Role of Myo/Nog Cells in Neuroprotection: Evidence from the Light Damaged Retina

نویسندگان

  • Alice Brandli
  • Jacquelyn Gerhart
  • Christopher K. Sutera
  • Sivaraman Purushothuman
  • Mindy George-Weinstein
  • Jonathan Stone
  • Arturo Bravo-Nuevo
چکیده

PURPOSE To identify Myo/Nog cells in the adult retina and test their role in protecting retinal photoreceptors from light damage. METHODS Light damage was induced by exposing albino rats raised in dim cyclic light to 1000 lux light for 24 hours. In one group of rats, Myo/Nog cells were purified from rat brain tissue by magnetic cell sorting following binding of the G8 monoclonal antibody (mAb). These cells were injected into the vitreous humour of the eye within 2 hours following bright light exposure. Retinal function was assessed using full-field, flash electroretinogram (ERG) before and after treatment. The numbers of Myo/Nog cells, apoptotic photoreceptors, and the expression of glial fibrillary acidic protein (GFAP) in Muller cells were assessed by immunohistochemistry. RESULTS Myo/Nog cells were present in the undamaged retina in low numbers. Light induced damage increased their numbers, particularly in the choroid, ganglion cell layer and outer plexiform layer. Intravitreal injection of G8-positive (G8+) cells harvested from brain mitigated all the effects of light damage examined, i.e. loss of retinal function (ERG), death of photoreceptors and the stress-induced expression of GFAP in Muller cells. Some of the transplanted G8+ cells were integrated into the retina from the vitreous. CONCLUSIONS Myo/Nog cells are a subpopulation of cells that are present in the adult retina. They increase in number in response to light induced stress. Intravitreal injection of Myo/Nog cells was protective to the retina, in part, by reducing retinal stress as measured by the Muller cell response. These results suggest that Myo/Nog cells, or the factors they produce, are neuroprotective and may be therapeutic in neurodegenerative retinal diseases.

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عنوان ژورنال:

دوره 12  شماره 

صفحات  -

تاریخ انتشار 2017