Abstract
Ocular angiogenesis, stimulated by VEGF165 in the retina and choroid, is the principal cause of vision loss in patients with diabetic retinopathy and wet age related macular degeneration. In these conditions there is an excess of VEGF165 over the anti‐angiogenic splice variant VEGF165b. Inhibitors of VEGF such as ranibizumab and pegabtanib are used clinically to treat AMD patients. We have compared the effect of VEGF165b with these anti‐VEGF antibody treatments. Western blotting showed that pegabtanib did not bind VEGF165b, whereas bevacizumab (the antibody from which ranibizumab was derived) bound VEGF165b. Chemotaxis assays of HMVE Cells using a Boyden chamber showed a 2.6 fold decrease of HMVEC migration at 10nM pegabtanib after challenging the cells with 1nM VEGF165 (p<0.01). The same impairment in migration occurred with only 1nM VEGF165b. Treatment of RPE cells with 10mg/ml neutralising antibody to VEGF165b showed a significant increase in cytotoxicity compared to control IgG, measured by lactase dehydrogenase release, indicating that VEGF165b is a survival factor for retinal pigmented epithelial cells. Together these results support the use of VEGF165b as an anti‐angiogenic treatment in ocular neovascularization.
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