December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Neuron-Specific Enolase in Cell Damage after Retinal Ischemia-Reperfusion Injury in Rats
GJ Ko; Q Chu; S Garg; R Sanchez; AA Sadun; J Sebag; TT Lam
Author Affiliations & Notes
  • GJ Ko
    Doheny Eye Institute and the Department of Ophthalmology Keck School of Medicine of the University of Southern California/ New York University School of Medicine Los Angeles CA
  • Q Chu
    Doheny Eye Institute and the Department of Ophthalmology Keck School of Medicine of the University of Southern California Los Angeles CA
  • S Garg
    Doheny Eye Institute and the Department of Ophthalmology Keck School of Medicine of the University of Southern California Los Angeles CA
  • R Sanchez
    Doheny Eye Institute and the Department of Ophthalmology Keck School of Medicine of the University of Southern California Los Angeles CA
  • AA Sadun
    Doheny Eye Institute and the Department of Ophthalmology Keck School of Medicine of the University of Southern California Los Angeles CA
  • J Sebag
    Doheny Eye Institute and the Department of Ophthalmology Keck School of Medicine of the University of Southern California Los Angeles CA
  • TT Lam
    Doheny Eye Institute and the Department of Ophthalmology Keck School of Medicine of the University of Southern California Los Angeles CA
  • Footnotes
    Commercial Relationships   G.J. Ko, None; Q. Chu, None; S. Garg, None; R. Sanchez, None; A.A. Sadun, None; J. Sebag, None; T.T. Lam, None. Grant Identification: Supported in part by a NIH Grant EY03040 and an unrestricted grant from RPB.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3614. doi:
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      GJ Ko, Q Chu, S Garg, R Sanchez, AA Sadun, J Sebag, TT Lam; Neuron-Specific Enolase in Cell Damage after Retinal Ischemia-Reperfusion Injury in Rats . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3614.

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Abstract

Abstract: : Purpose:Neuron-specific enolase (NSE), a neuron and neuroendocrine cell-specific glycolytic enzyme, is released into the serum, the CSF and other tissues following neuronal injury. This study was conducted to investigate whether tissue and/or serum levels of NSE may be indicators of inner retinal degeneration after retinal ischemia-reperfusion injury in rats. Methods:Intraocular pressure was maintained for 60 minutes at 110mm Hg in anesthetized male albino Lewis rats. Retinal and blood samples were obtained at 0, 2, 4, 18, 24, 48 and 72 hours after the insult. Dot-blot and Western analysis were performed using a monoclonal mouse anti-human neuron-specific enolase (dot-blot: 1:500; Western: 1:200) (DAKO Corp., Carpinteria, CA). Immunohistochemistry was used to localize NSE in retinal sections. Results:Retinal NSE levels increased at 0, 2 and 4 hours after the insult, reached maximal levels from 18 to 24 hours, and decreased from 48 to 72 hours. Serum NSE levels also increased gradually, reaching maximal levels from 8 to 18 hours and showing noticeably elevated levels even at 72 hours. Western blotting confirmed the detection of the NSE gamma subunit detected at 46 kDa. Immunohistochemistry showed mild NSE immunoreactivity (IM) in the retina except the inner and outer segments with moderate IM in the cell bodies of scattered cells in the retinal ganglion cell layer (RGCL) and the inner nuclear layer (INL) in the normal retinas. After the insult and up to 48 hours, intense IM was noted in the inner limiting membrane (ILM), the nerve fiber layer (NFL) and RGCL. Conclusion: Both tissue and serum NSE levels are reliable indicators of inner retinal cell damage.

Keywords: 448 ischemia • 554 retina • 399 enzymes/enzyme inhibitors 
© 2002, The Association for Research in Vision and Ophthalmology, Inc., all rights reserved. Permission to republish any abstract or part of an abstract in any form must be obtained in writing from the ARVO Office prior to publication.
Copyright © 2025 Association for Research in Vision and Ophthalmology.
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