May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Analysis of Apelin-13 (F13A) in an Animal Model of Choroidal Neovascularization
Author Affiliations & Notes
  • T. P. McDonald
    Ophthalmics Research, Merck Research Labs, Merck and Co, West Point, Pennsylvania
  • J. Wiler Maxwell
    Ophthalmics Research, Merck Research Labs, Merck and Co, West Point, Pennsylvania
  • A. C. Hughes
    Ophthalmics Research, Merck Research Labs, Merck and Co, West Point, Pennsylvania
  • C. J. Thut
    Ophthalmics Research, Merck Research Labs, Merck and Co, West Point, Pennsylvania
  • A. L. Webber
    Ophthalmics Research, Merck Research Labs, Merck and Co, West Point, Pennsylvania
  • Footnotes
    Commercial Relationships  T.P. McDonald, Merck and Co., E; J. Wiler Maxwell, Merck and Co., E; A.C. Hughes, Merck and Co., E; C.J. Thut, Merck and Co., E; A.L. Webber, Merck and Co., E.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 291. doi:https://doi.org/
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      T. P. McDonald, J. Wiler Maxwell, A. C. Hughes, C. J. Thut, A. L. Webber; Analysis of Apelin-13 (F13A) in an Animal Model of Choroidal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2008;49(13):291. doi: https://doi.org/.

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

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Abstract

Purpose: : Apelin is the endogenous peptide ligand for the G-protein coupled receptor, APJ. Apelin and APJ are widely expressed and have been shown to play a role in a broad array of physiological activities, including cardiovascular regulation, fluid homeostasis, and angiogenesis. Expression of the ligand and the receptor are associated with nascent retinal vessels, and the APJ receptor has been shown to be upregulated during pathological angiogenesis in the murine ROP model of ischemia-induced retinopathy. To investigate the role of apelin signaling in choroidal neovascularization, we tested the antagonist apelin-13 (F13A) in the rat laser model of choroidal neovascularization (CNV).

Methods: : Apelin-13 (F13A) was delivered by intravitreal injection at a dose of 2ug or 10ug per eye in a rat laser model of choroidal neovascularization. The APJ-specific antagonist was delivered intravitreally on days 0 (day of laser injury) and 6. Animals were perfused with FITC-dextran on day 12, and neovascularization was quantitated using fluorescence image analysis of CNV lesions.

Results: : 10ug intravitreal administration of Apelin-13 (F13A) demonstrated a 44% reduction in lesion size compared to vehicle control PBS in the rat laser model of choroidal neovascularization. This reached statistical significance with a P value < 0.01. No reduction in lesion size was observed with the 2ug dose of Apelin-13 (F13A) compared to PBS control.

Conclusions: : A 10ug dose of the Apelin-13 (F13A) delivered on day 0 and day 6 can significantly reduce neovasularization and lesion size in the rat laser model of choroidal neovascularization.

Keywords: choroid: neovascularization • age-related macular degeneration • inhibitory receptors 
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