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 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).
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Abbreviations
- α-GAPDH:
-
glyceraldehyde phosphate dehydrogenase
- GFP:
-
green fluorescent protein
- HUVEC:
-
human umbilical vein endothelial cells
- shRNA:
-
short hairpin RNA
- siRNA:
-
small interfering RNA
- SRE:
-
serum response element
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Original Russian Text © E. V. Semina, K. A. Rubina, P. N. Rutkevich, T. A. Voyno-Yasenetskaya, Y. V. Parfyonova, V. A. Tkachuk, 2009, published in Biokhimiya, 2009, Vol. 74, No. 4, pp. 448–458.
Originally published in Biochemistry (Moscow) On-Line Papers in Press, as Manuscript BM08-318, February 15, 2009.
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Semina, E.V., Rubina, K.A., Rutkevich, P.N. et al. T-cadherin activates Rac1 and Cdc42 and changes endothelial permeability. Biochemistry Moscow 74, 362–370 (2009). https://doi.org/10.1134/S0006297909040026
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DOI: https://doi.org/10.1134/S0006297909040026