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Effect of an inducer of BiP, a molecular chaperone, on endoplasmic reticulum (ER) stress-induced retinal cell death.
Invest Ophthalmol Vis Sci. 2009 Jan; 50(1):334-44.IO

Abstract

PURPOSE

The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.

METHODS

In vitro, BiP mRNA was measured after BIX treatment using semi-quantitative RT-PCR or real-time PCR. The effect of BIX on tunicamycin (at 2 microg/mL)-induced damage was evaluated by measuring the cell-death rate and CHOP protein expression. In vivo, BiP protein induction was examined by immunostaining. The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression.

RESULTS

In vitro, BIX preferentially induced BiP mRNA expression both time- and concentration-dependently in RGC-5 cells. BIX (1 and 5 microM) significantly reduced tunicamycin-induced cell death, and BIX (5 microM) significantly reduced tunicamycin-induced CHOP protein expression. In vivo, intravitreal injection of BIX (5 nmol) significantly induced BiP protein expression in the mouse retina. Co-administration of BIX (5 nmol) significantly reduced both the retinal cell death and the CHOP protein expression in GCL induced by intravitreal injection of tunicamycin or NMDA.

CONCLUSIONS

These findings suggest that this BiP inducer may have the potential to be a therapeutic agent for endoplasmic reticulum (ER) stress-induced retinal diseases.

Authors+Show Affiliations

Department of Biofunctional Evaluation, Molecular Pharmacology, Gifu Pharmaceutical University, Gifu, JapanNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18757512

Citation

Inokuchi, Yuta, et al. "Effect of an Inducer of BiP, a Molecular Chaperone, On Endoplasmic Reticulum (ER) Stress-induced Retinal Cell Death." Investigative Ophthalmology & Visual Science, vol. 50, no. 1, 2009, pp. 334-44.
Inokuchi Y, Nakajima Y, Shimazawa M, et al. Effect of an inducer of BiP, a molecular chaperone, on endoplasmic reticulum (ER) stress-induced retinal cell death. Invest Ophthalmol Vis Sci. 2009;50(1):334-44.
Inokuchi, Y., Nakajima, Y., Shimazawa, M., Kurita, T., Kubo, M., Saito, A., Sajiki, H., Kudo, T., Aihara, M., Imaizumi, K., Araie, M., & Hara, H. (2009). Effect of an inducer of BiP, a molecular chaperone, on endoplasmic reticulum (ER) stress-induced retinal cell death. Investigative Ophthalmology & Visual Science, 50(1), 334-44. https://doi.org/10.1167/iovs.08-2123
Inokuchi Y, et al. Effect of an Inducer of BiP, a Molecular Chaperone, On Endoplasmic Reticulum (ER) Stress-induced Retinal Cell Death. Invest Ophthalmol Vis Sci. 2009;50(1):334-44. PubMed PMID: 18757512.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of an inducer of BiP, a molecular chaperone, on endoplasmic reticulum (ER) stress-induced retinal cell death. AU - Inokuchi,Yuta, AU - Nakajima,Yoshimi, AU - Shimazawa,Masamitsu, AU - Kurita,Takanori, AU - Kubo,Mikiko, AU - Saito,Atsushi, AU - Sajiki,Hironao, AU - Kudo,Takashi, AU - Aihara,Makoto, AU - Imaizumi,Kazunori, AU - Araie,Makoto, AU - Hara,Hideaki, Y1 - 2008/08/29/ PY - 2008/9/2/pubmed PY - 2009/1/17/medline PY - 2008/9/2/entrez SP - 334 EP - 44 JF - Investigative ophthalmology & visual science JO - Invest Ophthalmol Vis Sci VL - 50 IS - 1 N2 - PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated. METHODS: In vitro, BiP mRNA was measured after BIX treatment using semi-quantitative RT-PCR or real-time PCR. The effect of BIX on tunicamycin (at 2 microg/mL)-induced damage was evaluated by measuring the cell-death rate and CHOP protein expression. In vivo, BiP protein induction was examined by immunostaining. The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression. RESULTS: In vitro, BIX preferentially induced BiP mRNA expression both time- and concentration-dependently in RGC-5 cells. BIX (1 and 5 microM) significantly reduced tunicamycin-induced cell death, and BIX (5 microM) significantly reduced tunicamycin-induced CHOP protein expression. In vivo, intravitreal injection of BIX (5 nmol) significantly induced BiP protein expression in the mouse retina. Co-administration of BIX (5 nmol) significantly reduced both the retinal cell death and the CHOP protein expression in GCL induced by intravitreal injection of tunicamycin or NMDA. CONCLUSIONS: These findings suggest that this BiP inducer may have the potential to be a therapeutic agent for endoplasmic reticulum (ER) stress-induced retinal diseases. SN - 1552-5783 UR - https://www.unboundmedicine.com/medline/citation/18757512/Effect_of_an_inducer_of_BiP_a_molecular_chaperone_on_endoplasmic_reticulum__ER__stress_induced_retinal_cell_death_ L2 - https://iovs.arvojournals.org/article.aspx?doi=10.1167/iovs.08-2123 DB - PRIME DP - Unbound Medicine ER -