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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.
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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).
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.
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.
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.
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