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Related Experiment Video

Updated: Jun 17, 2026

Endothelial Cell Transcytosis Assay as an In Vitro Model to Evaluate Inner Blood-Retinal Barrier Permeability
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Src-induced tyrosine phosphorylation of VE-cadherin is not sufficient to decrease barrier function of endothelial

Alejandro P Adam1, Amy L Sharenko, Kevin Pumiglia

  • 1Center for Cardiovascular Sciences, Albany Medical College, Albany, New York 12208, USA.

The Journal of Biological Chemistry
|January 6, 2010
PubMed
Summary
This summary is machine-generated.

Src-induced VE-cadherin phosphorylation alone does not increase vascular permeability. Additional signaling pathways are likely required for inflammatory mediators and growth factors to alter endothelial barrier function.

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Barrier Functional Integrity Recording on bEnd.3 Vascular Endothelial Cells via Transendothelial Electrical Resistance Detection

Published on: September 29, 2023

Area of Science:

  • Cell biology
  • Molecular signaling
  • Vascular biology

Background:

  • Src family kinases (SFK) and VE-cadherin phosphorylation regulate vascular permeability.
  • Investigating Src signaling independently of other pathways is crucial.

Purpose of the Study:

  • To determine if Src-induced VE-cadherin phosphorylation alone increases endothelial cell monolayer permeability.
  • To elucidate the role of Src signaling in vascular barrier function.

Main Methods:

  • Activation of Src/SFKs via dominant-negative Csk or constitutively active Src expression, and Csk knockdown.
  • Analysis of VE-cadherin phosphorylation at specific tyrosine sites.
  • Assessment of endothelial cell monolayer permeability and protein interactions.

Main Results:

  • Dominant-negative Csk expression induced VE-cadherin phosphorylation but not permeability changes.
  • Constitutively active Src decreased barrier function and increased VE-cadherin phosphorylation.
  • Csk knockdown induced VE-cadherin phosphorylation without affecting barrier function.
  • VE-cadherin phosphorylation did not disrupt binding to p120/beta-catenin or plasma membrane localization.

Conclusions:

  • Src-induced VE-cadherin tyrosine phosphorylation is insufficient to increase endothelial monolayer permeability.
  • Concurrent signaling pathways alongside VE-cadherin phosphorylation are necessary for inflammatory mediator/growth factor-induced permeability changes.