Purpose : Myo/Nog cells, named for their expression of the skeletal muscle specific transcription factor MyoD and bone morphogenetic protein inhibitor noggin, are critical regulators of embryonic development, including eye morphogenesis. In the normal adult eye, Myo/Nog cells are present in low numbers throughout the anterior and posterior segments. Here we study the behaviors of Myo/Nog cells in different models of retinal stress and degeneration.

Methods : The numbers and distribution of Myo/Nog cells and cell death were determined by immunofluorescence microscopy in the following models: 1) the critical period of physiological culling of photoreceptors, 2) hypoxia induced cell death, 3) light damage, 4) genetically induced retinal degeneration, and 5) increased intraocular pressure. Optical coherence tomography and electroretinography were used to imagine the retina and measure visual function, respectively.

Results : Myo/Nog cells increase in number and migrate to areas of stress and cell death in the retina. Depletion of Myo/Nog cells leads to increased neuronal cell damage. Addition of exogenous Myo/Nog cells significantly reduces neuronal cell death and improves visual function.

Conclusions : Myo/Nog cells are highly responsive to a perturbation in retinal homeostasis induced by different forms of stress and injury. Myo/Nog cells are neuroprotective under these conditions. However, their capacity to differentiate into myofibroblasts must be taken into account when considering an approach of Myo/Nog cell based therapy.

This is a 2020 ARVO Annual Meeting abstract.