T-cadherin activates Rac1 and Cdc42 and changes endothelial permeability.
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).
Semina
E V
EV
Institute of Experimental Cardiology, Cardiology Research Center, Moscow, 121552, Russia.
Rubina
K A
KA
Rutkevich
P N
PN
Voyno-Yasenetskaya
T A
TA
Parfyonova
Y V
YV
Tkachuk
V A
VA
D000818:Animals; D015820:Cadherins / Q000235:genetics / Q000378:metabolism*; D002463:Cell Membrane Permeability; D002478:Cells, Cultured; D015536:Down-Regulation; D042783:Endothelial Cells / Q000737:chemistry / Q000378:metabolism*; D006801:Humans; D051379:Mice; D008870:Microtubules / Q000378:metabolism; D041681:NIH 3T3 Cells; D015398:Signal Transduction; D022502:Stress Fibers / Q000378:metabolism; D015533:Transcriptional Activation; D014471:Umbilical Veins / Q000737:chemistry / Q000378:metabolism; D020764:cdc42 GTP-Binding Protein / Q000235:genetics* / Q000378:metabolism; D020830:rac1 GTP-Binding Protein / Q000235:genetics* / Q000378:metabolism
D015820:Cadherins; C099972:H-cadherin; D020764:cdc42 GTP-Binding Protein; D020830:rac1 GTP-Binding Protein