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Venous stasis-induced fibrinolysis prevents thrombosis in mice: role of α2-antiplasmin.
Blood
September 2019
Department of Medicine, The University of Arizona, College of Medicine, Phoenix, AZ; and.
Stasis of venous blood triggers deep vein thrombosis by activating coagulation, yet its effects on the fibrinolytic system are not fully understood. We examined the relationship between stasis, fibrinolysis, and the development of experimental venous thrombosis. Effects of stasis-induced deep vein thrombosis and fibrinolysis on thrombosis were examined by inferior vena cava ligation in congenic mice with and without α2-antiplasmin (α2AP), the primary inhibitor of plasmin.
View Article and Find Full Text PDFThrombin-activatable fibrinolysis inhibitor in human abdominal aortic aneurysm disease.
J Thromb Haemost
November 2017
Thrombosis and Tissue Repair Group, Division of Cardiovascular and Diabetes Research, Leeds Institute of Cardiovascular and Metabolic Medicine, School of Medicine, University of Leeds, Leeds, UK.
Unlabelled: Essentials Patients with abdominal aortic aneurysms (AAA) develop dense clots that are resistant to lysis. This study explores the role of thrombin-activatable fibrinolysis inhibitor (TAFI) in human AAA. There is evidence of chronically increased TAFI activation in patients with AAA.
View Article and Find Full Text PDFReleasing the Brakes on the Fibrinolytic System in Pulmonary Emboli: Unique Effects of Plasminogen Activation and α2-Antiplasmin Inactivation.
Circulation
March 2017
From Department of Medicine, University of Tennessee Health Science Center, Memphis.
Background: In patients with hemodynamically significant pulmonary embolism, physiological fibrinolysis fails to dissolve thrombi acutely and r-tPA (recombinant tissue-type plasminogen activator) therapy may be required, despite its bleeding risk. To examine potential mechanisms, we analyzed the expression of key fibrinolytic molecules in experimental pulmonary emboli, assessed the contribution of α2-antiplasmin to fibrinolytic failure, and compared the effects of plasminogen activation and α2-antiplasmin inactivation on experimental thrombus dissolution and bleeding.
Methods: Pulmonary embolism was induced by jugular vein infusion of I-fibrin or fluorescein isothiocyanate-fibrin labeled emboli in anesthetized mice.
α2-Antiplasmin: New Insights and Opportunities for Ischemic Stroke.
Semin Thromb Hemost
March 2017
Department of Medicine, University of Tennessee Health Sciences Center, Memphis, Tennessee.
Thrombotic vascular occlusion is the leading cause of ischemic stroke. High blood levels of α-antiplasmin (a2AP), an ultrafast, covalent inhibitor of plasmin, have been linked in humans to increased risk of ischemic stroke and failure of tissue plasminogen activator (tPA) therapy. Consistent with these observations, a2AP neutralizes the therapeutic benefit of tPA therapy in experimental stroke.
View Article and Find Full Text PDFStreptokinase (SK) is a potent clot dissolver but lacks fibrin clot specificity as it activates human plasminogen (HPG) into human plasmin (HPN) throughout the system leading to increased risk of bleeding. Another major drawback associated with all thrombolytics, including tissue plasminogen activator, is the generation of transient thrombin and release of clot-bound thrombin that promotes reformation of clots. In order to obtain anti-thrombotic as well as clot-specificity properties in SK, cDNAs encoding the EGF 4,5,6 domains of human thrombomodulin were fused with that of streptokinase, either at its N- or C-termini, and expressed these in Pichia pastoris followed by purification and structural-functional characterization, including plasminogen activation, thrombin inhibition, and Protein C activation characteristics.
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