Protection of the structure and function of the retina by body-wide mechanism

Abstract

Photoreceptor degeneration causes the loss of vision, and if extensive, severe blindness. Photoreceptor degenerations such as retinitis pigmentosa and age-related macular degeneration account for the majority of blindness in the developed world. To date there are limited therapies available that slow the progressive loss of photoreceptors. Consequently, there is a need to test novel interventions that are capable of stabilizing photoreceptors from degeneration. In this project, I used a rodent model to induce photoreceptor degeneration and test the potential of retinal protectants; remote ischemic preconditioning (RIP) a well-established form of stress conditioning, and the application of Myo/Nog cells, a cell understood to contribute to retinal development. RIP was shown to affect retinal function in healthy animals. Pathological and function testing of the retina revealed that both of these interventions are capable of preserving photoreceptors immediately before or after initiation of photoreceptor degeneration. Further testing of RIP implicated brain derived neurotrophic factor as a potential mediator of photoreceptor protection. In summary there are two findings to report. Firstly, this project expands our understanding of RIP effects on the body and the mechanism underlying RIP induced projection. Secondly, this project shows for the first time that Myo/Nog cells are expressed in adult retina, are active during periods of stress and importantly their presence is able to stabilize photoreceptors.