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L. Zhao, Y. Liu, Y. Li, Y. Song, A.M. Laties, J.S. Rudge, S.J. Wiegand, R. Wen; Complete Inhibition of Neovascularization by VEGF Trap in a Matrigel CNV Model . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5300.
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Age–related macular degeneration (AMD) is the leading cause of visual disability and blindness in the population 65 years or older in the United States. The majority of the cases of severe vision loss with AMD are due to choroidal neovascularization (CNV) with devastating complications. Although the pathogenesis of CNV is not entirely understood, VEGF is implicated in its development. The present work uses VEGF Trap, a potent soluble VEGF receptor composed of ligand–binding portions of human VEGF receptor–1 (VEGFR–1) and VEGFR–2 fused to the Fc segment of IgG1, to bind and neutralize VEGF in a subretinal Matrigel model of CNV.
Sprague–Dawley rats (2.5 months old females) were injected with Matrigel into the subretinal space on the temporal side of both eyes through a 33–gauge needle connected to a 10–µl Hamilton microsyringe. VEGF Trap (12.5 mg/kg) or an equimolar concentration of a control protein (human Fc, 6.25 mg/kg) was injected subcutaneously on day 2 and 6. Animals were sacrificed 10 days post–Matrigel injection, and were perfused with a DiI solution to stain blood vessels. Eyes were harvested and serial sections (100 µm each) covering the entire Matrigel–injected area were cut on a Vibratome and examined by fluorescence microscopy. The maximal width W of CNV network in each section was measured (in µm) and the CNV index was calculated by multiply W by the thickness of the section T (100 µm). The sum of CNV indexes of all the sections was taken as the CNV index of an eye.
CNV was detected in every eye in the control group, but was completely absent from all eyes of the VEGF Trap treated group. The CNV index for each group was calculated and is presented in the table below.
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