March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Oncostatin M Protects Retinal Ganglion Cells in an Optic Nerve Crush Mouse Model
Author Affiliations & Notes
  • Xin Xia
    Bascom Palmer Eye Institute, University of Miami, Miami, Florida
    Department of Ophthalmology, Shanghai First People’s Hospital, Jiaotong University, Shanghai, China
  • Yiwen Li
    Bascom Palmer Eye Institute, University of Miami, Miami, Florida
  • Zhengying Wang
    Bascom Palmer Eye Institute, University of Miami, Miami, Florida
  • Lingyu Luo
    Bascom Palmer Eye Institute, University of Miami, Miami, Florida
  • Rong Wen
    Bascom Palmer Eye Institute, University of Miami, Miami, Florida
  • Footnotes
    Commercial Relationships  Xin Xia, None; Yiwen Li, None; Zhengying Wang, None; Lingyu Luo, None; Rong Wen, None
  • Footnotes
    Support  NIH Grant R01EY018586, P30EY14801; Hope for Vision, the James and Esther King Biomedical Research Program of the State of Florida JEK 08-KN-09; the Department of Defense Grant W81XWH-09-1-0674; RPB.
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 6588. doi:
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    • Get Citation

      Xin Xia, Yiwen Li, Zhengying Wang, Lingyu Luo, Rong Wen; Oncostatin M Protects Retinal Ganglion Cells in an Optic Nerve Crush Mouse Model. Invest. Ophthalmol. Vis. Sci. 2012;53(14):6588.

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

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Abstract
 
Purpose:
 

Oncostatin M (OSM) is a member of the IL-6 family of cytokines, which includes interleukin 6 (IL-6), IL-11, ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF), cardiotropin 1 (CT-1), and cardiotrophin-like cytokine (CLC). We have shown previously that OSM protects rod and cone photoreceptors in the transgenic rat that carries the rhodopsin S334ter mutation. In the present work, we studied the neuroprotective effects on retinal ganglion cells (RGCs) after optic nerve crush (ONC) in mouse.

 
Methods:
 

BALB/C mice were used in all experiments. RGCs were retrogradely labeled 7 days before ONC by placing a small piece of gelform containing 3µl of 2% FluoroGold on the surface of the superior colliculi on both sides of the brain. The left optic nerve was exposed from the superior side and crushed by a pair of self-closing forceps (RS-5027, Roboz Surgical Instrument Co., Gaithersburg, MD) for 4 second. The right optic nerve was exposed but not crushed to serve as a sham-operated control. Intravitreal OSM (3µg in 2µl PBS) or PBS (2µl) was given immediately after ONC. Retinas were collected 14 days after, flat-mounted, and examined by the confocal microscopy. Three rectangular areas of 0.64 x 0.64 mm at 0.5, 1.0, and 1.5 mm from the optic nerve disc (OND) in the central region of each retinal quadrant (superior, nasal, inferior and temporal) were examined and the average cell densities were presented as mean±SD/mm2.

 
Results:
 

RGCs in the sham-operated control retinas are 3,176.46±440.77, 3,062.29±371.21, and 2708.85±303.10 at 0.5, 1.0, and 1.5 mm from OND, respectively (n=6). In PBS-treated retinas, the RCG densities are 402.5±37.73, 397.29±38.95, and 363.33±23.21 at 0.5, 1.0, and 1.5 mm from OND respectively (n=6). RGC densities in OSM-treated retinas are 1,224.90±142.57, 1,311.77±114.21, and 1,182.08±98.00 at 0.5, 1.0, and 1.5 mm from OND, respectively (n=6). RGC densities in OSM-treated are significantly higher than those in the PBS-treated retinas (P<0.001, triple asterisks).

 
Conclusions:
 

OSM treatment significantly protected RGCs from optic nerve crush induced cell death.  

 
Keywords: ganglion cells • neuroprotection • optic nerve 
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