Endothelial Rho signaling is required for monocyte transendothelial migration

被引:38
作者
Strey, A
Janning, A
Barth, H
Gerke, V
机构
[1] Univ Munster, Inst Med Biochem, ZMBE, D-48149 Munster, Germany
[2] Univ Freiburg, Inst Expt & Clin Pharmacol & Toxicol, Freiburg, Germany
关键词
actin cytoskeleton; bacterial toxin; cell-cell contact; leukocyte extravasation;
D O I
10.1016/S0014-5793(02)02643-1
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Bacterial toxins affecting Rho activity in microvascular endothelial cells were employed to elucidate whether endothelial Rho participates in regulating the migration of monocytes across monolayers of cultured endothelial cells. Inactivation of Rho by the Clostridium C3 exoenzyme resulted in an increased adhesion of peripheral blood monocytes to the endothelium and a decreased rate of transendothelial monocyte migration. Cytotoxic necrotizing factor 1-mediated activation of endothelial Rho also reduced the rate of monocyte transmigration, but did not affect monocyte-endothelium adhesion. Thus, efficient leukocyte extravasation requires Rho signaling not only within the migrating leukocytes but also within the endothelial lining of the vessel wall. (C) 2002 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:261 / 266
页数:6
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