December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
VEGF Increases Paracellular transport in Retinal Endothelial Cells
Author Affiliations & Notes
  • TW Gardner
    Department of Ophthalmology Penn State Univ Coll of Med Hershey PA
  • L DeMaio
    Chemical Engineering Penn State University University Park PA
  • JM Tarbell
    Chemical Engineering Penn State University University Park PA
  • DA AntonettiPenn State Retina Research Group
    Cellular and Molecular Physiology Penn State University Hershey PA
  • Footnotes
    Commercial Relationships   T.W. Gardner, None; L. DeMaio, None; J.M. Tarbell, None; D.A. Antonetti, None. Grant Identification: EY12021,HL57093
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3297. doi:
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      TW Gardner, L DeMaio, JM Tarbell, DA AntonettiPenn State Retina Research Group; VEGF Increases Paracellular transport in Retinal Endothelial Cells . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3297.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: Vascular endothelial growth factor (VEGF) increases microvascular permeability in vivo and contributes to decreased blood-retinal and blood-brain barrier integrity in diseases such as diabetic retinopathy and brain glioma. However, the physical transport pathways by which water and solutes cross the endothelium in response to VEGF are not completely understood. Methods: We developed an in vitro system to record simultaneous, real-time measures of water and solute flux across cell monolayers. This study tested the hypothesis that VEGF increases convective transport of water and solutes through a single paracellular pathway across bovine retinal endothelial cell monolayers (BRECs). Results: VEGF (50 ng/ml) induced a 3.5-fold increase in both water (Jv) and 70 kDa dextran (Pe) transport after 120 min. However, VEGF did not alter the osmotic reflection coefficient (s) of BREC monolayers to dextran over the time course of the experiment. Conclusion: This observation suggests that water and dextran share common paracellular pathways across the endothelium and that VEGF increases the number of paracellular "pores" or the size of existing "pores". These conclusions are consistent with previously observed VEGF-induced alterations of tight junctions, such as occludin and ZO-1 phosphorylation, which may regulate the opening of paracellular "pores".

Keywords: 614 vascular cells • 388 diabetic retinopathy • 533 pump/barrier function 
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