Systemic administration of a free radical scavenger, edaravone, protects against light-induced photoreceptor degeneration in the mouse retina

Imai, Shunsuke; Inokuchi, Yuta; Nakamura, Shinsuke; Tsuruma, Kazuhiro; Shimazawa, Masamitsu; Hara, Hideaki

doi:10.1016/j.ejphar.2010.05.057

Cited by 55 publications

(44 citation statements)

References 29 publications

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“…It has been reported that lightinduced photoreceptor apoptosis was related to MAPKs activation in vitro and in vivo (Imai et al, 2010). Furthermore, Yang et al indicated that SB203580, a p38 inhibitor, inhibits the light-induced 661W cell death (Yang et al, 2007).…”

Section: Discussionmentioning

confidence: 98%

Maqui berry (Aristotelia chilensis) and the constituent delphinidin glycoside inhibit photoreceptor cell death induced by visible light

et al. 2013

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Section: Discussionmentioning

confidence: 98%

Maqui berry (Aristotelia chilensis) and the constituent delphinidin glycoside inhibit photoreceptor cell death induced by visible light

et al. 2013

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“…45 Extracellular signaling-regulated kinase (ERK) and protein kinase B (Akt) are known to be downstream of HB-EGF signaling, 31 and ERK and Akt activations are thought to have protective effects against light-induced retinal damage. 7,46 Thus, ERK and Akt signaling may be downregulated, and their protective effects eliminated, by Hb-egf knockdown. HB-EGF-C causes nuclear export of promyelocytic leukemia zinc finger protein, one of the transcriptional repressors, and activates a proliferative suppression abreaction.…”

Section: Discussionmentioning

confidence: 99%

“…3,4 Many researchers have reported the efficacy of antioxidants such as ascorbate 5 and curcumin 6 against lightinduced retinal damage. In addition, we previously described both the mechanism of disease progression and the efficacies of drugs such as antioxidants (edaravone, 7,8 crocetin, 9 anthocyanin 10 ) and a calpain inhibitor 11 against light-induced retinal damage. Thus, oxidative stress is likely to be involved in the pathogenesis of light-induced retinal degeneration.…”

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confidence: 99%

Role of Heparin-Binding Epidermal Growth Factor–Like Growth Factor in Light-Induced Photoreceptor Degeneration in Mouse Retina

Inoue

Tsuruma²,

Nakanishi³

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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Citation: Inoue Y, Tsuruma K, Nakanishi T, et al. Role of heparin-binding epidermal growth factor-like growth factor in light-induced photoreceptor degeneration in mouse retina. Invest Ophthalmol Vis Sci. 2013;54:3815-3829. DOI:10.1167/iovs.12-11236 PURPOSE. Although heparin-binding epidermal growth factor-like growth factor (HB-EGF) has been reported to have protective effects against various neuronal cell damage, its role in the retina has not been elucidated. Here, we investigated its role in light-induced photoreceptor degeneration using retinas and ventral forebrain-specific Hb-egf knockout (KO) mice.METHODS. Disruption of Hb-egf was confirmed by b-galactosidase (LacZ) staining and RT-PCR. Time-dependent changes in retinal HB-EGF were measured using quantitative RT-PCR and Western blotting. Retinal damage was induced by exposure to light. Recombinant human HB-EGF was injected intravitreally. Electroretinogram (ERG) and histological analyses were performed. To evaluate the effect of HB-EGF against light irradiation-induced cell death, 661W cells, a transformed mouse cone cell line, were used. RESULTS.LacZ-positive cells were observed and Hb-egf deletion was confirmed in the retinas of Hb-egf KO mice. Hb-egf and pro-HB-EGF levels were increased after light exposure in wildtype (WT) mice. Exposure to light reduced the a-and b-wave amplitudes of the dark-adapted ERG, and also outer nuclear layer (ONL) thickness, in Hb-egf KO mice versus WT mice. Treatment with HB-EGF improved both the a-and b-wave amplitudes and the thickness of the ONL. The 661W cell death induced by light irradiation was exacerbated by Hb-egf knockdown. HB-EGF also protected against light-induced cell death and reduced reactive oxygen species (ROS) production in 661W cells. HB-EGF treatment improved the a-wave amplitudes and the thickness of the ONL in Hb-egf KO mice.CONCLUSIONS. These data suggest that HB-EGF plays a pivotal role in light-induced photoreceptor degeneration. It therefore warrants investigation as a potential therapeutic target for such light-induced retinal diseases as age-related macular degeneration.

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“…Light irradiation to retina induces oxidative stress, 20 and inflammatory cytokines, 21 which lead to the ER stress in RPE cells. 11,22 The RPE is also constantly subjected to oxidative stress as a result of exposure to arterial blood.…”

Section: Susceptibility Of Sema4a Mutants To Er Stress and Oxidative mentioning

confidence: 99%

SEMA4A Mutations Lead to Susceptibility to Light Irradiation, Oxidative Stress, and ER Stress in Retinal Pigment Epithelial Cells

Tsuruma

Nishimura

Kishi

et al. 2012

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. RP is a retinal degeneration disorder that is caused by mutations of various genes, including semaphorin-4A (SEM-A4A). A number of retinal diseases, including RP, are associated with light exposure, oxidative stress, and endoplasmic reticulum (ER) stress. In this study, we investigated whether mutant SEMA4A causes retinal dysfunction via light exposure, oxidative stress, and ER stress.METHODS. Mutant SEMA4A (D345H or F350C) was overexpressed in a human retinal epithelium cell line ARPE19. Intracellular localization of mutant SEMA4A was investigated using confocal laser scanning microscopy. The ARPE-19 cells were also irradiated with white light, and expression of 78 kDa glucose-regulated protein (GRP78), a marker of ER stress, and phagocytosis were measured. The cells were treated with an ER stress inducer, tunicamycin, or an oxidative stressor, H 2 O 2 , and cell death was measured. Human SEMA4A mutants were expressed in zebrafish embryos with tunicamycin and mRNA of DNA damage-inducible transcript 3 (ddit3) was measured as an ER stress marker.RESULTS. Mutant SEMA4A was localized in the ER, whereas wild type (WT) SEMA4A was observed in cell membranes. The expression of GRP78 was increased by mutant SEMA4A following light irradiation, and phagocytosis was suppressed in mutant SEMA4A-transfected cells. Mutant SEMA4A induced susceptibility to ER stress and oxidative stress. In zebrafish, human mutant SEMA4A increased ddit3 mRNA compared with WT under the ER stress condition. CONCLUSIONS.Our results suggest that mutations in SEMA4A may cause susceptibility to light exposure, oxidative stress, and ER stress, which may be involved in the progression and pathology of RP. (Invest Ophthalmol Vis Sci. 2012;53:6729-6737)

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Systemic administration of a free radical scavenger, edaravone, protects against light-induced photoreceptor degeneration in the mouse retina

Cited by 55 publications

References 29 publications

Maqui berry (Aristotelia chilensis) and the constituent delphinidin glycoside inhibit photoreceptor cell death induced by visible light

Maqui berry (Aristotelia chilensis) and the constituent delphinidin glycoside inhibit photoreceptor cell death induced by visible light

Role of Heparin-Binding Epidermal Growth Factor–Like Growth Factor in Light-Induced Photoreceptor Degeneration in Mouse Retina

SEMA4A Mutations Lead to Susceptibility to Light Irradiation, Oxidative Stress, and ER Stress in Retinal Pigment Epithelial Cells

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