Plasminogen/plasmin system function in mice deficient in stromelysin-1 (MMP-3) or in tissue inhibitor of metalloproteinases type-1 (TIMP-1)

摘要: Summary Specific interactions between the plasminogen/plasmin (fibrinolytic) and matrix metalloproteinase (MMP) systems suggest that both may cooperate in extracellular degradation. Therefore, system function was evaluated mice with stromelysin-1 (MMP-3) or tissue inhibitor of MMP type-1 (TIMP-1) gene inactivation. Urinary urokinase-type plasminogen activator (u-PA) antigen (120–190 ng/ml) activity (13–18 IU/ml) levels were similar wild-type gene-deficient mice. Vascular activity, measured aorta extracts, for tissue-type (t-PA)-mediated (8–14 arbitrary units (AU) per mg protein) u-PA-mediated (25–34 AU protein). The spontaneous thrombolytic potential (lysis a 125 I-fibrin labelled pulmonary embolus) comparable (MMP-3 +/+ ) MMP-3 −/− (36 ± 6% versus 49 5% after 8 h; P = 0.13), (TIMP-1 TIMP-1 (48 4% 48 2% h). Organ sections did not reveal significant fibrin deposition liver any genotypes. Furthermore, vivo thioglycollate-stimulated macrophages all 4 genotypes expressed activating degrading potential. Thus, these data do play major role generation fibrinolytic mediated via system.