CDH5

(redirected from VE-cadherin)

CDH5

A gene on chromosome 16q22.1 that encodes a calcium-dependent cell–cell adhesion glycoprotein (cadherin), which is involved in regulating cell–cell adhesions, mobility and proliferation of epithelial cells. CDH5 is thought to play a key role in endothelial cell biology by controlling cohesion and organisation of intercellular junctions.
References in periodicals archive ?
Diabetic hyperglycemia is toxic to the retinal microvasculature, causing pericyte apoptosis, which in turn disrupts microvascular intracellular trafficking of the adherent cadherin:catenin (e.g., VE-cadherin) components of retinal vascular endothelial cell-cell junctions.
HMGB1, TLR4, phospho-NF-[kappa]B (p-NF-[kappa]B), and VE-cadherin expression in LPS-stimulated HPMEC cells
Delayed vasculogenesis and impaired angiogenesis due to altered Ang-2 and VE-cadherin levels in the chick embryo model following exposure to cadmium.
VE-cadherin, which is only expressed in the epithelial cell, and JAM-1 are key factors in vascular hemostasis and angiogenesis [5, 6].
PB-MNC, stimulated or not with ephrin-B2, did not modify Evans blue extravasation (N = 6 - 7) or occludin, claudin-5, ZO-1, or VE-cadherin mRNA expression compared to PBS (N =5 - 7) (Figure 5).
Adherens junctions are a major part of the complex, in which VE-cadherin, an endothelium-specific component of adhesion proteins, controls both adherens junctions and endothelial barrier integrity [20, 21].
The protective role of Sirt1 in LPS-induced EC hyperpermeability was then verified by monitoring the monolayer barrier and detecting the morphological alterations of F-actin and VE-cadherin. It was revealed that the decrease in TER level induced by LPS was remarkably reversed by both pretreatment and simultaneous treatment with SRT1720, consistent with the reversed decrease in flux of dextran (Figure 3(a)).
Further activation of Src was mediated by tumor cell-derived IL8 and VLA-4/VCAM-1 interactions leading to phosphorylation of VE-cadherin, a major component of endothelial junctions and finally to disruption of the endothelial barrier [83].
We measured the HUVEC permeability, proliferation, and the secretion of VE-cadherin into culture medium using fluorescein isothiocyanate-dextran assay, 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay, and enzyme-linked immunosorbent assay, respectively, in response to treatment with MMP9 and/or rhubarb monomers.
In TGF-[beta]1 stimulated HPMECs, treatment with GA resulted in a reduction of EndoMT with a decrease in vimentin, and an increase in VE-cadherin instead.
(29.) Chiasson CM, Wittich KB, Vincent PA, Faundez V, Kowalczyk AP p120-catenin inhibits VE-cadherin internalization through a Rho-independent mechanism.
In addition, [beta]-cadherin is found in the placenta (36), VE-cadherin is found in the vascular endothelium, and R-and K-cadherin are found in the retina and kidney, respectively (38).