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Updated: Jun 23, 2026

Study of the Actin Cytoskeleton in Live Endothelial Cells Expressing GFP-Actin
Published on: November 18, 2011
T-cadherin activates Rac1 and Cdc42 and changes endothelial permeability
E V Semina1, K A Rubina, P N Rutkevich
1Institute of Experimental Cardiology, Cardiology Research Center, Moscow, 121552, Russia.
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).
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