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MERTK mutation reduces the ability of retinal pigment epithelial (RPE) cells to phagocytize the photoreceptor outer segments, which leads to accumulation of debris separating photoreceptors from RPE cells, resulting in their degeneration and loss of vision. In a rat model of Retinitis Pigmentosa due to  MERTK  mutation, we demonstrate that surgical removal of debris performed when about half of photoreceptors are lost (P38), allows the remaining photoreceptor cells to renew their outer segments and survive for at least 6 months – 3 times longer than in untreated eyes. In another set of experiments, patterned laser photocoagulation was performed before the debris formation (P19-25) to destroy a fraction of photoreceptors and thereby reduce the phagocytic load of shed outer segment fragments. This treatment also delayed the degeneration of the remaining photoreceptors. Both approaches were assessed functionally and morphologically, using electroretinography, optical coherence tomography, and histology. The long-term preservation of photoreceptors we observed indicates that  MERTK -related form of inherited retinal degeneration, which has currently no cure, could be amenable to laser therapy or subretinal surgery, to extend the visual function, potentially for life.

Long-term Rescue of Photoreceptors in a Rodent Model of Retinitis Pigmentosa Associated with MERTK Mutation