Local injection of receptor tyrosine kinase inhibitor MAE 87 reduces retinal neovascularization in mice.

摘要: Purpose Retinal neovascularization occurs under the influence of angiogenic factors like vascular endothelial growth factor (VEGF). VEGF signaling is enhanced by insulin-like factor-1 (IGF-1). In vitro, oxoindolinone MAE 87 inhibits signal transduction blocking tyrosine kinase receptors including receptor 2 (VEGFR-2), IGF-1R, fibroblast GF-1R and epidermal GFR. We investigated effect in vivo using mouse model for oxygen induced retinopathy. Methods From postnatal day seven (P7) on, C57BL/6J mice were kept a 75% environment five days. On 12 (P12) they received an intravitreal injection one eye control substance fellow eye. The animals sacrificed intracardial perfusion with fluorescein-dextran solution on P17. whole mounts prepared ischemic retinopathy was evaluated 26 standardized score. Results After single there significantly less angioproliferative changes (blood vessel tufts, extra-retinal neovascularization, blood tortuosity) than (p=0.007). median score (maximal 13) treated eyes 6 (25th percentile: 5; 75th 7) 8 10). Conclusions inhibitor may be promising local treatment retinal neovascularization. Due to its ability inhibit not only but also IGF-1 cascade, prove especially valuable diabetic