammation that leads to progressive destruction of cartilage and bone [ 1 ]. Immunological mechanisms are thought to initiate synovial inflammation, which becomes persistent with the disease progression. Among the many histopathological features described, one of the most striking is the accumulation of fibrin [ 2 , 3 ]. We have recently provided evidence that synovial deposition of this protein plays a deleterious role in arthritic joints in antigen-induced arthritis (AIA), a well-established model of RA [ 4 ]. This accumulation of fibrin could result from a local imbalance between its formation and dissolution. Previous studies have revealed enhanced coagulation activity in rheumatoid synovial fluid and membrane [ 3 , 5 ] as well as increased activity of synovial urokinase plasminogen activator (uPA) in rheumatoid synovial membrane [ 6 ]. Little is known about the expression of procoagulant molecules in the arthritic synovial membrane, and the molecular events that tip the natural balance between synovial procoagulant and fibrinolysis in favor of coagulation remain to be elucidated.