May 2007
Volume 48, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2007
LIF Protection of Photoreceptor from Light Damage Correlates with Stat3 Activation
Author Affiliations & Notes
  • Y. Ueki
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Oklahoma Center for Neuroscience,
  • J. Wang
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Department of Ophthalmology,
  • S. Chollangi
    Department of Bioengineering, University of Oklahoma, Norman, Oklahoma
  • J. D. Ash
    University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma
    Oklahoma Center for Neuroscience,
    Department of Ophthalmology,
  • Footnotes
    Commercial Relationships Y. Ueki, None; J. Wang, None; S. Chollangi, None; J.D. Ash, None.
  • Footnotes
    Support R01 EY016459 HIGHWIRE EXLINK_ID="48:5:3052:1" VALUE="EY016459" TYPEGUESS="GEN" /HIGHWIRE -01A1(Ash PI), P20 RR017703 HIGHWIRE EXLINK_ID="48:5:3052:2" VALUE="RR017703" TYPEGUESS="GEN" /HIGHWIRE -01, P30 EY012190 HIGHWIRE EXLINK_ID="48:5:3052:3" VALUE="EY012190" TYPEGUESS="GEN" /HIGHWIRE , Research to Prevent Blindness
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 3052. doi:
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    • Get Citation

      Y. Ueki, J. Wang, S. Chollangi, J. D. Ash; LIF Protection of Photoreceptor from Light Damage Correlates with Stat3 Activation. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3052.

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

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Abstract

Purpose:: Activation of the receptor gp130 by IL-6 family cytokines, including leukemia inhibitory factor (LIF) and ciliary neurotrophic factor (CNTF), is neuroprotective and prevents photoreceptor cell death in vivo. However, the mechanisms of protection in the retina remain largely unknown. The purpose of this study was to determine the signaling pathways downstream of gp130 that are responsible for neuroprotection.

Methods:: Recombinant human LIF or a LIF antagonist, LIF05, was injected intravitreally to one eye of 5-6 week-old Balb/c mice. PBS was injected in the other eye as a control (n=6 mice per group). The first experiment was designed to determine if LIF prevented photoreceptor degeneration. To accomplish this, mice were exposed to 3000 lux of light for 4 hours, 2 days post injections. Following light exposure mice were retuned to normal mouse room lighting. Electroretinograms (ERG) were recorded 5 days after the light damage, and eyes were then collected for measurements of photoreceptor cell loss by histological evaluation. In the second experiment, retinas were collected 2 days after the injections for analysis of Stat3, Akt, and ERK1/2 activation. Activation was quantified by Western Blot using antibodies to phosphorylated and unphosphorylated proteins. The cellular localization of active signaling was measured by immunohistochemistry.

Results:: We observed LIF prevented loss of photoreceptors in a dose dependent manner. In the ERG analysis the a- and b- wave amplitudes were preserved by LIF injections. In LIF injected eye the thickness of the outer nuclear layer (ONL) was also preserved relative to uninjected, PBS or LIF05 injected eyes. Significant Stat3 activation was detected in LIF, but not in LIF05 or PBS injected retinas at the time of light exposure (2 days). Activated Stat3 was mainly localized in nuclei of inner retinal neurons and Muller cells. Neither LIF nor LIF05 lead to significant activation of Akt or Erk1/2 pathways at the time of light exposure.

Conclusions:: LIF, but not PBS or LIF05, protects photoreceptors from degeneration induced by light damage. This protection correlated well with activation of Stat3 but not with activation of Akt or Erk1/2 pathways.

Keywords: neuroprotection • signal transduction • retinal degenerations: cell biology 
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