June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Sigma-1 Receptor Increases Mitochondrial Membrane Potential in Glucose and Oxygen deprived Retinal Ganglion Cells.
Author Affiliations & Notes
  • Dorette Z Ellis
    North Texas Eye Rresearch Institute, UNTHSC, Fort Worth, TX
  • Linya Li
    North Texas Eye Rresearch Institute, UNTHSC, Fort Worth, TX
  • Yong H Park
    North Texas Eye Rresearch Institute, UNTHSC, Fort Worth, TX
  • Brett H Mueller
    North Texas Eye Rresearch Institute, UNTHSC, Fort Worth, TX
  • Hai-Ying Ma
    North Texas Eye Rresearch Institute, UNTHSC, Fort Worth, TX
  • Thomas Yorio
    North Texas Eye Rresearch Institute, UNTHSC, Fort Worth, TX
  • Footnotes
    Commercial Relationships Dorette Ellis, None; Linya Li, None; Yong Park, None; Brett Mueller, None; Hai-Ying Ma, None; Thomas Yorio, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 4258. doi:
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      Dorette Z Ellis, Linya Li, Yong H Park, Brett H Mueller, Hai-Ying Ma, Thomas Yorio, North Texas Eye Research Institute; Sigma-1 Receptor Increases Mitochondrial Membrane Potential in Glucose and Oxygen deprived Retinal Ganglion Cells. . Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):4258.

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

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Abstract

Purpose: Understanding the role of mitochondria in retinal ganglion cells (RGCs) is relevant to human disease, as studies showed mitochondrial abnormalities in primary open angle glaucoma patients. Recent studies in our laboratory demonstrated that glucose and oxygen deprivation (OGD) decreased mitochondrial movement in RGCs and sigma-1 receptors (σ-1r) agonists restored mitochondrial movement following OGD. This study determined the role of the σ-1r in regulating mitochondrial membrane potential in RGCs.

Methods: RGCs were isolated from rat pups and subjected to OGD in the presence or absence of σ-1r agonist and antagonist and AAV-σ-1r vector, used to increase σ-1r expression. Mitochondrial membrane potential was measured using JC1 dye. Caspase 3 and 7 activities were measured using luminescent assay kit.

Results: OGD in RGCs resulted in decreased mitochondrial membrane potential when compared to normoxic RGCs. Addition of σ-1r agonists restored the mitochondrial membrane potential comparable to normoxic conditions while σ-1r antagonists abolished these effects. Overexpression of the σ-1r resulted in the restoration of RGCs’ health following OGD deprivation. Caspase activity was increased in response to ODG and decreased by σ-1r agonist, pentazocine and σ-1r overexpression.

Conclusions: These data suggest that σ-1r restores RGCs function following OGD; particularly mitochondrial function which is vital to the health of the cells.

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