T-cadherin activates Rac1 and Cdc42 and changes endothelial permeability

Biochemistry (Mosc). 2009 Apr;74(4):362-70. doi: 10.1134/s0006297909040026.

Abstract

In the present study, expression of T-cadherin was shown to induce intracellular signaling in NIH3T3 fibroblasts: it activated Rac1 and Cdc42 (p < 0.01) but not RhoA. T-Cadherin overexpression in human umbilical vein endothelial cells (HUVEC) using adenoviral constructs induced disassembly of microtubules and polymerization of actin stress fibers, whereas down-regulation of endogenous T-cadherin expression in HUVEC using lentiviral constructs resulted in microtubule polymerization and a decrease in the number of actin stress fibers. Moreover, suppression of the T-cadherin expression significantly decreased the endothelial monolayer permeability as compared to the control (p < 0.001).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cadherins / genetics
  • Cadherins / metabolism*
  • Cell Membrane Permeability*
  • Cells, Cultured
  • Down-Regulation
  • Endothelial Cells / chemistry
  • Endothelial Cells / metabolism*
  • Humans
  • Mice
  • Microtubules / metabolism
  • NIH 3T3 Cells
  • Signal Transduction
  • Stress Fibers / metabolism
  • Transcriptional Activation*
  • Umbilical Veins / chemistry
  • Umbilical Veins / metabolism
  • cdc42 GTP-Binding Protein / genetics*
  • cdc42 GTP-Binding Protein / metabolism
  • rac1 GTP-Binding Protein / genetics*
  • rac1 GTP-Binding Protein / metabolism

Substances

  • Cadherins
  • H-cadherin
  • cdc42 GTP-Binding Protein
  • rac1 GTP-Binding Protein