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Comparison of lectin binding of drusen, RPE, Bruch's membrane, and photoreceptors.

ABSTRACT: PURPOSE: Drusen are deposits located between the retinal pigment epithelium and Bruch's membrane in age-related maculopathy. They are believed to be photoreceptor byproducts that are incompletely metabolized by the retinal pigment epithelium. This study therefore compares the lectin histochemistry of drusen, photoreceptors, retinal pigment epithelium, and Bruch's membrane. METHODS: Semithin sections of three eyes with age-related maculopathy were studied using 19 biotinylated lectins and an avidin-peroxidase-revealing system with and without neuraminidase pretreatment. RESULTS: High mannose, bi and tri-antennary nonbisected and bisected complex N-glycan, N-acetyl glucosamine and galactose were expressed by drusen, retinal pigment epithelium, Bruch's membrane, and photoreceptors while N-acetyl galactosamine and fucose were absent; treatment with neuraminidase exposed subterminal galactose in both sites and sparse N-acetyl galactosamine residues in drusen alone. Overall, there were striking similarities between the lectin binding of drusen, retinal pigment epithelium, and the photoreceptor outer segments, though cone outer segments were distinct in some features of their O-linked glycosylation. CONCLUSIONS: The results suggest that the pathogenesis of drusen is a combined mechanism, involving photoreceptors, Bruch's membrane, and the retinal pigment epithelium.

SUBMITTER: D'Souza YB

PROVIDER: S-EPMC2676197 | biostudies-literature | 2009

REPOSITORIES: biostudies-literature

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Comparison of lectin binding of drusen, RPE, Bruch's membrane, and photoreceptors.

D'Souza Yvonne B YB Jones Carolyn J P CJ Bonshek Richard E RE

Molecular vision 20090504

<h4>Purpose</h4>Drusen are deposits located between the retinal pigment epithelium and Bruch's membrane in age-related maculopathy. They are believed to be photoreceptor byproducts that are incompletely metabolized by the retinal pigment epithelium. This study therefore compares the lectin histochemistry of drusen, photoreceptors, retinal pigment epithelium, and Bruch's membrane.<h4>Methods</h4>Semithin sections of three eyes with age-related maculopathy were studied using 19 biotinylated lectin ...[more]

PMID: 19421409

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Project description: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;Sod2flox/flox BALB/cJ mice were housed in either 12-h dark, 12-h 200 lux white lighting (normal light), or 12-h dark, 12-h <10 lux red lighting (dim light). Electroretinography (ERG) and spectral-domain optical coherence tomography (SD-OCT) were performed to assess retinal function and morphology. Immunofluorescence was used to examine protein expression; quantitative RT-PCR was used to measure gene expression. Sod2 knockout (KO) mice had reduced RPE function with age and increased oxidative stress compared to wild type (WT) controls as expected by the cell-specific deletion of Sod2. This was associated with alterations in RPE morphology and the structure and function of RPE mitochondria. In addition, data show a compensatory increase in RPE glycolytic metabolism. The metabolic shift in RPE correlated with severe disruption of photoreceptor mitochondria including a reduction in TOMM20 expression, mitochondrial fragmentation, and reduced COXIII/β-actin levels. These findings demonstrate that mitochondrial oxidative stress can lead to RPE dysfunction and metabolic reprogramming of RPE. Secondary to these changes, photoreceptors also undergo metabolic stress with increased mitochondrial damage. These data are consistent with the hypothesis of a linked metabolism between RPE and photoreceptors and suggest a mechanism of retinal degeneration in dry AMD.

Dataset Information

Comparison of lectin binding of drusen, RPE, Bruch's membrane, and photoreceptors.

Publications

Comparison of lectin binding of drusen, RPE, Bruch's membrane, and photoreceptors.

Similar Datasets

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