May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Modulation of VEGF Receptor Expression by Human Choroidal Endothelial Cells During Oxidative Stress
Author Affiliations & Notes
  • P.L. Penfold
    Ophthalmology, University of Sydney, Sydney, Australia
  • L. Wen
    Ophthalmology, University of Sydney, Sydney, Australia
  • D. Pow
    Biomedical Sciences, University of Queensland, Brisbane, Australia
  • Footnotes
    Commercial Relationships  P.L. Penfold, RetMed Inc R; L. Wen, RetMed Inc R; D. Pow, None.
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 1706. doi:
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      P.L. Penfold, L. Wen, D. Pow; Modulation of VEGF Receptor Expression by Human Choroidal Endothelial Cells During Oxidative Stress . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1706.

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

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Abstract

Abstract: : Purpose:Oxidative stress has been reported to play a role in the pathogenesis of age related macular degeneration (AMD) (1). Our previously reports have shown that triamcinolone acetonide (TA) modulates permeability and intercellular adhesion molecule-1 (ICAM-1) expression of both ECV304 epithelial cell line (2) and human choroidal endothelial cells (HCEC) (3). In the present study, we investigate the expression profiles of VEGF receptor flk-1 and flt-1 on HCEC during oxidative stress. The effects of TA after cellular exposure to H2O2 also has been examined. Methods: HCEC were isolated from post-mortem human eyes. Confluent HCEC were incubated with H2O2 in a series of concentrations for 48h. Specimens/doses with upregulated flk-1 and flt-1 expression were also treated with TA. The expression of flk-1 and flt-1 on HCEC was determined by immunocytochemistry, and was quantified by flow cytometry from 15 donor’s eyes Results:H2O2 upregulated flk-1 and flt-1 expression on HCEC occured in a dose-dependent manner, concentrations of 10-6M or 10-7M of H2O2 appeared the optimal doses for upregulation of both receptors. More obvious induction was shown in the donors above 45 year of age, however, these changes are varied between individuals. TA treatment produced a moderate down-regulation of flk-1 and flt-1 expression. Conclusions: Exposure of HCEC cells to H2O2 represents a useful model for the study of oxidative stress influences on human choroidal blood vessels, which may contribute understanding the pathogenesis of choroidal neovescularization. Constitutively expressed levels of VEGF receptors flk-1 and flt-1 on HCEC may be subject to modulation by oxidative stress. TA mediated down-regulation of VEGF receptor expression on HCEC illustrates a further mode of action of glucocorticoids. (1) Beatty S et al., Surv Ophthalmol, 2000 45:115-134. (2) Penfold PL, Wen L, Madigan MC, Gillies MC, King, NJC & Provis JM. Clin Exp Immunol, 2000 121:458-465. (3) Penfold PL, Wen L, Madigan MC, King, NJC & Provis JM. IOVS 2002;43:3125-3130

Keywords: vascular cells • retinal degenerations: cell biology • age-related macular degeneration 
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