June 2013
Volume 54, Issue 15
Free
ARVO Annual Meeting Abstract  |   June 2013
Myo/Nog Cells Promote Photoreceptor Cell Survival in the Stressed Retina
Author Affiliations & Notes
  • Arturo Bravo-Nuevo
    Lankenau Institute for Medical Research, Wynnewood, PA
  • alice brandli
    Physiology, University of Sydney, Sydney, NSW, Australia
  • Jacquelyn Gerhart
    Lankenau Institute for Medical Research, Wynnewood, PA
  • Meghan Pitts
    Lankenau Institute for Medical Research, Wynnewood, PA
  • Jonathan Stone
    Physiology, University of Sydney, Sydney, NSW, Australia
  • Mindy George-Weinstein
    Lankenau Institute for Medical Research, Wynnewood, PA
  • Footnotes
    Commercial Relationships Arturo Bravo-Nuevo, None; alice brandli, None; Jacquelyn Gerhart, None; Meghan Pitts, None; Jonathan Stone, None; Mindy George-Weinstein, Lankenau Institute for Medical Research (P)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2013, Vol.54, 4177. doi:https://doi.org/
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      Arturo Bravo-Nuevo, alice brandli, Jacquelyn Gerhart, Meghan Pitts, Jonathan Stone, Mindy George-Weinstein; Myo/Nog Cells Promote Photoreceptor Cell Survival in the Stressed Retina. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4177. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: Myo/Nog cells express the MyoD transcription factor, the BMP inhibitor noggin and cell surface G8 antigen. During embryogenesis, Myo/Nog cells are integrated into the developing retina. Their release of noggin is critical for normal morphogenesis of the retina. The purpose of this study was to examine the stressed retina of neonatal and adult rodents for Myo/Nog cells and explore their role in photoreceptor survival.

Methods: Sv129 mice and Sprague Dawley rats were subjected to oxygen induced retinopathy and light damage, respectively. Myo/Nog cells were ablated in the retina by injecting into the vitreous a monoclonal antibody (mAb) to the G8 antigen complexed with complement. Some animals received an intravitreal injection of Myo/Nog cells harvested from the brain. Prior to inducing light damage, some rats were treated with infrared light or saffron, both of which are neuroprotective. Retinas were analyzed by immunofluorescence localization of Myo/Nog cells, TUNEL assay and electroretinography (ERG).

Results: Myo/Nog cells were increased in the retina during the critical period of photoreceptor development and in areas of oxygen- and light-induced stress. Administration of infrared light or saffron prior to inducing light damage reduced photoreceptor cell death and the number of Myo/Nog cells in the retina. Depletion of Myo/Nog cells led to increased photoreceptor cell death and a reduction in the A and B waves of the ERG. Addition of Myo/Nog cells into the vitreous increased photoreceptor survival and both the A and B waves.

Conclusions: Myo/Nog cells are present in the neonatal and adult retina. Their prevalence in the retina correlates with the extent of photoreceptor cell death. Myo/Nog cells appear to be neuroprotective under conditions of stress. Myo/Nog cells, or the factors they release, have potential therapeutic value for promoting photoreceptor survival in retinopathies.

Keywords: 695 retinal degenerations: cell biology • 648 photoreceptors • 426 apoptosis/cell death  
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