Endothelial Rho signaling is required for monocyte transendothelial migration

FEBS Letters

Barth, Holger²  Gerke, Volker¹  Strey, Anke¹  Janning, Annette¹ 

[1] Institute of Medical Biochemistry, ZMBE, University of Münster, von-Esmarch-Str. 56, D-48149 Münster, Germany;Institute of Experimental and Clinical Pharmacology and Toxicology, University of Freiburg, Freiburg, Germany

关键词: Actin cytoskeleton;    Bacterial toxin;    Cell–cell contact;    Leukocyte extravasation;   

DOI  :  10.1016/S0014-5793(02)02643-1

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 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.

【 授权许可】

Unknown