December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Cyclooxygenase 2 in Ischemic Proliferative Retinopathy
Author Affiliations & Notes
  • F Sennlaub
    Unite 450 INSERM Paris France
  • F Valamanes
    Paris France
  • G Lefevre
    Paris France
  • R Thuret
    Paris France
  • Y Courtoisand
    Paris France
  • F Behar Cohen
    Paris France
  • Footnotes
    Commercial Relationships   F. Sennlaub, None; F. Valamanes , None; G. Lefevre , None; R. Thuret , None; Y. Courtoisand , None; F. Behar Cohen , None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 4020. doi:
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    • Get Citation

      F Sennlaub, F Valamanes, G Lefevre, R Thuret, Y Courtoisand, F Behar Cohen; Cyclooxygenase 2 in Ischemic Proliferative Retinopathy . Invest. Ophthalmol. Vis. Sci. 2002;43(13):4020.

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

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Abstract: : Purpose: Cyclooxygenas 2 (Cox-2) is induced in many hypoxic conditions. Prostaglandine E2 (PGE2), produce of Cox-2 activity, has been shown to promote angiogenesis in many models. To investigate the role of Cox-2 in retinal neovascularization, we studied the expression of Cox-2 and the effect of a specific Cox-2 inhibitor in the mouse ischemic proliferative retinopathy model. Methods: Mice were exposed from post-natal day 7 (P7) to P12 to 75±2% oxygen, leading to vessel rarefaction and the development of a central avascular area. From P12 to P17 mice were raised in room air, resulting in relative hypoxia. Cox-2 mRNA expression was determined by RT-PCR. Cox2 protein was evaluated by western blot analysis and immunohistochemistry. The influence of Cox-2 on normal vascular development and in ischemic proliferative retinopathy was evaluated by comparing intraretinal and intravitreal endothelial cell proliferation in mice treated with two intravitreal injections (P13 and P15 (n=6+ per group)) of either a specific Cox-2 inhibitor (APHS 0,6 / 3 / 15 mg/ml) or PGE-2. (0,5 / 5 mg/ml). Results: RT PCR (at P12, P14 and P17) and Western blot analysis (at P14) demonstrated the expression and the translation of Cox-2 messenger in room air raised and in oxygen incubated animals. Immunohistochemistry at P14 revealed Cox-2 in the ROP layer and in the inner plexiform layer of normoxic and hypoxic retinas.. Inhibition of Cox-2 by APHS had no effect on the retinal vasculature of room air raised mice. The inhibition of Cox-2 by APHS injection in the hypoxic phase of the model, resulted in a dose dependent inhibition of intravitreal neovascularization (up to 50%). No effect was observed on intraretinal revascularization. On the other hand, the injectionof PGE2 exacerbated pre-retinal neovascularization. Conclusion: Cox-2 is expressed in normal retinal development between P12 and P17, as well as under hyperoxic and hypoxic conditions in the murine retina. However Cox-2 activity, or PGE2 endothelial cell sensitivity, seems to be upregulated under hypoxic conditions, as specific inhibition of Cox-2 inhibited intravitreal neovascularization in a dose dependent manner. Intraretinal revascularization was not altered by Cox-2 inhibition. Cox-2 inhibitors could have potential therapeutic interest in pre retinal neovascularization in ischemic prliferative retinopathy.

Keywords: 566 retinal neovascularization • 316 animal model • 476 molecular biology 

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