A preliminary study of endothelial cell migration during angiogenesis using a meshless method approach

2020 ◽  
Vol 36 (11) ◽  
Author(s):  
Ana Guerra ◽  
Jorge Belinha ◽  
Renato Natal Jorge
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Meshless Method ◽  
Endothelial Cell Migration ◽  
Preliminary Study ◽  
Method Approach

Cyclic strain-mediated regulation of vascular endothelial cell migration and tube formation

2005 ◽  
Vol 329 (2) ◽  
pp. 573-582 ◽  
Author(s):  
Nicholas Von Offenberg Sweeney ◽  
Philip M. Cummins ◽  
Eoin J. Cotter ◽  
Paul A. Fitzpatrick ◽  
Yvonne A. Birney ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Cyclic Strain ◽  
Tube Formation ◽  
Endothelial Cell Migration ◽  
Vascular Endothelial

scholarly journals Ablation of SGK1 Impairs Endothelial Cell Migration and Tube Formation Leading to Decreased Neo-Angiogenesis Following Myocardial Infarction

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e80268 ◽  
Author(s):  
Elham Zarrinpashneh ◽  
Tommaso Poggioli ◽  
Padmini Sarathchandra ◽  
Jonas Lexow ◽  
Laurent Monassier ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Tube Formation ◽  
Endothelial Cell Migration

scholarly journals VEGF-induced endothelial cell migration requires urokinase receptor (uPAR)-dependent integrin redistribution

2012 ◽  
Vol 94 (1) ◽  
pp. 125-135 ◽  
Author(s):  
Revu Ann Alexander ◽  
Gerald W. Prager ◽  
Judit Mihaly-Bison ◽  
Pavel Uhrin ◽  
Stefan Sunzenauer ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Urokinase Receptor ◽  
Endothelial Cell Migration

Mafba and  Mafbb Differentially Regulate Lymphatic Endothelial Cell Migration in Topographically Distinct Manners

2021 ◽  
Author(s):  
Hannah Arnold ◽  
Virginia Panara ◽  
Beata Filipek-Gorniok ◽  
Renae Skoczylas ◽  
Petter Ranefall ◽  
...  
Keyword(s):  
Cell Migration ◽  
Endothelial Cell ◽  
Lymphatic Endothelial Cell ◽  
Endothelial Cell Migration

Reactive oxygen species mediate Rac-induced loss of cell-cell adhesion in primary human endothelial cells

2002 ◽  
Vol 115 (9) ◽  
pp. 1837-1846 ◽  
Author(s):  
Sandra van Wetering ◽  
Jaap D. van Buul ◽  
Safira Quik ◽  
Frederik P. J. Mul ◽  
Eloise C. Anthony ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Cell Migration ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Reactive Oxygen ◽  
Small Gtpases ◽  
Endothelial Cell Migration ◽  
Oxygen Species ◽  
Cell Cell

The integrity of the endothelium is dependent on cell-cell adhesion, which is mediated by vascular-endothelial (VE)-cadherin. Proper VE-cadherin-mediated homotypic adhesion is, in turn, dependent on the connection between VE-cadherin and the cortical actin cytoskeleton. Rho-like small GTPases are key molecular switches that control cytoskeletal dynamics and cadherin function in epithelial as well as endothelial cells. We show here that a cell-penetrating, constitutively active form of Rac (Tat-RacV12) induces a rapid loss of VE-cadherin-mediated cell-cell adhesion in endothelial cells from primary human umbilical veins (pHUVEC). This effect is accompanied by the formation of actin stress fibers and is dependent on Rho activity. However,transduction of pHUVEC with Tat-RhoV14, which induces pronounced stress fiber and focal adhesion formation, did not result in a redistribution of VE-cadherin or an overall loss of cell-cell adhesion. In line with this observation, endothelial permeability was more efficiently increased by Tat-RacV12 than by Tat-RhoV14. The loss of cell-cell adhesion, which is induced by Tat-RacV12, occurred in parallel to and was dependent upon the intracellular production of reactive oxygen species (ROS). Moreover, Tat-RacV12 induced an increase in tyrosine phosphorylation of a component the VE-cadherin-catenin complex, which was identified as α-catenin. The functional relevance of this signaling pathway was further underscored by the observation that endothelial cell migration, which requires a transient reduction of cell-cell adhesion, was blocked when signaling through ROS was inhibited. In conclusion, Rac-mediated production of ROS represents a previously unrecognized means of regulating VE-cadherin function and may play an important role in the (patho)physiology associated with inflammation and endothelial damage as well as with endothelial cell migration and angiogenesis.

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