Endothelial Rho signaling is required for monocyte transendothelial migration

FEBS Lett. 2002 Apr 24;517(1-3):261-6. doi: 10.1016/s0014-5793(02)02643-1.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • ADP Ribose Transferases / pharmacology
  • Actin Cytoskeleton / physiology
  • Acute-Phase Proteins / metabolism*
  • Bacterial Toxins / pharmacology
  • Botulinum Toxins*
  • Cell Adhesion / drug effects
  • Cell Adhesion / physiology
  • Cell Movement / physiology*
  • Cells, Cultured
  • Cytotoxins / pharmacology
  • Endothelium, Vascular / physiology*
  • Escherichia coli Proteins*
  • Humans
  • Monocytes / physiology*
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*

Substances

  • Acute-Phase Proteins
  • Bacterial Toxins
  • Cytotoxins
  • Escherichia coli Proteins
  • acute-phase protein rho
  • cytotoxic necrotizing factor type 1
  • ADP Ribose Transferases
  • exoenzyme C3, Clostridium botulinum
  • Botulinum Toxins