Anti-angiogenic state in mice and humans with retinal photorecptor cell degeneration

Abstract

Neonatal mice with classic inherited retinal degeneration (Pdebrd1/Pdebrd1) are disclosed which fail to mount reactive retinal neovascularization in a mouse model of oxygen-induced proliferative retinopathy. Also disclosed is a comparable human paradigm: spontaneous regression of retinal neovascularization associated with long-standing diabetes mellitus which occurs when retinitis pigmentosa becomes clinically evident. Both mouse and human data indicate that reactive retinal neovascularization either fails to develop or regresses when the number of photoreceptor cells is markedly reduced. The results show that a functional mechanism underlying this anti-angiogenic state is failure of the predicted up-regulation of vascular endothelial growth factor (VEGF), although other growth factors may also be involved. Preventive and therapeutic methods useful against both proliferative and degenerative retinopathies are also disclosed.

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