scholarly journals Dynamic Regulation of Vascular Permeability by Vascular Endothelial Cadherin-Mediated Endothelial Cell-Cell Junctions

2017 ◽  
Vol 84 (4) ◽  
pp. 148-159 ◽  
Author(s):  
Seung-Sik Rho ◽  
Koji Ando ◽  
Shigetomo Fukuhara
Keyword(s):  
Endothelial Cell ◽  
Vascular Permeability ◽  
Cell Junctions ◽  
Vascular Endothelial ◽  
Dynamic Regulation ◽  
Vascular Endothelial Cadherin ◽  
Cell Cell

Stealthy Nanoparticles Protecting Endothelium Barrier from Leakiness by Resisting the Absorption of VE-cadherin

Nanoscale ◽  
2021 ◽  
Author(s):  
Yuan Huang ◽  
Suxiao Wang ◽  
Jin-Zhi Zhang ◽  
Hang-Xing Wang ◽  
Qichao Zou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Interstitial Space ◽  
Cell Interactions ◽  
Vascular Endothelial ◽  
Vascular Endothelial Cadherin ◽  
Cell Cell

Nanomaterial induced endothelial cells leakiness (NanoEL) is caused because nanomaterials enter the interstitial space of endothelial cells and disrupt the endothelial cell-cell interactions by interacting with vascular endothelial cadherin (VE-cad)....

scholarly journals RAF dimers control vascular permeability and cytoskeletal rearrangements at endothelial cell‐cell junctions

FEBS Journal ◽  
2019 ◽  
Vol 286 (12) ◽  
pp. 2277-2294 ◽  
Author(s):  
Coralie Dorard ◽  
Botond Cseh ◽  
Karin Ehrenreiter ◽  
Reiner Wimmer ◽  
Andrea Varga ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Permeability ◽  
Cell Junctions ◽  
Cytoskeletal Rearrangements ◽  
Cell Cell

PDZRN3 destabilizes endothelial cell-cell junctions through a PKCζ-containing polarity complex to increase vascular permeability

2017 ◽  
Vol 10 (464) ◽  
pp. eaag3209 ◽  
Author(s):  
Raj N. Sewduth ◽  
Héléna Kovacic ◽  
Béatrice Jaspard-Vinassa ◽  
Vincent Jecko ◽  
Thomas Wavasseur ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Permeability ◽  
Cell Junctions ◽  
Cell Cell

Vascular Endothelial Cadherin (VE-Cadherin): Cloning and Role in Endothelial Cell-Cell Adhesion

1997 ◽  
Vol 4 (2) ◽  
pp. 267-277 ◽  
Author(s):  
Jahanara Ali ◽  
Fang Liao ◽  
Eric Martens ◽  
William A. Muller
Keyword(s):  
Cell Adhesion ◽  
Endothelial Cell ◽  
Vascular Endothelial ◽  
Vascular Endothelial Cadherin ◽  
Cell Cell

scholarly journals Phosphorylation of VE-cadherin controls endothelial phenotypes via p120-catenin coupling and Rac1 activation

2011 ◽  
Vol 300 (1) ◽  
pp. H162-H172 ◽  
Author(s):  
Kunihiko Hatanaka ◽  
Michael Simons ◽  
Masahiro Murakami
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Permeability ◽  
Cell Junctions ◽  
Endothelial Cell Migration ◽  
Wild Type ◽  
P120 Catenin ◽  
Cell Functions ◽  
Preferential Binding ◽  
Cell Cell

To establish the role of vascular endothelial (VE)-cadherin in the regulation of endothelial cell functions, we investigated the effect of phosphorylation of a VE-cadherin site sought to be involved in p120-catenin binding on vascular permeability and endothelial cell migration. To this end, we introduced either wild-type VE-cadherin or Y658 phosphomimetic (Y658E) or dephosphomimetic (Y658F) VE-cadherin mutant constructs into an endothelial cell line (rat fat pad endothelial cells) lacking endogenous VE-cadherin. Remarkably, neither wild-type- nor Y658E VE-cadherin was retained at cell-cell contacts because of p120-catenin preferential binding to N-cadherin, resulting in the targeting of N-cadherin to cell-cell junctions and the exclusion of VE-cadherin. However, Y658F VE-cadherin was able to bind p120-catenin and to localize at adherence junctions displacing N-cadherin. This resulted in an enhanced barrier function and a complete abrogation of Rac1 activation and lamellipodia formation, thereby inhibiting cell migration. These findings demonstrate that VE-cadherin, through the regulation of Y658 phosphorylation, competes for junctional localization with N-cadherin and controls vascular permeability and endothelial cell migration.

VE-cadherin Y685F knock-in mouse is sensitive to vascular permeability in recurrent angiogenic organs

2014 ◽  
Vol 307 (3) ◽  
pp. H455-H463 ◽  
Author(s):  
Adama Sidibé ◽  
Helena Polena ◽  
Karin Pernet-Gallay ◽  
Jeremy Razanajatovo ◽  
Tiphaine Mannic ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cell ◽  
Growth Factor ◽  
Vascular Permeability ◽  
Reproductive Tract ◽  
Cell Junctions ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor

Covalent modifications such as tyrosine phosphorylation are associated with the breakdown of endothelial cell junctions and increased vascular permeability. We previously showed that vascular endothelial (VE)-cadherin was tyrosine phosphorylated in vivo in the mouse reproductive tract and that Y685 was a target site for Src in response to vascular endothelial growth factor in vitro. In the present study, we aimed to understand the implication of VE-cadherin phosphorylation at site Y685 in cyclic angiogenic organs. To achieve this aim, we generated a knock-in mouse carrying a tyrosine-to-phenylalanine point mutation of VE-cadherin Y685 (VE-Y685F). Although homozygous VE-Y685F mice were viable and fertile, the nulliparous knock-in female mice exhibited enlarged uteri with edema. This phenotype was observed in 30% of females between 4 to 14 mo old. Histological examination of longitudinal sections of the VE-Y685F uterus showed an extensive disorganization of myometrium and endometrium with highly edematous uterine glands, numerous areas with sparse cells, and increased accumulation of collagen fibers around blood vessels, indicating a fibrotic state. Analysis of cross section of ovaries showed the appearance of spontaneous cysts, which suggested increased vascular hyperpermeability. Electron microscopy analysis of capillaries in the ovary showed a slight but significant increase in the gap size between two adjacent endothelial cell membranes in the junctions of VE-Y685F mice (wild-type, 11.5 ± 0.3, n = 78; and VE-Y685F, 12.48 ± 0.3, n = 65; P = 0.045), as well as collagen fiber accumulation around capillaries. Miles assay revealed that either basal or vascular endothelial growth factor-stimulated permeability in the skin was increased in VE-Y685F mice. Since edema and fibrotic appearance have been identified as hallmarks of initial increased vascular permeability, we conclude that the site Y685 in VE-cadherin is involved in the physiological regulation of capillary permeability. Furthermore, this knock-in mouse model is of potential interest for further studies of diseases that are associated with abnormal vascular permeability.

scholarly journals Autoregulatory “Multitasking” at Endothelial Cell Junctions by Junction-Associated Intermittent Lamellipodia Controls Barrier Properties

2021 ◽  
Vol 11 ◽  
Author(s):  
Jochen Seebach ◽  
Nadine Klusmeier ◽  
Hans Schnittler
Keyword(s):  
Endothelial Cell ◽  
Transcriptional Activation ◽  
Plasma Membranes ◽  
Current Knowledge ◽  
Vascular Endothelial Cell ◽  
Barrier Properties ◽  
Cell Junctions ◽  
Local Concentration ◽  
Vascular Endothelial ◽  
Dynamic Regulation

Vascular endothelial cell (EC) junctions are key structures controlling tissue homeostasis in physiology. In the last three decades, excellent studies have addressed many aspects of this complex and highly dynamic regulation, including cell signaling, remodeling processes of the proteins of tight junctions, adherens junctions, and gap junctions, the cytoskeleton, and post-transcriptional modifications, transcriptional activation, and gene silencing. In this dynamic process, vascular endothelial cadherin (VE-cadherin) provides the core structure of EC junctions mediating the physical adhesion of cells as well as the control of barrier function and monolayer integrity via remodeling processes, regulation of protein expression and post-translational modifications. In recent years, research teams have documented locally restricted dynamics of EC junctions in which actin-driven protrusions in plasma membranes play a central role. In this regard, our research group showed that the dynamics of VE-cadherin is driven by small (1–5 μm) actin-mediated protrusions in plasma membranes that, due to this specific function, were named “junction-associated intermittent lamellipodia” (JAIL). JAIL form at overlapping, adjacent cells, and exactly at this site new VE-cadherin interactions occur, leading to new VE-cadherin adhesion sites, a process that restores weak or lost VE-cadherin adhesion. Mechanistically, JAIL formation occurs locally restricted (1–5 μm) and underlies autoregulation in which the local VE-cadherin concentration is an important parameter. A decrease in the local concentration of VE-cadherin stimulates JAIL formation, whereas an increase in the concentration of VE-cadherin blocks it. JAIL mediated VE-cadherin remodeling at the subjunctional level have been shown to be of crucial importance in angiogenesis, wound healing, and changes in permeability during inflammation. The concept of subjunctional regulation of EC junctions is strongly supported by permeability assays, which can be employed to quantify actin-driven subjunctional changes. In this brief review, we summarize and discuss the current knowledge and concepts of subjunctional regulation in the endothelium.

scholarly journals Vascular Endothelial Integrity Affects the Severity of Enterovirus-Mediated Cardiomyopathy

2021 ◽  
Vol 22 (6) ◽  
pp. 3053
Author(s):  
Jin-Ho Park ◽  
Ha-Hyeon Shin ◽  
Hyun-Seung Rhyu ◽  
So-Hee Kim ◽  
Eun-Seok Jeon ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vascular Permeability ◽  
Germ Line ◽  
Vascular Endothelial Cell ◽  
Cell Junctions ◽  
Blue Dye ◽  
Vascular Endothelial ◽  
Knock Out ◽  
Endothelial Junction

Coxsackievirus and adenovirus receptor (CAR) is present in epithelial and vascular endothelial cell junctions. We have previously shown a hemorrhagic phenotype in germ-line CAR knock-out mouse embryos; we have also found that CAR interacts with ZO-1 and β-catenin. However, the role of CAR in vascular endothelial junction permeability has not been proven. To understand the roles of CAR in the vascular endothelial junctions, we generated endothelium-specific CAR knockout (CAR-eKO) mice. In the absence of CAR, the endothelial cell layer showed an increase in transmembrane electrical resistance (TER, Ω) and coxsackievirus permeability. Evans blue dye and 70 kDa dextran-FITC were delivered by tail vein injection. We observed increased vascular permeability in the hearts of adult CAR-eKO mice compare with wild-type (WT) mice. There was a marked increase in monocyte and macrophage penetration into the peritoneal cavity caused by thioglycolate-induced peritonitis. We found that CAR ablation in endothelial cells was not significantly increased coxsackievirus B3 (CVB3) induced myocarditis in murine model. However, tissue virus titers were significantly higher in CAR-eKO mice compared with WT. Moreover, CVB3 was detected in the brain of CAR-eKO mice. Endothelial CAR deletion affects the expression of major endothelial junction proteins, such as cadherin and platelet endothelial cell adhesion molecule-1 (PECAM-1) in the cultured endothelial cells as well as liver vessel. We suggest that CAR expression is required for normal vascular permeability and endothelial tight junction homeostasis. Furthermore, CVB3 organ penetration and myocarditis severities were dependent on the endothelial CAR level.

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