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Quantitation of Endothelial Cell Adhesiveness In Vitro
10:24

Quantitation of Endothelial Cell Adhesiveness In Vitro

Published on: June 18, 2015

Caveolin-1 scaffolding domain promotes leukocyte adhesion by reduced basal endothelial nitric oxide-mediated ICAM-1

Sulei Xu1, Xueping Zhou, Dong Yuan

  • 1Department of Physiology and Pharmacology, School of Medicine, West Virginia University, Morgantown, West Virginia.

American Journal of Physiology. Heart and Circulatory Physiology
|September 18, 2013
PubMed

Insights

Caveolin-1 scaffolding domain (CAV) reduces basal nitric oxide (NO), increasing leukocyte adhesion via ICAM-1 phosphorylation. This effect is independent of microvessel barrier function unless secondary stimulation occurs.

Area of Science:

  • Endothelial biology
  • Vascular physiology
  • Immunology

Background:

  • Caveolin-1 scaffolding domain (CAV) inhibits inflammatory mediator-induced nitric oxide (NO) and microvessel permeability.
  • The role of CAV in endothelial basal NO production and leukocyte adhesion is not well understood.

Purpose of the Study:

  • To investigate the effects of exogenously applied CAV on basal NO production.
  • To determine CAV's impact on leukocyte adhesion and adhesion-induced microvessel permeability changes.

Main Methods:

  • Experiments performed in individually perfused rat mesenteric venules.
  • Quantification of NO using fluorescence imaging (DAF-2).
  • Measurement of microvessel permeability (hydraulic conductivity, Lp) and leukocyte adhesion.

Main Results:

  • CAV perfusion inhibited basal NO production but did not alter basal Lp.
  • CAV treatment significantly increased leukocyte adhesion, mediated by ICAM-1 phosphorylation via Src activation.
  • NO synthase inhibition mimicked CAV effects; NO donor abolished CAV-induced adhesion.
  • Leukocyte adhesion was uncoupled from barrier function unless secondary stimulation was applied.

Conclusions:

  • Exogenous CAV reduces basal NO, promoting ICAM-1-mediated leukocyte adhesion through Src-dependent ICAM-1 phosphorylation.
  • CAV's effects on leukocyte adhesion are distinct from its previously known inhibitory effects on inflammatory mediator-induced permeability.
  • CAV-induced leukocyte adhesion does not compromise microvessel barrier integrity on its own.
Keywords:
ICAM-1 phorsphorylationcaveolin-1leukocyte adhesionmicrovessel permeabilityreactive oxygen species

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