Purpose : Myo/Nog cells play an essential role in normal eye development. Previous studies have shown that they migrate to areas of stress and injury in the retina and are neuroprotective. In this study, we observed the behavior of Myo/Nog cells in a congenital murine model of retinitis pigmentosa (C3H mice), which results in the loss of photoreceptor cells within the outer nuclear layer of the retina (ONL).

Methods : C3H and C57 control mice were assessed at weeks 2.5, 3, 4, 5, and 6 using Scotopic Electroretinographs (ERG), Ocular Computer Topography (OCT), and immunofluorescence microscopy. Enucleated eyes were fixed in paraformaldehyde and cryo-sectioned. Cryosections were labeled with Myo/Nog specific G8 monoclonal antibody.

Results : ERGs demonstrated decreased amplitudes of the A and B waves in the C3H group compared to the C57 group (p<0.05). OCTs revealed a significant difference in retinal thickness between the two groups (p<0.05). Progressive thinning of the retina in the C3H mice was confirmed by microscopy. Myo/Nog cells were significantly more numerous in C3H mice compared to controls (p<0.05). The majority of Myo/Nog cells were found in the outer nuclear layer and within the neighboring choroid.

Conclusions : Progressive retinal degeneration and visual deterioration in C3H mice is accompanied by an increase in Myo/Nog cells. They accumulate in parallel with an increase in photoreceptor cell death in the ONL. These findings are consistent with the behaviors of Myo/Nog cells in other forms of retinal stress and injury. Future studies will characterize the functions of Myo/Nog cells in this severe model of retinitis pigmentosa.

This is a 2020 ARVO Annual Meeting abstract.