March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
VEGF165B Prevents Tight Junctional Re-organisation In Retinal Pigmented Epithelial Cells Induced by VEGF165
Author Affiliations & Notes
  • Nikita Ved
    School of Physiology and Pharmacology, University of Bristol, Bristol, United Kingdom
  • James W. Bainbridge
    UCL Institute of Ophthalmology, London, United Kingdom
  • David O. Bates
    School of Physiology and Pharmacology, University of Bristol, Bristol, United Kingdom
  • Footnotes
    Commercial Relationships  Nikita Ved, None; James W. Bainbridge, None; David O. Bates, None
  • Footnotes
    Support  Diabetes UK
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 5778. doi:
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      Nikita Ved, James W. Bainbridge, David O. Bates; VEGF165B Prevents Tight Junctional Re-organisation In Retinal Pigmented Epithelial Cells Induced by VEGF165. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5778.

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

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Abstract
 
Purpose:
 

Proliferative diabetic retinopathy (PDR) is associated with increased pro-angiogenic vascular endothelial growth factor (VEGF) and macular edema. VEGF promotes the increased neovascularisation observed in PDR, breakdown of the blood-retinal barrier (BRB) and degradation of the tight-junctions formed between retinal pigment epithelial (RPE) cells by downregulating the tight junctional protein ZO-1, which may also facilitate fluid movement into the retina1. This study aimed to determine the effects of the pro-angiogenic and anti-angiogenic isoforms of VEGF, VEGF165 and VEGF165b respectively, on tight-junctional integrity in retinal pigment epithelial cells.

 
Methods:
 

Primary RPEs received one of four treatments: untreated, VEGF165 treated (2.5nM), VEGF165b treated (2.5nM) and treated with both (2.5nM each). 24 hours following treatment, changes in ZO1 expression were observed using immunofluorescence

 
Results:
 

Results RPEs treated with VEGF165, showed a significantly decreased (p<0.05) ZO1 staining intensity by 51.1% (±11%, n=9, figure 1a) relative to untreated cells, (figure 1b). VEGF165b treated cells showed no change in ZO1 staining intensity (88.7±17.9%) compared to VEGF165 treated. Cells treated with both isoforms showed no change in ZO1 staining intensity of (84.3±4.5%) when compared to untreated cells.

 
Conclusions:
 

The VEGF mediated decrease in ZO1 expression in RPEs, is limited to the pro-angiogenic VEGF165 isoform and blocked by the anti-angiogenic VEGF165b isoform.1. R. Ghassemifar, C. M. Lai, P. E. Rakoczy (2006) VEGF differentially regulates transcription and translation of ZO-1alpha+ and ZO-1alpha- and mediates trans-epithelial resistance in cultured endothelial and epithelial cells Cell Tissue Res 323:117-25  

 
Keywords: diabetic retinopathy • retinal pigment epithelium • vascular endothelial growth factor 
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