BASIC FIBROBLAST-GROWTH-FACTOR IS NEITHER NECESSARY NOR SUFFICIENT FOR THE DEVELOPMENT OF RETINAL NEOVASCULARIZATION

Basic fibroblast growth factor (FGF2) is constitutively expressed in t he retina and its expression is increased by a number of insults, but its role in the retina is still uncertain. This study was designed to test the hypothesis that altered expression of FGF2 in the retina affe cts the development of retinal neovascularization. Mice with targeted disruption of the Fgf2 gene had no detectable expression of FGF2 in th e retina by Western blot, but retinal vessels were: not different in a ppearance or total area from wild-type mice. When FGF2-deficient mice were compared with wild-type mice in a murine model of oxygen induced ischemic retinopathy, they developed the same amount of retinal neovas cularization. Transgenic mice with a rhodopsin promoter/Fgf2 gene fusi on expressed high levels of FGF2 in retinal photoreceptors but develop ed no retinal neovascularization or other abnormalities of retinal ves sels; in the ischemic retinopathy model, they showed no significant di fference in the amount of retinal neovascularization compared with wil d-type mice. These data indicate that FGF2 expression is not necessary nor sufficient for the development of retinal neovascularization. Thi s suggests that agents that specifically antagonize FGF2 are not Likel y to be useful adjuncts in the treatment of retinal neovascularization and therapies designed to increase FGF2 expression are not likely to be complicated by retinal neovascularization.