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 Pathogenic Hantaviruses Andes Virus and Hantaan Virus Induce Adherens Junction Disassembly by Directing Vascular Endothelial Cadherin Internalization in Human Endothelial Cells

2010 ◽  
Vol 84 (14) ◽  
pp. 7405-7411 ◽  
Author(s):  
Elena Gorbunova ◽  
Irina N. Gavrilovskaya ◽  
Erich R. Mackow
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Adherens Junctions ◽  
Paracellular Permeability ◽  
Cell Permeability ◽  
Hantaan Virus ◽  
Vascular Endothelial ◽  
Vascular Endothelial Cadherin ◽  
Andes Virus ◽  
Endothelial Cell Permeability

ABSTRACT Hantaviruses infect endothelial cells and cause 2 vascular permeability-based diseases. Pathogenic hantaviruses enhance the permeability of endothelial cells in response to vascular endothelial growth factor (VEGF). However, the mechanism by which hantaviruses hyperpermeabilize endothelial cells has not been defined. The paracellular permeability of endothelial cells is uniquely determined by the homophilic assembly of vascular endothelial cadherin (VE-cadherin) within adherens junctions, which is regulated by VEGF receptor-2 (VEGFR2) responses. Here, we investigated VEGFR2 phosphorylation and the internalization of VE-cadherin within endothelial cells infected by pathogenic Andes virus (ANDV) and Hantaan virus (HTNV) and nonpathogenic Tula virus (TULV) hantaviruses. We found that VEGF addition to ANDV- and HTNV-infected endothelial cells results in the hyperphosphorylation of VEGFR2, while TULV infection failed to increase VEGFR2 phosphorylation. Concomitant with the VEGFR2 hyperphosphorylation, VE-cadherin was internalized to intracellular vesicles within ANDV- or HTNV-, but not TULV-, infected endothelial cells. Addition of angiopoietin-1 (Ang-1) or sphingosine-1-phosphate (S1P) to ANDV- or HTNV-infected cells blocked VE-cadherin internalization in response to VEGF. These findings are consistent with the ability of Ang-1 and S1P to inhibit hantavirus-induced endothelial cell permeability. Our results suggest that pathogenic hantaviruses disrupt fluid barrier properties of endothelial cell adherens junctions by enhancing VEGFR2-VE-cadherin pathway responses which increase paracellular permeability. These results provide a pathway-specific mechanism for the enhanced permeability of hantavirus-infected endothelial cells and suggest that stabilizing VE-cadherin within adherens junctions is a primary target for regulating endothelial cell permeability during pathogenic hantavirus infection.

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

Vascular Endothelial Dysfunction during Cardiac Surgery: On-Pump versus Off-Pump Coronary Surgery

2017 ◽  
Vol 58 (5-6) ◽  
pp. 354-368 ◽  
Author(s):  
Florian Brettner ◽  
Daniel Chappell ◽  
Lisa Schwartz ◽  
Alexander Lukasz ◽  
Philipp Kümpers ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cardiac Surgery ◽  
Endothelial Cell ◽  
Coronary Artery ◽  
Coronary Artery Bypass ◽  
Artery Bypass ◽  
Vascular Endothelial ◽  
Off Pump ◽  
Opcab Group ◽  
Cell Cell

Background: Cardiac surgery often causes ischemia and development of a systemic inflammatory response syndrome, which impairs vascular barrier function, normally maintained by the endothelial cell line and the endothelial glycocalyx (EG). The EG normally covers and protects healthy endothelial cells throughout the vasculature. The aim of the present study was to assess the disruption of the cellular part of the microvascular barrier by determining parameters of endothelial cell activation known to influence and reflect cell-cell junctional integrity. Particular attention was placed on angiopoietins and their important effects on endothelial gap junctions. Furthermore, comparative measurements were undertaken in patients undergoing on- and off-pump cardiac surgery, the latter group presumably experiencing less ischemic stress. Methods: 30 patients undergoing elective coronary artery bypass surgery were assigned to the conventional coronary artery bypass (CCAB) group (n = 15) or the off-pump coronary artery bypass grafting (OPCAB) group (n = 15). Blood samples were obtained for measuring angiopoietin-1 (Ang-1), angiopoietin-2 (Ang-2), vascular endothelial (VE)-cadherin, and endocan at various time points. Results: There were significant increases in all measured parameters in both study groups versus the respective basal values. Maximal increases were as follows: Ang-1: CCAB +220%, OPCAB +166%, p < 0.05 each; Ang-2: CCAB +150%, OPCAB +20%, p < 0.05 each; VE-cadherin: CCAB +87%, OPCAB +66%, p < 0.05 each; endocan: CCAB +323%, OPCAB +72%, p < 0.05 each. Conclusion: The present study demonstrates the activation of endothelial cells, shedding of cell-cell contacts and a potential intrinsic counterregulation by Ang-1 and endocan in patients undergoing major cardiac surgery. Quantitatively greater deviations of parameters in the CCAB than in the OPCAB group suggest a relation between the occurrence of ischemia/reperfusion and the extent of endothelial activation.

scholarly journals The effect of quercetin on endothelial cells is modified by heterocellular interactions

2020 ◽  
Vol 11 (5) ◽  
pp. 3916-3925
Author(s):  
Sarka Tumova ◽  
Michael J. Houghton ◽  
Gary Williamson
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Single Cell ◽  
Cell Function ◽  
Cell Interactions ◽  
Cell Type ◽  
Endothelial Cell Function ◽  
Single Cell Type ◽  
Cell Cell

Single cell-type models are useful for determining mechanisms, but in vivo, cell–cell interactions are important, and neighbouring cells can impact endothelial cell function.

scholarly journals Neutrophil-mediated protection of cultured human vascular endothelial cells from damage by growing Candida albicans hyphae

Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1450-1457 ◽  
Author(s):  
JE Jr Edwards ◽  
D Rotrosen ◽  
JW Fontaine ◽  
CC Haudenschild ◽  
RD Diamond
Keyword(s):  
Endothelial Cells ◽  
Candida Albicans ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Cell Interactions ◽  
Morphological Observation ◽  
Human Neutrophils ◽  
Vascular Endothelial ◽  
Human Vascular Endothelial Cell ◽  
Cell Monolayers

Abstract Interactions were studied between human neutrophils and cultured human umbilical vein endothelial cells invaded by Candida albicans. In the absence of neutrophils, progressive Candida germination and hyphal growth extensively damaged endothelial cell monolayers over a period of 4 to 6 hours, as determined both by morphological changes and release of 51Cr from radiolabeled endothelial cells. Monolayers were completely destroyed and replaced by hyphae after 18 hours of incubation. In contrast, when added 2 hours after the monolayers had been infected with Candida, neutrophils selectively migrated toward and attached to hyphae at points of hyphal penetration into individual endothelial cells (observed by time-lapse video-microscopy). Attached neutrophils spread over hyphal surfaces both within and beneath the endothelial cells; neutrophil recruitment to initial sites of leukocyte-Candida- endothelial cell interactions continued throughout the first 60 minutes of observation. Neutrophil spreading and stasis were observed only along Candida hyphae and at sites of Candida-endothelial cell interactions. These events resulted in 58.0% killing of Candida at 2 hours and subsequent clearance of Candida from endothelial cell monolayers, as determined by microcolony counts and morphological observation. On introduction of additional neutrophils to yield higher ratios of neutrophils to endothelial cells (10 neutrophils:1 endothelial cell), neutrophil migration toward hyphal elements continued. Despite retraction or displacement of occasional endothelial cells by invading Candida and neutrophils, most endothelial cells remained intact, viable, and motile as verified both by morphological observations and measurement of 51Cr release from radiolabeled monolayers. From these studies, we conclude that neutrophils are capable of killing Candida hyphae selectively within human vascular endothelial cell monolayers and may have protective rather than detrimental effects on endothelial cell integrity.

Cadherin dependent regulatory mechanisms of vascular endothelial cell-cell interactions

1993 ◽  
Vol 6 (1) ◽  
pp. 50 ◽  
Author(s):  
Norihisa Matsuyoshi ◽  
Ken-ichi Toda ◽  
Yuji Horiguchi ◽  
Toshihiro Tanaka ◽  
Sadao Imamura
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Cell Interactions ◽  
Regulatory Mechanisms ◽  
Vascular Endothelial ◽  
Cell Cell
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