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Prepublished online as a Blood First Edition Paper on February 6, 2003; DOI 10.1182/blood-2002-11-3338.
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Blood, 1 June 2003, Vol. 101, No. 11, pp. 4446-4448
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Brief report
Inhibition of coagulation, fibrinolysis, and endothelial cell activation by a p38 mitogen-activated protein kinase inhibitor during human endotoxemia
Judith Branger,
Bernt van den Blink,
Sebastiaan Weijer,
Abhya Gupta,
Sander J.H. van Deventer,
C. Erik Hack,
Maikel P. Peppelenbosch, and
Tom van der Poll
From the Laboratory of Experimental Internal Medicine and the Department of Infectious Diseases, Tropical Medicine and AIDS, the Academic Medical Center, and the Central Laboratory of the Netherlands Red Cross Blood Transfusion Service (CLB) and Laboratory for Clinical and Experimental Immunology, University of Amsterdam, Amsterdam, the Netherlands; and Boehringer Ingelheim Pharma KG, Biberach, Germany
P38 mitogen-activated protein kinase (MAPK) is an important component of intracellular signaling cascades that initiate various inflammatory cellular responses. To determine the role of p38 MAPK in the procoagulant response to lipopolysaccharide (LPS), 24 healthy subjects were exposed to an intravenous dose of LPS (4 ng/kg), preceded 3 hours earlier by orally administered 600 or 50 mg BIRB 796 BS (a specific p38 MAPK inhibitor), or placebo. The 600-mg dose of BIRB 796 BS strongly inhibited LPS-induced coagulation activation, as measured by plasma concentrations of the prothrombin fragment F1 + 2. BIRB 796 BS also dose dependently attenuated the activation and subsequent inhibition of the fibrinolytic system (plasma tissue-type plasminogen activator, plasmin- 2-antiplasmin complexes, and plasminogen activator inhibitor type 1) and endothelial cell activation (plasma soluble E-selectin and von Willebrand factor). Activation of p38 MAPK plays an important role in the procoagulant and endothelial cell response after in vivo exposure to LPS.
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