May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Effect of Tauroursodeoxycholic Acid on Mouse Retinal Ganglion Cell Degeneration Following Optic Nerve Transection
Author Affiliations & Notes
  • J.H. Boatright
    Ophthalmology, Emory Univ School of Medicine, Atlanta, GA
  • A.P. Boyd
    Ophthalmology, Emory Univ School of Medicine, Atlanta, GA
  • E. Garcia–Valenzuela
    Ophthalmology, Emory Univ School of Medicine, Atlanta, GA
  • Footnotes
    Commercial Relationships  J.H. Boatright, None; A.P. Boyd, None; E. Garcia–Valenzuela, None.
  • Footnotes
    Support  RPB, FFB, NIH R01EY014026, P30EY06360
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3180. doi:
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      J.H. Boatright, A.P. Boyd, E. Garcia–Valenzuela; Effect of Tauroursodeoxycholic Acid on Mouse Retinal Ganglion Cell Degeneration Following Optic Nerve Transection . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3180.

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

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Abstract

Abstract: : Purpose: Tauroursodeoxycholic acid (TUDCA) is a naturally–occurring bile acid that is neuroprotective in models of neurodegenerative disease. We tested whether TUDCA was similarly protective in mouse retinal ganglion cells (RGCs) following optic nerve transection, an animal model of glaucoma. Methods: Adult C57/Bl6 mice were injected subcutaneously with TUDCA or vehicle (sodium bicarbonate) every three days during the course of the experiment. Ten days after the start of injections, mice were anesthetized and their optic nerves transected. The central retinal arteries were uninjured. A gelfoam sponge soaked in 3% Fluorogold was applied to the cut optic nerve stumps. At 5, 7, and 10 days post–surgery, mice were sacrificed and eyes fixed. Retina flatmounts were observed under fluorescent microscopy. Fluorescing RGCs were counted in a blinded fashion. Results: RGC somas were readily observed to be fluorescing in retina flatmounts from both TUDCA– and vehicle–treated mice, indicating that the severed RGCs took up Fluorogold following surgery. The number of fluorescing RGCs in vehicle–treated retinas declined with time. The number of fluorescing RGCs in TUDCA–treated retinas overall did not decline during the course of the experiment. The number of fluorescing RGCs in retinas from TUDCA–treated mice was higher than the number from vehicle–treated mice, regardless of post–operative day observation. RGC number was 34%, 214%, and 116% greater in TUDCA–treated versus vehicle–treated retinas at post–operative day 5, 7, and 10, respectively. Conclusions: RGCs have the ability to take up Fluorogold after transection and can be visualized by fluoroscent microscopy. RGC counts from vehicle–treated mice declined over the course of the experiment, suggesting that RGCs die following transection. RGC counts from TUDCA–treated mice did not similarly decline, suggesting that TUDCA treatment delayed or suppressed RGC death. The longevity of this protective effect and a possible anti–apoptotic mechanism of action are being studied in additional experiments. As TUDCA is FDA–approved and tolerated at high doses, these results may have implications for RGC–related diseases such as glaucoma.

Keywords: ganglion cells • apoptosis/cell death • neuroprotection 
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