Kruppel-Like Factor 2 Inhibits Protease Activated Receptor-1 Expression and Thrombin-Mediated Endothelial Activation

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Kruppel-like factor 2 inhibits protease activated receptor-1 expression and thrombin-mediated endothelial activation.

OBJECTIVE The serine protease thrombin can dramatically alter endothelial gene expression in a manner that confers a proinflammatory phenotype. Recent studies have identified the Kruppel-like factor 2 (KLF2) as a critical regulator of endothelial gene expression. Herein, we provide evidence that KLF2 inhibits thrombin-mediated endothelial activation via alterations in expression of its principa...

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Rapid Communication Kruppel-Like Factor 2 Inhibits Protease Activated Receptor-1 Expression and Thrombin-Mediated Endothelial Activation

Thrombin-Mediated Endothelial Activation Kruppel-Like Factor 2 Inhibits Protease Activated Receptor-1 Expression and Print ISSN: 1079-5642. Online ISSN: 1524-4636 Copyright © 2006 American Heart Association, Inc. All rights reserved. Greenville Avenue, Dallas, TX 75231 is published by the American Heart Association, 7272 Arteriosclerosis, Thrombosis, and Vascular Biology doi: 10.1161/01.ATV.000...

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Aprotinin inhibits proinflammatory activation of endothelial cells by thrombin through the protease-activated receptor 1.

OBJECTIVE Thrombin is generated in significant quantities during cardiopulmonary bypass and mediates adverse events, such as platelet aggregation and proinflammatory responses, through activation of the high-affinity thrombin receptor protease-activated receptor 1, which is expressed on platelets and endothelium. Thus antagonism of protease-activated receptor 1 might have broad therapeutic sign...

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The serine protease thrombin activates Protease-Activated Receptors (PARs), a family of G-protein-coupled receptors (GPCRs) activated by the proteolytic cleavage of their extracellular N-terminal domain. Four members of this family have been identified: PAR1-4. The activation of Protease-Activated Receptor 1(PAR1), the prototype of this receptor family, leads to an increase in intracellular Ca+...

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Kruppel-like factor 2 regulates endothelial barrier function.

OBJECTIVE A central function of the endothelium is to serve as a selective barrier that regulates fluid and solute exchange. Although perturbation of barrier function can contribute to numerous disease states, our understanding of the molecular mechanisms regulating this aspect of endothelial biology remains incompletely understood. Accumulating evidence implicates the Kruppel-like factor 2 (KL...

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ژورنال

عنوان ژورنال: Arteriosclerosis, Thrombosis, and Vascular Biology

سال: 2006

ISSN: 1079-5642,1524-4636

DOI: 10.1161/01.atv.0000215638.53414.99