Novel mechanism regulating endothelial permeability via T-cadherin-dependent VE-cadherin phosphorylation and clathrin-mediated endocytosis

Semina, E.; KA, R.; VY, S.; PN, R.; NM, K.; VA, T.

Авторы: Semina EV, Rubina KA, Sysoeva VY, Rutkevich PN, Kashirina NM, Tkachuk VA
Журнал: Molecular and Cellular Biochemistry
Том: 387
Номер: 1-2
Год издания: 2014
Издательство: Kluwer Academic/Plenum Publishers
Местоположение издательства: United States
Первая страница: 39
Последняя страница: 53
DOI: 10.1007/s11010-013-1867-4
Аннотация: T-cadherin is a unique member of the cadherin superfamily of adhesion molecules. In contrast to ‘‘classical’’ cadherins, T-cadherin lacks transmembrane and cytoplasmic domains and is anchored to the cell membrane via a glycosilphosphoinositol moiety. T-cadherin is predominantly expressed in cardiovascular system. Clinical and biochemical studies evidence that expression of T-cadherin increases in post-angioplasty restenosis and atherosclerotic lesions—conditions associated with endothelial dysfunction and pathological expression of adhesion molecules. Here, we provide data suggesting a new signaling mechanism by which T-cadherin regulates endothelial permeability. T-cadherin overexpression leads to VE-cadherin phosphorylation on Y731 (b-catenin-binding site), VE-cadherin clathrin-dependent endocytosis and its degradation in lysosomes. Moreover, T-cadherin overexpression results in activation of Rho GTPases signaling and actin stress fiber formation. Thus, T-cadherin up-regulation is involved in degradation of a key endothelial adhesion molecule, VE-cadherin, resulting in the disruption of endothelial barrier function. Our results point to the role of T-cadherin in regulation of endothelial permeability and its possible engagement in endothelial dysfunction.
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Novel mechanism regulating endothelial permeability via T-cadherin-dependent VE-cadherin phosphorylation and clathrin-mediated endocytosisстатья

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