April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
The Effect of an Inducer of Bip, an ER-Resident Molecular Chaperone, on Light-Induced Retinal Damages
Author Affiliations & Notes
  • T. Nakanishi
    Biofunctional Evaluation, Molecular Pharmacology,
    Gifu Pharmaceutical University, Gifu, Japan
  • S. Imai
    Biofunctional Evaluation, Molecular Pharmacology,
    Gifu Pharmaceutical University, Gifu, Japan
  • Y. Inokuchi
    Biofunctional Evaluation, Molecular Pharmacology,
    Gifu Pharmaceutical University, Gifu, Japan
  • K. Tsuruma
    Biofunctional Evaluation, Molecular Pharmacology,
    Gifu Pharmaceutical University, Gifu, Japan
  • M. Shimazawa
    Biofunctional Evaluation, Molecular Pharmacology,
    Gifu Pharmaceutical University, Gifu, Japan
  • Y. Monguchi
    Medical Chemistry,
    Gifu Pharmaceutical University, Gifu, Japan
  • H. Sajiki
    Medical Chemistry,
    Gifu Pharmaceutical University, Gifu, Japan
  • T. Kudo
    Psychiatry, Osaka University Graduate School of Medicine, Osaka, Japan
  • H. Hara
    Biofunctional Evaluation, Molecular Pharmacology,
    Gifu Pharmaceutical University, Gifu, Japan
  • Footnotes
    Commercial Relationships  T. Nakanishi, None; S. Imai, None; Y. Inokuchi, None; K. Tsuruma, None; M. Shimazawa, None; Y. Monguchi, None; H. Sajiki, None; T. Kudo, None; H. Hara, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 2255. doi:
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      T. Nakanishi, S. Imai, Y. Inokuchi, K. Tsuruma, M. Shimazawa, Y. Monguchi, H. Sajiki, T. Kudo, H. Hara; The Effect of an Inducer of Bip, an ER-Resident Molecular Chaperone, on Light-Induced Retinal Damages. Invest. Ophthalmol. Vis. Sci. 2010;51(13):2255.

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

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Abstract

Purpose: : Recent evidence suggests that endoplasmic reticulum (ER) stress is activated during light-induced retinal damage. A preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin binding protein (BiP; Bip inducer X, BIX) has the protective effect against ER stress-induced cell death. Here, we investgated changes of ER stress-related factors in retina after the light exposure and effect of BIX on light-induced retinal cell death in mice.

Methods: : To examine the ER stress activation, we measured time-dependent changes of ER stress-related factors in retina after light exposure using quantitative RT-PCR: The expressions of GRP78/BiP, C/EBP-homologous (CHOP), calreticulin, ER degradation enhancing α-mannosidase like protein (EDEM), asparagine synthetase (ASNS), 94 kDa glucose-regulated protein (GRP94), and 52 kDa repressor of the inhibitor of the protein kinase (p58IPK) were measured. Retinal light damage was induced by exposure to constant white fluorescent light for 3 h at an illumination of 8000 lux. To evaluate the effect of BIX on retinal damages, a- and b-wave amplitudes of the dark-adapted electroretinogram (ERG) were recorded at 5 days after light exposure, then outer nuclear layer (ONL) thickness was measured on hematoxylin-eosin-stained sections. BIX (5 nmol/eye) was intravitreously injected at 6 h before light exposure.

Results: : RT-PCR revealed that all ER stress-related factors except ASNS were increased after light exposure. The a- and b-wave amplitudes of the dark-adapted ERG were reduced at 5 days after light exposure, and BIX treatment significantly prevented the retinal dysfunctions as compared with those in vehicle-treated group. In histological analysis, the light exposure reduced ONL thickness, and treatment with BIX significantly inhibited the ONL atrophy as compared with that in vehicle-treated group.

Conclusions: : These data indicate that ER stress may play a pivotal role in light exposure-induced retinal damage, and treatment with BIX may prevent the retinal damage.

Keywords: apoptosis/cell death • chaperones • retina 
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