April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Involvement of Endoplasmic Reticulum Stress on Neuronal Degeneration in the Lateral Geniculate Nucleus in the Monkey Glaucoma Model
Y. Ito; M. Shimazawa; Y. Inokuchi; A. Miwa; H. Yamanaka; K. Tsuruma; H. Onoe; M. Araie; H. Hara
Author Affiliations & Notes
  • Y. Ito
    Biofunctnl Evaluation, Gifu Pharmaceutical University, Gifu, Japan
  • M. Shimazawa
    Biofunctnl Evaluation, Gifu Pharmaceutical University, Gifu, Japan
    Functional Probe Research Laboratory, Molecular Imaging Research Program, RIKEN, Kobe, Japan
  • Y. Inokuchi
    Biofunctnl Evaluation, Gifu Pharmaceutical University, Gifu, Japan
  • A. Miwa
    Biofunctnl Evaluation, Gifu Pharmaceutical University, Gifu, Japan
  • H. Yamanaka
    Functional Probe Research Laboratory, Molecular Imaging Research Program, RIKEN, Kobe, Japan
  • K. Tsuruma
    Biofunctnl Evaluation, Gifu Pharmaceutical University, Gifu, Japan
  • H. Onoe
    Functional Probe Research Laboratory, Molecular Imaging Research Program, RIKEN, Kobe, Japan
  • M. Araie
    Department of Ophthalmology, University of Tokyo School of Medicine, Tokyo, Japan
  • H. Hara
    Biofunctnl Evaluation, Gifu Pharmaceutical University, Gifu, Japan
    Functional Probe Research Laboratory, Molecular Imaging Research Program, RIKEN, Kobe, Japan
  • Footnotes
    Commercial Relationships  Y. Ito, None; M. Shimazawa, None; Y. Inokuchi, None; A. Miwa, None; H. Yamanaka, None; K. Tsuruma, None; H. Onoe, None; M. Araie, None; H. Hara, None.
  • Footnotes
    Support  JSPS Grant No. 20•10786, MEXT Grant No. 18209053
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 6117. doi:
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      Y. Ito, M. Shimazawa, Y. Inokuchi, A. Miwa, H. Yamanaka, K. Tsuruma, H. Onoe, M. Araie, H. Hara; Involvement of Endoplasmic Reticulum Stress on Neuronal Degeneration in the Lateral Geniculate Nucleus in the Monkey Glaucoma Model. Invest. Ophthalmol. Vis. Sci. 2010;51(13):6117.

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Abstract

Purpose: : Endoplasmic reticulum (ER) stress is involved in neurodegenerative diseases, including glaucoma. However, it has been unclear yet whether ER stress induces the neuronal death in the glaucomatous LGN. In this study, we investigated the involvement of ER stress on the pathophysiological mechanisms underlying neuronal death of the LGN after the intraocular pressure (IOP) elevation.

Methods: : Two cynomolgus monkeys, each with a glaucomatous left eye by laser-photocoagulation treatment, were studied. At 4 and 24 weeks after the laser-photocoagulation treatment, the numbers of LGN neuron and atrophy were evaluated by immunohistchemistry using parvalbumin-antibody that was used to specifically label relay neurons connecting to the visual cortex.

Results: : Loss of neurons and/or neuronal atrophy in layer 1 of LGN (magnocellular layer) were observed at both 4 and 24 weeks after the laser-photocoagulation treatment, and in layers 4 and 6 of LGN (parvocellular layer) at 24 weeks. In the LGN region, the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL)-positive cells, polyubiquitin, and production of ER stress-related proteins, such as the phosphorylation of eukaryotic initiation factor 2α (p-eIF2α) and C/EBP-homologous protein (CHOP), were also detected by in situ hybridization and immunostaining.

Conclusions: : These findings indicate that ER-stress may play some roles in neuronal death of the LGN after the IOP elevation.

Keywords: apoptosis/cell death • pathology: experimental • immunohistochemistry 
© 2010, 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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