July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Characterization of Expression of Key Enzymes of Glycogen Metabolism in the Mouse Retina
Author Affiliations & Notes
  • Tedi Begaj
    Medicine, Cambridge Health Alliance, Harvard Medical School, Cambridge, Massachusetts, United States
  • Yashodhan Chinchore
    Genetics, Harvard Medical School, Boston, Massachusetts, United States
  • Constance L Cepko
    Genetics, Harvard Medical School, Boston, Massachusetts, United States
  • Footnotes
    Commercial Relationships   Tedi Begaj, None; Yashodhan Chinchore, None; Constance Cepko, None
  • Footnotes
    Support  Howard Hughes Medical Institute Medical Research Fellowship 2015-2016
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 3055. doi:https://doi.org/
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      Tedi Begaj, Yashodhan Chinchore, Constance L Cepko; Characterization of Expression of Key Enzymes of Glycogen Metabolism in the Mouse Retina. Invest. Ophthalmol. Vis. Sci. 2018;59(9):3055. doi: https://doi.org/.

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

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Abstract

Purpose : Glycogen is present in the retina of many vertebrate species. It is believed to serve as an important energy reserve, especially in times of higher oxygen consumption and glucose utilization (e.g. dark adapted states). In avascular retinae (e.g. rabbit), glycogen is abundant in the inner retina while in vascular retinae, (e.g. human, or mice) there is less histochemically demonstrable glycogen. In the adult mouse retina, the cellular distribution of glycogen storage has not been characterized. Moreover, a description of the cell-specific RNA expression of genes in the glycogen storage and degradation pathways has not been published. One important implication of elucidating these pathways involves inherited retinal degeneration, where genetic mutations are thought to cause significant perturbations in glucose metabolism. Indeed, in retinal degeneration 7 mice, several genes involved in glycogen metabolism are upregulated in cones. Thus understanding which retinal cells are involved in glycogen metabolism could provide insight for potential therapeutic targets.

Methods : To first characterize glycogen storage in the adult mouse retina, histochemical analysis via a periodic acid-Schiff (PAS) technique with hematoxylin counterstain was performed on thin sections. Retinae were pre-treated with amylase to ensure specificity of the reaction. PAS staining was also performed on light and dark-adapted mice. Finally, we systematically characterized the expression of RNAs encoding enzymes for both glycogen synthesis and degradation, aiming to elucidate any cell specific patterns, using RNA in situ hybridization.

Results : In the mouse retina, PAS-positive staining was observed in the photoreceptor layer as well as the inner retina. Light and dark-adapted mice showed no detectable variation in glycogen content. Expression analysis of transcripts for glycogenin (a scaffold protein involved in the first steps of glycogen synthesis), and key enzymes for both synthesis and degradation, were found to be enriched in the inner retina. In line with previous work in the rat, transcript enrichment was observed for glycogen phosphorylase, brain and muscle isoform, but not liver isoform.

Conclusions : Glycogen in the mouse retina seems to be limited to the photoreceptor layer and inner retina. The transcripts encoding key enzymes involved in glycogen synthesis and degradation appear to be enriched in the inner retina.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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