Biochemistry (Moscow)

, Volume 74, Issue 4, pp 362–370 | Cite as

T-cadherin activates Rac1 and Cdc42 and changes endothelial permeability

  • E. V. Semina
  • K. A. RubinaEmail author
  • P. N. Rutkevich
  • T. A. Voyno-Yasenetskaya
  • Y. V. Parfyonova
  • V. A. Tkachuk
Accelerated Publication


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 micro-tubule 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).

Key words

T-cadherin Rho GTPases endothelial cell permeability microtubules actin 



glyceraldehyde phosphate dehydrogenase


green fluorescent protein


human umbilical vein endothelial cells


short hairpin RNA


small interfering RNA


serum response element


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Supplementary material

10541_2009_4002_MOESM1_ESM.pdf (489 kb)
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Copyright information

© Pleiades Publishing, Ltd. 2009

Authors and Affiliations

  • E. V. Semina
    • 1
  • K. A. Rubina
    • 2
    Email author
  • P. N. Rutkevich
    • 1
  • T. A. Voyno-Yasenetskaya
    • 3
  • Y. V. Parfyonova
    • 1
  • V. A. Tkachuk
    • 2
  1. 1.Institute of Experimental CardiologyCardiology Research CenterMoscowRussia
  2. 2.Faculty of Fundamental MedicineLomonosov Moscow State UniversityMoscowRussia
  3. 3.Department of PharmacologyIllinois UniversityChicagoUSA

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