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Related Experiment Videos

VEGF-induced permeability increase is mediated by caveolae

Y Feng1, V J Venema, R C Venema

  • 1Vascular Biology Center, The Medical College of Georgia, Augusta 30912, USA.

Investigative Ophthalmology & Visual Science
|January 15, 1999
PubMed
Summary

Vascular Endothelial Cell Growth Factor (VEGF) increases retinal endothelial cell permeability via nitric oxide synthase (NOS)-dependent transcytosis in caveolae. This pathway involves VEGF receptor Flk-1/KDR, eNOS, and caveolin-1 localization within caveolae.

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Area of Science:

  • Endothelial cell biology
  • Molecular signaling
  • Vascular physiology

Background:

  • Vascular Endothelial Cell Growth Factor (VEGF) is crucial for angiogenesis and vascular permeability.
  • The precise cellular mechanisms by which VEGF modulates endothelial barrier function are not fully elucidated.
  • Nitric oxide (NO) produced by NO synthase (NOS) is implicated in various endothelial cell signaling pathways.

Purpose of the Study:

  • To investigate the cellular pathway of VEGF-induced permeability in retinal endothelial cells.
  • To determine the involvement of NO production by NOS in mediating VEGF's effects on permeability.
  • To explore the structural relationships between VEGF receptors, NOS, and caveolae.

Main Methods:

  • Utilized cultured bovine retinal microvascular endothelial (BRE) cells for permeability bioassays.

Related Experiment Videos

  • Employed an NOS inhibitor to assess the role of NOS activity in VEGF-induced permeability.
  • Analyzed structural associations using double-label immunofluorescence and cell fractionation.

    • Main Results:

    • VEGF increases BRE cell permeability through an NOS-dependent transcytotic process within caveolae.
    • VEGF receptor Flk-1/KDR and endothelial NOS (eNOS) were found to colocalize with caveolin-1 in plasma membrane caveolae.
    • Cell fractionation confirmed higher levels of Flk-1/KDR, eNOS, and caveolin-1 in caveolar fractions.

    Conclusions:

    • VEGF enhances endothelial cell permeability via an eNOS-dependent mechanism involving transcytosis in caveolae.
    • VEGF signaling appears to be initiated within the caveolar compartment, indicated by the colocalization of key signaling molecules.
    • These findings provide insights into the molecular regulation of endothelial barrier function by VEGF.