April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
HE3286 Reduces Axonal Loss and Preserves Retinal Ganglion Cell Function in Experimental Optic Neuritis
Author Affiliations & Notes
  • Reas Sulaimankutty
    Ophthalmology, Univ of Pennsylvania, Scheie Eye Inst, Philadelphia, PA
  • Kimberly Dine
    Ophthalmology, Univ of Pennsylvania, Scheie Eye Inst, Philadelphia, PA
  • Esteban Luna
    Ophthalmology, Univ of Pennsylvania, Scheie Eye Inst, Philadelphia, PA
  • Clarence Ahlem
    Harbor Therapeutics Inc, San Diego, CA
  • Kenneth S Shindler
    Ophthalmology, Univ of Pennsylvania, Scheie Eye Inst, Philadelphia, PA
  • Footnotes
    Commercial Relationships Reas Sulaimankutty, None; Kimberly Dine, None; Esteban Luna, None; Clarence Ahlem, Harbor Therapeutics (E), Harbor Therapeutics (I); Kenneth Shindler, Harbor Therapeutics (F)
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 5771. doi:
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      Reas Sulaimankutty, Kimberly Dine, Esteban Luna, Clarence Ahlem, Kenneth S Shindler; HE3286 Reduces Axonal Loss and Preserves Retinal Ganglion Cell Function in Experimental Optic Neuritis. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5771.

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

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Abstract

Purpose: Optic nerve inflammation, demyelination and axonal loss are all prominent features of optic neuritis. While corticosteroids can hasten visual recovery in optic neuritis, no treatment is available to improve visual outcomes. HE3286 (17α-ethynyl-5-androstene-3β, 7β, 17β-triol), a synthetic derivative of a natural steroid, β-AET (5-androstene-3β, 7β, 17β-triol), exerts anti-inflammatory effects in several disease models, and has purported direct neuroprotective effects as well. The ability of HE3286 to suppress optic neuritis in the experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis was examined.

Methods: EAE was induced in C57/Bl6 mice by immunization with myelin oligodendroglial glycoprotein peptide. Mice were treated daily with vehicle or 40 mg/kg HE3286 i.p. Visual function was assessed by optokinetic responses (OKR) at baseline and every 10 days until sacrifice 6 weeks post-immunization. Retinas and optic nerves were isolated. Inflammation was assessed by H&E staining, demyelination was assessed by luxol fast blue staining and axonal loss was assessed by neurofilament staining of optic nerve sections. Retinal ganglion cells (RGCs) were immunolabeled with Brn3a antibodies to quantify RGC survival.

Results: Progressive decreases in OKR occurred in vehicle-treated EAE mice, and HE3286 treatment significantly reduced the level of this vision loss. HE3286 also significantly attenuated the degree of inflammation, demyelination and axonal loss in EAE optic nerves as compared to nerves from vehicle-treated EAE mice. RGC loss was observed in eyes from both vehicle- and HE3286-treated EAE mice, with a trend toward increased RGC survival in the HE3286-treated mice.

Conclusions: HE3286 suppresses inflammation and reduces demyelination and axonal loss during experimental optic neuritis. Importantly, HE3286 treatment also preserves some RGC function. Results suggest HE3286 is a potential novel treatment for optic neuritis and MS that warrants further study.

Keywords: 613 neuro-ophthalmology: optic nerve • 629 optic nerve • 531 ganglion cells  
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