Protection of Rpe65-deficient mice identifies rhodopsin as a mediator of light-induced retinal degeneration

Grimm, Christian; Wenzel, Andreas; Hafezi, Farhad; Yu, Song; Redmond, T. Michael; Remé, Charlotte E.

doi:10.1038/75614

Cited by 238 publications

(223 citation statements)

References 25 publications

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“…The second concerns the RPE which is selectively vulnerable to high‐energy blue light 41, 42. RPE sensitivity to LED lighting was previously explored by Chamorro et al .…”

Section: Discussionmentioning

confidence: 99%

Effects of white light‐emitting diode (LED) exposure on retinal pigment epithelium in vivo

Jaadane

Rodriguez

Boulenguez

et al. 2017

J Cellular Molecular Medi

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Ageing and alteration of the functions of the retinal pigment epithelium (RPE) are at the origin of lost of vision seen in age‐related macular degeneration (AMD). The RPE is known to be vulnerable to high‐energy blue light. The white light‐emitting diodes (LED) commercially available have relatively high content of blue light, a feature that suggest that they could be deleterious for this retinal cell layer. The aim of our study was to investigate the effects of “white LED” exposure on RPE. For this, commercially available white LEDs were used for exposure experiments on Wistar rats. Immunohistochemical stain on RPE flat mount, transmission electron microscopy and Western blot were used to exam the RPE. LED‐induced RPE damage was evaluated by studying oxidative stress, stress response pathways and cell death pathways as well as the integrity of the outer blood–retinal barrier (BRB). We show that white LED light caused structural alterations leading to the disruption of the outer blood–retinal barrier. We observed an increase in oxidized molecules, disturbance of basal autophagy and cell death by necrosis. We conclude that white LEDs induced strong damages in rat RPE characterized by the breakdown of the BRB and the induction of necrotic cell death.

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“…The second concerns the RPE which is selectively vulnerable to high‐energy blue light 41, 42. RPE sensitivity to LED lighting was previously explored by Chamorro et al .…”

Section: Discussionmentioning

confidence: 99%

Effects of white light‐emitting diode (LED) exposure on retinal pigment epithelium in vivo

Jaadane

Rodriguez

Boulenguez

et al. 2017

J Cellular Molecular Medi

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“…Photoreceptors lacking rhodopsin in genetically modified mice are completely protected against light-induced cell death. 16 …”

Section: History Of Action Spectramentioning

confidence: 99%

Light damage to the retina: an historical approach

Norren

Vos²

2015

Eye

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A brief review of retinal light damage is presented. Thermal damage requires a local rise in temperature of at least 10°C, causing an instant denaturation of proteins. The primary absorber is melanin. Photochemical damage occurs at body temperature and involves cellular damage by reactive forms of oxygen. The photosensitizers are photoproducts of the visual pigments. First indications that non-thermal damage might exist, in particular in the case of eclipse blindness, was presented by Vos in 1962. Attribution thereof to photochemical action was presented in 1966 by Noell et al who also measured the first action spectrum, in rat. It turned out to be identical to the absorption spectrum of rhodopsin. However, in 1976 and 1982 Ham et al found a quite different spectrum in monkeys, peaking at short wavelengths. The latter spectrum, but not the former, was confirmed since in numerous publications with animal models including rat. In ophthalmological practice a 'sunburn' was at first the only complaint caused by light damage. To avoid this, patients with dilated pupils should always be advised to wear sunglasses. Since the invention of the laser accidents have been reported, the most recent development is youth playfully pointing a strong laser pen in their eyes with marked consequences. The operation microscope and endoilluminators should always be used as brief as possible to avoid photochemical damage. Arguments for implant lenses that block not only the UV but also part of the visible spectrum seem too weak to justify extra costs.

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“…17,45 PCR amplification of c-jun was done on cDNA representing 12 ng of total retinal RNA using the upstream primer 5'-GAT CCT AAA ACA GAG CAT GAC-3' and the downstream primer 5'-GAA GTT GCT GAG GTT GGC G-3'. Amplification was for 35 cycles at 948C (30 s, denaturation), 558C (45 s, annealing) and 728C (45 s, extension).…”

Section: Ampli®cation and Sequencing Of C-junmentioning

confidence: 99%

“…4,13 ± 16 The light stimulus is absorbed by the visual pigment rhodopsin and converted into an intracellular death signal. 17 In mice, this process depends on the activation of the transcription factor AP-1 18,19 (and Wenzel et al,56 ). AP-1 is a dimeric complex consisting either of heterodimers of the Fos (c-Fos, FosB, Fra-1, Fra-2) and Jun (c-Jun, JunD, JunB) family of proteins or of homodimers of the Jun family of proteins.…”

Section: Introductionmentioning

confidence: 99%

AP-1 mediated retinal photoreceptor apoptosis is independent of N-terminal phosphorylation of c-Jun

et al. 2001

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Protection of Rpe65-deficient mice identifies rhodopsin as a mediator of light-induced retinal degeneration

Cited by 238 publications

References 25 publications

Effects of white light‐emitting diode (LED) exposure on retinal pigment epithelium in vivo

Effects of white light‐emitting diode (LED) exposure on retinal pigment epithelium in vivo

Light damage to the retina: an historical approach

AP-1 mediated retinal photoreceptor apoptosis is independent of N-terminal phosphorylation of c-Jun

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