September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Over Expression of Sigma-1 Receptor Protects Against Retinal Ganglion Cell loss in an Optic Nerve Crush Model
Author Affiliations & Notes
  • Dorette Z Ellis
    North Texas Eye Research Institute, UNTHSC, Fort Worth, Texas, United States
  • Linya Li
    North Texas Eye Research Institute, UNTHSC, Fort Worth, Texas, United States
  • Yang Liu
    North Texas Eye Research Institute, UNTHSC, Fort Worth, Texas, United States
  • Yong H Park
    North Texas Eye Research Institute, UNTHSC, Fort Worth, Texas, United States
  • Thomas Yorio
    North Texas Eye Research Institute, UNTHSC, Fort Worth, Texas, United States
  • Footnotes
    Commercial Relationships   Dorette Ellis, None; Linya Li, None; Yang Liu, None; Yong Park, None; Thomas Yorio, None
  • Footnotes
    Support  DOD (W81XWH-10-2-0003)
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 85. doi:
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    • Get Citation

      Dorette Z Ellis, Linya Li, Yang Liu, Yong H Park, Thomas Yorio; Over Expression of Sigma-1 Receptor Protects Against Retinal Ganglion Cell loss in an Optic Nerve Crush Model. Invest. Ophthalmol. Vis. Sci. 2016;57(12):85.

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

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Abstract

Purpose : Recent studies in sigma-1 receptors (σ-1r)- deficient mice demonstrated increased losses of retinal ganglion cells (RGCs) in oxidative stress and optic nerve crush mice models (ONC) . This study determines the neuroprotective role of the σ-1r in σ-1r- deficient mice ONC model.

Methods : ONC was performed in σ-1r k/o mice and wild type mice. Briefly, the left optic nerve (ON) were exposed intraorbitally through a small window made between the surrounding muscles. The ON was crushed approximately 1mm behind the globe with self-closing forceps for 4 seconds under visualization. The contralateral eye was used as controls for ONC. Two weeks prior to ONC, mice were intravitreally injected with AAV2-CAG-σ-1r-GFP vector (1.2 x 1010) and expression of σ-1r was assessed; AAV2 empty vector (1.2 x 1010) served as controls. Retinal activity was measured using electroretinogram (ERG, positive scotopic threshold response) before surgery and different times after surgery. Termination experiments include counting RGCs using RNA-binding protein with multiple splicing antibodies (RBPMS antibodies) in experimental animals to determine neuroprotective activities of the σ-1r.

Results : RGC death was accelerated in σ-1r k/o ONC animals when compared with wild-type mice. σ-1r k/o ONC mice injected with AAV2-CAG-σ-1r-GFP vector demonstrated significant increases in RGCs numbers and activity when compared with σ-1r k/o ONC mice injected with empty vector or non-injected σ-1r k/o ONC animals.

Conclusions : Our studies which involved the expression of σ-1r in a system devoid of σ-1rs, provided direct evidence of neuroprotection of RGCs due to the expression of σ-1rs. These findings support a protective role of σ-1r in RGCs when they are challenged by neurodegenerative insults.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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