T-Cadherin Activates Rac1 and Cdc42 and Changes Endothelial Permeability

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E. V. Semina¹, K. A. Rubina^2*, P. N. Rutkevich¹, T. A. Voyno-Yasenetskaya³, Y. V. Parfyonova¹, and V. A. Tkachuk²

¹Institute of Experimental Cardiology, Cardiology Research Center, 3-ya Cherepkovskaya ul. 15a, 121552 Moscow, Russia; fax: (495) 414-6712

²Faculty of Fundamental Medicine, Lomonosov Moscow State University, Lomonosovskii pr. 31, Build. 5, 117192 Moscow, Russia; fax: (495) 932-9904; E-mail: rkseniya@mail.ru

³Department of Pharmacology, Illinois University, Chicago, USA; fax: (312) 996-1225

^* To whom correspondence should be addressed.

Received October 2, 2008; Revision received November 20, 2008

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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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KEY WORDS: T-cadherin, Rho GTPases, endothelial cell permeability, microtubules, actin

DOI: 10.1134/S0006297909040026

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