[Experimental study on inhibition of retinal neovascularisation by gene transfer of extracellular 1-3 domain of VEGF receptor KDR].

Objective: To evaluate the effect of liposome mediated plasmids KDRn3 injected into the vitreous to inhibit experimental retinal neovascularization.
Methods: One-week-old C57BL/6N mice were exposed to 75% ± 2% oxygen for 5 days, then returned to the room air to induce retinal neovascularization. Cationic liposome mediated KDRn3 comp-lex (1 µl) was injected into the vitreous in the treatment group. PBS 1µl or liposome were injected in the control group. The pEGFP-N1/KDRn3 expression was observed by using fluorescence microscope. Retinal neovascularization was evaluated by counting the number of vascular endothelial cell nuclei on the vitreal side of the inner limiting membrane of the retina and measuring the areas of non-perfusions in central retina.
Results: KDRn3 protein was expressed both in the ganglion layer and in the inner layer. Retinal wholemount preparation of retinal neovascular animal model showed that prominent neovascular tuft and fluorescein leakage and large areas of non-perfusions in central retina. Fewer neovascular tufts and fewer areas of non-perfusions could be seen after pEGFP-N1/KDRn3 injection. There were statistic differences between control group and pEGFP-N1/KDRn3 injecting group with the number of vascular endothelial cell nuclei on the vitreal side of the inner limiting membrane of the retina (0.20 ± 0.51, 13.58 ± 2.48, 23.05 ± 3.40, 21.70 ± 2.89; F = 1085.25, P < 0.05) and the areas of non-perfusions in central retina [(1.33 ± 0.49), (2.75 ± 0.70), (2.12 ± 0.35) mm(2); F = 17.61, P < 0.01].
Conclusion: pEGFP-N1/KDRn3 gene transfer can inhibit retinal neovascularisation in C57Bl/6J mice of ischaemia-induced retinal neovascularisation on some extent.