Endothelial cell polarization and chemotaxis in a microfluidic device

Lab on a Chip ◽  
2008 ◽  
Vol 8 (8) ◽  
pp. 1292 ◽  
Author(s):  
Amir Shamloo ◽  
Ning Ma ◽  
Mu-ming Poo ◽  
Lydia L. Sohn ◽  
Sarah C. Heilshorn
Keyword(s):  
Endothelial Cell ◽  
Microfluidic Device ◽  
Cell Polarization

scholarly journals Endothelial cell polarization and orientation to flow in a novel microfluidic multimodal shear stress generator

Lab on a Chip ◽  
2020 ◽  
Vol 20 (23) ◽  
pp. 4373-4390
Author(s):  
Utku M. Sonmez ◽  
Ya-Wen Cheng ◽  
Simon C. Watkins ◽  
Beth L. Roman ◽  
Lance A. Davidson
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Microfluidic Device ◽  
Cell Polarization ◽  
Orientation Analysis ◽  
Stress Gradients ◽  
Multiple Levels

Endothelial cell polarization and orientation analysis using a novel microfluidic device that can simultaneously generate multiple levels of shear stress and shear stress gradients for systematic mechanobiology studies under flow.

scholarly journals Loss of Caveolin-1 Polarity Impedes Endothelial Cell Polarization and Directional Movement

2004 ◽  
Vol 280 (5) ◽  
pp. 3541-3547 ◽  
Author(s):  
Andrew Beardsley ◽  
Kai Fang ◽  
Heather Mertz ◽  
Vince Castranova ◽  
Sherri Friend ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Polarization ◽  
Caveolin 1 ◽  
Directional Movement

RhoA and Rac mediate endothelial cell polarization and detachment induced by T‐cadherin

2005 ◽  
Vol 19 (6) ◽  
pp. 1-23 ◽  
Author(s):  
Maria Philippova ◽  
Danila Ivanov ◽  
Roy Allenspach ◽  
Yoh Takuwa ◽  
Paul Erne ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Polarization

scholarly journals Control of endothelial cell polarity and sprouting angiogenesis by non-centrosomal microtubules

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Maud Martin ◽  
Alexandra Veloso ◽  
Jingchao Wu ◽  
Eugene A Katrukha ◽  
Anna Akhmanova
Keyword(s):  
Endothelial Cell ◽  
Cell Polarity ◽  
Cell Polarization ◽  
Sprouting Angiogenesis ◽  
Cell Protrusion ◽  
Radial Microtubule System ◽  
3D Environments ◽  
Cell Asymmetry ◽  
Vessel Development

Microtubules control different aspects of cell polarization. In cells with a radial microtubule system, a pivotal role in setting up asymmetry is attributed to the relative positioning of the centrosome and the nucleus. Here, we show that centrosome loss had no effect on the ability of endothelial cells to polarize and move in 2D and 3D environments. In contrast, non-centrosomal microtubules stabilized by the microtubule minus-end-binding protein CAMSAP2 were required for directional migration on 2D substrates and for the establishment of polarized cell morphology in soft 3D matrices. CAMSAP2 was also important for persistent endothelial cell sprouting during in vivo zebrafish vessel development. In the absence of CAMSAP2, cell polarization in 3D could be partly rescued by centrosome depletion, indicating that in these conditions the centrosome inhibited cell polarity. We propose that CAMSAP2-protected non-centrosomal microtubules are needed for establishing cell asymmetry by enabling microtubule enrichment in a single-cell protrusion.

Endothelial Cell Polarization During Lumen Formation, Tubulogenesis, and Vessel Maturation in 3D Extracellular Matrices

2015 ◽  
pp. 205-220 ◽  
Author(s):  
George E. Davis ◽  
Katherine R. Speichinger ◽  
Pieter R. Norden ◽  
Dae Joong Kim ◽  
Stephanie L. K. Bowers
Keyword(s):  
Endothelial Cell ◽  
Cell Polarization ◽  
Extracellular Matrices ◽  
Lumen Formation ◽  
Vessel Maturation

scholarly journals Endothelial Cell Culture Under Perfusion On A Polyester-Toner Microfluidic Device

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Ana Carolina Urbaczek ◽  
Paulo Augusto Gomes Carneiro Leão ◽  
Fayene Zeferino Ribeiro de Souza ◽  
Ana Afonso ◽  
Juliana Vieira Alberice ◽  
...  
Keyword(s):  
Cell Culture ◽  
Endothelial Cell ◽  
Microfluidic Device ◽  
Endothelial Cell Culture

scholarly journals Regulation of Endothelial Cell Motility by Complexes of Tetraspan Molecules CD81/TAPA-1 and CD151/PETA-3 with α3β1 Integrin Localized at Endothelial Lateral Junctions

1998 ◽  
Vol 141 (3) ◽  
pp. 791-804 ◽  
Author(s):  
María Yáñez-Mó ◽  
Arántzazu Alfranca ◽  
Carlos Cabañas ◽  
Mónica Marazuela ◽  
Reyes Tejedor ◽  
...  
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Cell Motility ◽  
Cell Polarization ◽  
Cell Junctions ◽  
Cell Junction ◽  
Cell Contact ◽  
Collagen Gels ◽  
Α3β1 Integrin ◽  
Cell Cell

Cell-to-cell junction structures play a key role in cell growth rate control and cell polarization. In endothelial cells (EC), these structures are also involved in regulation of vascular permeability and leukocyte extravasation. To identify novel components in EC intercellular junctions, mAbs against these cells were produced and selected using a morphological screening by immunofluorescence microscopy. Two novel mAbs, LIA1/1 and VJ1/16, specifically recognized a 25-kD protein that was selectively localized at cell–cell junctions of EC, both in the primary formation of cell monolayers and when EC reorganized in the process of wound healing. This antigen corresponded to the recently cloned platelet-endothelial tetraspan antigen CD151/PETA-3 (platelet-endothelial tetraspan antigen-3), and was consistently detected at EC cell–cell contact sites. In addition to CD151/PETA-3, two other members of the tetraspan superfamily, CD9 and CD81/ TAPA-1 (target of antiproliferative antibody-1), localized at endothelial cell-to-cell junctions. Biochemical analysis demonstrated molecular associations among tetraspan molecules themselves and those of CD151/ PETA-3 and CD9 with α3β1 integrin. Interestingly, mAbs directed to both CD151/PETA-3 and CD81/ TAPA-1 as well as mAb specific for α3 integrin, were able to inhibit the migration of ECs in the process of wound healing. The engagement of CD151/PETA-3 and CD81/TAPA-1 inhibited the movement of individual ECs, as determined by quantitative time-lapse video microscopy studies. Furthermore, mAbs against the CD151/PETA-3 molecule diminished the rate of EC invasion into collagen gels. In addition, these mAbs were able to increase the adhesion of EC to extracellular matrix proteins. Together these results indicate that CD81/TAPA-1 and CD151/PETA-3 tetraspan molecules are components of the endothelial lateral junctions implicated in the regulation of cell motility, either directly or by modulation of the function of the associated integrin heterodimers.

scholarly journals Defective flow-migration coupling causes arteriovenous malformations in hereditary hemorrhagic telangiectasia

2021 ◽  
Author(s):  
Hyojin Park ◽  
Jessica Furtado ◽  
Mathilde Poulet ◽  
Minhwan Chung ◽  
Sanguk Yun ◽  
...  
Keyword(s):  
Blood Flow ◽  
Endothelial Cell ◽  
Hereditary Hemorrhagic Telangiectasia ◽  
Arteriovenous Malformations ◽  
Nuclear Translocation ◽  
Vascular Malformations ◽  
Critical Role ◽  
Cell Polarization ◽  
Endothelial Cell Migration ◽  
Cardiovascular Development

Background: Activin receptor-like kinase 1 (ACVRL1, hereafter ALK1) is an endothelial transmembrane serine threonine kinase receptor for BMP family ligands that plays a critical role in cardiovascular development and pathology. Loss-of-function mutations in the ALK1 gene cause type 2 hereditary hemorrhagic telangiectasia (HHT), a devastating disorder that leads to arteriovenous malformations (AVMs). Here we show that ALK1 controls endothelial cell polarization against the direction of blood flow and flow-induced endothelial migration from veins through capillaries into arterioles. Methods: Using Cre lines that recombine in different subsets of arterial, capillary-venous or endothelial tip cells, we showed that capillary-venous Alk1 deletion was sufficient to induce AVM formation in the postnatal retina. Results: ALK1 deletion impaired capillary-venous endothelial cell polarization against the direction of blood flow in vivo and in vitro. Mechanistically, ALK1 deficient cells exhibited increased integrin signaling interaction with VEGFR2, which enhanced downstream YAP/TAZ nuclear translocation. Pharmacological inhibition of integrin or YAP/TAZ signaling rescued flow migration coupling and prevented vascular malformations in Alk1 deficient mice. Conclusions: Our study reveals ALK1 as an essential driver of flow-induced endothelial cell migration and identifies loss of flow-migration coupling as a driver of AVM formation in HHT disease. Integrin-YAP/TAZ signaling blockers are new potential targets to prevent vascular malformations in HHT patients.

scholarly journals Apelin receptor signaling: a novel mechanism of endothelial cell polarization

2016 ◽  
Vol 48 (12) ◽  
pp. 1138-1139 ◽  
Author(s):  
Hong Zhao ◽  
Pingbo Yao ◽  
Lanfang Li ◽  
Linxi Chen
Keyword(s):  
Endothelial Cell ◽  
Cell Polarization ◽  
Receptor Signaling ◽  
Apelin Receptor
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