|
|
Prepublished online as a Blood First Edition Paper on February 6, 2003; DOI 10.1182/blood-2002-11-3338.
 Previous Article | Table of Contents | Next Article 
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.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
T. Thalhamer, M. A. McGrath, and M. M. Harnett
MAPKs and their relevance to arthritis and inflammation
Rheumatology,
April 1, 2008;
47(4):
409 - 414.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. C. Marshall
Sepsis: rethinking the approach to clinical research
J. Leukoc. Biol.,
March 1, 2008;
83(3):
471 - 482.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Bahador and A. S. Cross
Review: From therapy to experimental model: a hundred years of endotoxin administration to human subjects
Innate Immunity,
October 1, 2007;
13(5):
251 - 279.
[Abstract]
[PDF]
|
|
|
|
|
|
|
M. D. de Kruif, L. C. Lemaire, I. A. Giebelen, M. A. D. van Zoelen, J. M. Pater, P. S. van den Pangaart, A. P. Groot, A. F. de Vos, P. J. Elliott, J. C. M. Meijers, et al.
Prednisolone Dose-Dependently Influences Inflammation and Coagulation during Human Endotoxemia
J. Immunol.,
February 1, 2007;
178(3):
1845 - 1851.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Renckens, J. M. Pater, and T. v. d. Poll
Plasminogen Activator Inhibitor Type-1-Deficient Mice Have an Enhanced IFN-{gamma} Response to Lipopolysaccharide and Staphylococcal Enterotoxin B
J. Immunol.,
December 1, 2006;
177(11):
8171 - 8176.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
K. Bijangi-Vishehsaraei, M. R. Saadatzadeh, A. Werne, K. A. W. McKenzie, R. Kapur, H. Ichijo, and L. S. Haneline
Enhanced TNF-{alpha}-induced apoptosis in Fanconi anemia type C-deficient cells is dependent on apoptosis signal-regulating kinase 1
Blood,
December 15, 2005;
106(13):
4124 - 4130.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
Y. Kuma, G. Sabio, J. Bain, N. Shpiro, R. Marquez, and A. Cuenda
BIRB796 Inhibits All p38 MAPK Isoforms in Vitro and in Vivo
J. Biol. Chem.,
May 20, 2005;
280(20):
19472 - 19479.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. Shiratsuchi and M. D. Basson
Activation of p38 MAPK{alpha} by extracellular pressure mediates the stimulation of macrophage phagocytosis by pressure
Am J Physiol Cell Physiol,
May 1, 2005;
288(5):
C1083 - C1093.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
B. Jilma, C. Marsik, F. Kovar, O. F. Wagner, P. Jilma-Stohlawetz, and G. Endler
The single nucleotide polymorphism Ser128Arg in the E-selectin gene is associated with enhanced coagulation during human endotoxemia
Blood,
March 15, 2005;
105(6):
2380 - 2383.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Bohgaki, T. Atsumi, Y. Yamashita, S. Yasuda, Y. Sakai, A. Furusaki, T. Bohgaki, O. Amengual, Y. Amasaki, and T. Koike
The p38 mitogen-activated protein kinase (MAPK) pathway mediates induction of the tissue factor gene in monocytes stimulated with human monoclonal anti-{beta}2Glycoprotein I antibodies
Int. Immunol.,
November 1, 2004;
16(11):
1633 - 1641.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
G. Schabbauer, M. Tencati, B. Pedersen, R. Pawlinski, and N. Mackman
PI3K-Akt Pathway Suppresses Coagulation and Inflammation in Endotoxemic Mice
Arterioscler. Thromb. Vasc. Biol.,
October 1, 2004;
24(10):
1963 - 1969.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
T. Force, K. Kuida, M. Namchuk, K. Parang, and J. M. Kyriakis
Inhibitors of Protein Kinase Signaling Pathways: Emerging Therapies for Cardiovascular Disease
Circulation,
March 16, 2004;
109(10):
1196 - 1205.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. Renckens, S. Weijer, A. F. de Vos, J. M. Pater, J. C. Meijers, C. E. Hack, M. Levi, and T. van der Poll
Inhibition of Plasmin Activity by Tranexamic Acid Does Not Influence Inflammatory Pathways During Human Endotoxemia
Arterioscler. Thromb. Vasc. Biol.,
March 1, 2004;
24(3):
483 - 488.
[Abstract]
[Full Text]
|
|
|
|
|
