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How VE-cadherin goes with the flow

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ABSTRACT

Study describes how the adhesion molecule’s transmembrane domain helps endothelial cells respond to fluid shear stress.

No MeSH data available.


FOCAL POINT  Brian Coon (left), Martin Schwartz (right), and colleagues (not pictured) reveal that the transmembrane domain of VE-cadherin allows endothelial cells to respond to fluid shear stress by binding to the transmembrane domains of the growth factor receptors VEGFR2 and VEGFR3, recruiting them into a mechanosensory complex at endothelial cell junctions. Fluid shear stress signaling can activate proinflammatory pathways and/or vascular remodeling. In vitro, human umbilical vein endothelial cells align in the direction of fluid flow, as shown in the images above. Cells are stained for VE-cadherin (green), F-actin (red), and DNA (blue).PHOTO COURTESY OF THE AUTHORS
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fig1: FOCAL POINT  Brian Coon (left), Martin Schwartz (right), and colleagues (not pictured) reveal that the transmembrane domain of VE-cadherin allows endothelial cells to respond to fluid shear stress by binding to the transmembrane domains of the growth factor receptors VEGFR2 and VEGFR3, recruiting them into a mechanosensory complex at endothelial cell junctions. Fluid shear stress signaling can activate proinflammatory pathways and/or vascular remodeling. In vitro, human umbilical vein endothelial cells align in the direction of fluid flow, as shown in the images above. Cells are stained for VE-cadherin (green), F-actin (red), and DNA (blue).PHOTO COURTESY OF THE AUTHORS


How VE-cadherin goes with the flow
FOCAL POINT  Brian Coon (left), Martin Schwartz (right), and colleagues (not pictured) reveal that the transmembrane domain of VE-cadherin allows endothelial cells to respond to fluid shear stress by binding to the transmembrane domains of the growth factor receptors VEGFR2 and VEGFR3, recruiting them into a mechanosensory complex at endothelial cell junctions. Fluid shear stress signaling can activate proinflammatory pathways and/or vascular remodeling. In vitro, human umbilical vein endothelial cells align in the direction of fluid flow, as shown in the images above. Cells are stained for VE-cadherin (green), F-actin (red), and DNA (blue).PHOTO COURTESY OF THE AUTHORS
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4384725&req=5

fig1: FOCAL POINT  Brian Coon (left), Martin Schwartz (right), and colleagues (not pictured) reveal that the transmembrane domain of VE-cadherin allows endothelial cells to respond to fluid shear stress by binding to the transmembrane domains of the growth factor receptors VEGFR2 and VEGFR3, recruiting them into a mechanosensory complex at endothelial cell junctions. Fluid shear stress signaling can activate proinflammatory pathways and/or vascular remodeling. In vitro, human umbilical vein endothelial cells align in the direction of fluid flow, as shown in the images above. Cells are stained for VE-cadherin (green), F-actin (red), and DNA (blue).PHOTO COURTESY OF THE AUTHORS

View Article: PubMed Central - HTML

ABSTRACT

Study describes how the adhesion molecule’s transmembrane domain helps endothelial cells respond to fluid shear stress.

No MeSH data available.