Mitochondrial oxidative stress in the retinal pigment epithelium (RPE) led to metabolic dysfunction in both the RPE and retinal photoreceptors

Age-related macular degeneration (AMD) is the leading cause of vision loss in the western world. Recent evidence suggests that RPE and photoreceptors have an interconnected metabolism and that mitochondrial damage in RPE is a trigger for degeneration in both RPE and photoreceptors in AMD. To test th...

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Bibliographic Details
Published in:Redox biology 2019-06, Vol.24, p.101201-101201, Article 101201
Main Authors: Brown, Emily E, DeWeerd, Alexander J, Ildefonso, Cristhian J, Lewin, Alfred S, Ash, John D
Format: Article
Language:English
Subjects:
Animals
Biomarkers
Disease Models, Animal
Electroretinography
Energy Metabolism
Female
Humans
Macular Degeneration - diagnostic imaging
Macular Degeneration - etiology
Macular Degeneration - metabolism
Macular Degeneration - pathology
Male
Mice, Knockout
Mitochondria - metabolism
Oxidative Stress
Photoreceptor Cells, Vertebrate - metabolism
Promoter Regions, Genetic
Research Paper
Retinal Pigment Epithelium - metabolism
Superoxide Dismutase - genetics
Superoxide Dismutase - metabolism
Tomography, Optical Coherence
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Summary:Age-related macular degeneration (AMD) is the leading cause of vision loss in the western world. Recent evidence suggests that RPE and photoreceptors have an interconnected metabolism and that mitochondrial damage in RPE is a trigger for degeneration in both RPE and photoreceptors in AMD. To test this hypothesis, this study was designed to induce mitochondrial damage in RPE in mice to determine whether this is sufficient to cause RPE and photoreceptor damage characteristic of AMD. In this study, we conditionally deleted the gene encoding the mitochondrial antioxidant enzyme, manganese superoxide dismutase (MnSOD encoded by Sod2) in the retinal pigment epithelium (RPE) of albino BALB/cJ mice. VMD2-Cre;Sod2 BALB/cJ mice were housed in either 12-h dark, 12-h 200 lux white lighting (normal light), or 12-h dark, 12-h
ISSN:2213-2317
2213-2317
DOI:10.1016/j.redox.2019.101201