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X. Shi, N. Kociok, A. M. Joussen; Changes in Retinal Vascularization After Intravitreal Injection of Avastin in a Mouse Model of Oxygen-Induced Retinopathy?. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4048.
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Substantial evidence indicate that vascular endothelial growth factor (VEGF), which is induced by hypoxia through several mediators, plays a key role in retinopathy of prematurity (ROP). The encouraging initial clinical reports of anti-VEGF therapy with intravitreal Bevacizumab (Avastin; Genentech, Inc), the full-length humanized monoclonal anti-VEGF neutralizing antibody, for choroidal neovascular and retinal neovascular diseases, prompt us to investigate the effect of Avastin of intravitreal injection using the mouse model for oxygen induced retinopathy.
From postnatal day seven (P7) on, C57BL/6J mice were kept in a 75% oxygen environment for five days. On P14 they received an intravitreal injection of Avastin (25mg/ml, 2µl) in one eye and control substance NaCl (0.9%, 2µl) in the fellow eye. On P17, retinal whole mounts were prepared and the retinal vessel area and the avascular area were quantified after perfusion of the mice with FITC-Concanavalin A.
After oxygen treatment and independent of the injected drug, the vascularization on P17 was retarded and great parts of the central retina remained non-vascularized as compared to age-matched controls held in normoxia. However, compared to the control eyes, in the eyes injected with Avastin, the area of retinal vessels was reduced additionally and the avascular area was increased as well without alteration of the vascular pattern.
Intravitreal injection of Avastin is able to inhibit retinal neovascularization in a mouse model for oxygen induced retinopathy. These data underline the potential utility of Avastin in ROP, besides its well tolerated intravitreal injection for effective management of choroidal neovascularization (CNV) associated with age-related macular degeneration (AMD) and retinal neovascularization in proliferative diabetic retinopathy.
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