A principal cause of blindness is subretinal neovascularization associated with age-related macular degeneration. Excised neovascular membranes from patients with age-related macular degeneration demonstrated a pattern of Fas+ new vessels in the center of the vascular complex, surrounded by FasL+ retinal pigment epithelial cells. In a murine model, Fas (CD95)-deficient (Ipr) and FasL-defective (gld) mice had a significantly increased incidence of neovascularization compared with normal mice. Furthermore, in gld mice there is massive subretinal neovascularization with uncontrolled growth of vessels. We found that cultured choroidal endothelial cells were induced to undergo apoptosis by retinal pigment epithelial cells through a Fas-FasL interaction. In addition, antibody against Fas prevented vascular tube formation of choroidal endothelial cells derived from the eye in a three-dimensional in vitro assay. Thus, FasL expressed on retinal pigment epithelial cells may control the growth and development of new subretinal vessels that can damage vision.
To determine whether macaque monkeys with infantile strabismus have latent nystagmus and directional asymmetries of horizontal optokinetic nystagmus (OKN) similar to those of humans with infantile strabismus, the authors recorded eye movements under conditions of monocular viewing. The presence of latent fixation nystagmus was tested by requiring the subjects to steadily fixate a stationary target subtending less than I deg of visual arc. OKN was tested using high-contrast, vertically-oriented moving stripes that filled 80 deg of the visual field. A macaque monkey who had infantile strabismus induced by alternating occlusion from birth showed latent nystagmus highly similar to that recorded in an adult human subject with infantile strabismus. The strabismic monkey also had asymmetric OKN similar to that of the strabismic human, favoring nasally-directed stimulus motion when viewing with either eye. Neither nystagmus nor an OKN asymmetry was observed in a normal macaque or in humans who had normal binocular vision. The findings of latent nystagmus and OKN asymmetries in the strabismic monkey support the notion that monkeys who have infantile-onset strabismus are an appropriate ocular motor model of human infantile strabismus.
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