Analysis of esterification of retinoids in the retinal pigmented epithelium of the Mitf-vit (vitiligo) mutant mouse.

B. L. Evans, Sylvia B Smith

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Abstract

PURPOSE: Mice homozygous for the vitiligo mutation of the microphthalmia (Mitf) gene have a retinal degeneration characterized by slow loss of photoreceptor cells and compromised retinal pigment epithelial (RPE) structure and function. The levels of retinyl esters, which are essential for generation of 11-cis-retinaldehyde for the formation of rhodopsin, were reported previously to be elevated by 6 weeks postnatally in the RPE of vitiligo mutant mice. The purpose of the present study was to determine whether this elevation was due to increased activity of lecithin:retinol acyl transferase (LRAT) the enzyme that converts all-trans-retinol to retinyl esters. METHODS: Retinoids extracted from the RPE and neural retina of mutant and normal mice ages 2, 4, 6 and 8 weeks were analyzed by reversed-phase HPLC. The esterification capacity of the RPE to convert 3H-retinol to 3H-retinyl ester was determined by HPLC in mutant and normal mice at 3 and 9 weeks. RESULTS: Retinyl ester levels were elevated significantly in the mutant RPE as early as postnatal week 2 and were four-fold greater by 8 weeks. The esterification assay indicated no significant differences between mutants and controls at 3 weeks. At 9 weeks, the esterification activity of the mutant RPE was significantly reduced compared to controls rather than elevated. CONCLUSIONS: The data suggest that the accumulation of retinyl esters is not due to increased LRAT activity. Alternative explanations for the retinyl ester accumulation are discussed.

Original languageEnglish (US)
Number of pages1
JournalMolecular Vision
Volume3
StatePublished - Jan 1 1997

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Vitiligo
Retinal Pigments
Esterification
Retinoids
Esters
Epithelium
Vitamin A
Lecithins
Transferases
High Pressure Liquid Chromatography
Retinaldehyde
Microphthalmos
Photoreceptor Cells
Retinal Degeneration
Rhodopsin
Retina
Mutation
Enzymes
Genes

ASJC Scopus subject areas

  • Ophthalmology

Cite this

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title = "Analysis of esterification of retinoids in the retinal pigmented epithelium of the Mitf-vit (vitiligo) mutant mouse.",
abstract = "PURPOSE: Mice homozygous for the vitiligo mutation of the microphthalmia (Mitf) gene have a retinal degeneration characterized by slow loss of photoreceptor cells and compromised retinal pigment epithelial (RPE) structure and function. The levels of retinyl esters, which are essential for generation of 11-cis-retinaldehyde for the formation of rhodopsin, were reported previously to be elevated by 6 weeks postnatally in the RPE of vitiligo mutant mice. The purpose of the present study was to determine whether this elevation was due to increased activity of lecithin:retinol acyl transferase (LRAT) the enzyme that converts all-trans-retinol to retinyl esters. METHODS: Retinoids extracted from the RPE and neural retina of mutant and normal mice ages 2, 4, 6 and 8 weeks were analyzed by reversed-phase HPLC. The esterification capacity of the RPE to convert 3H-retinol to 3H-retinyl ester was determined by HPLC in mutant and normal mice at 3 and 9 weeks. RESULTS: Retinyl ester levels were elevated significantly in the mutant RPE as early as postnatal week 2 and were four-fold greater by 8 weeks. The esterification assay indicated no significant differences between mutants and controls at 3 weeks. At 9 weeks, the esterification activity of the mutant RPE was significantly reduced compared to controls rather than elevated. CONCLUSIONS: The data suggest that the accumulation of retinyl esters is not due to increased LRAT activity. Alternative explanations for the retinyl ester accumulation are discussed.",
author = "Evans, {B. L.} and Smith, {Sylvia B}",
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journal = "Molecular Vision",
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AU - Smith, Sylvia B

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Y1 - 1997/1/1

N2 - PURPOSE: Mice homozygous for the vitiligo mutation of the microphthalmia (Mitf) gene have a retinal degeneration characterized by slow loss of photoreceptor cells and compromised retinal pigment epithelial (RPE) structure and function. The levels of retinyl esters, which are essential for generation of 11-cis-retinaldehyde for the formation of rhodopsin, were reported previously to be elevated by 6 weeks postnatally in the RPE of vitiligo mutant mice. The purpose of the present study was to determine whether this elevation was due to increased activity of lecithin:retinol acyl transferase (LRAT) the enzyme that converts all-trans-retinol to retinyl esters. METHODS: Retinoids extracted from the RPE and neural retina of mutant and normal mice ages 2, 4, 6 and 8 weeks were analyzed by reversed-phase HPLC. The esterification capacity of the RPE to convert 3H-retinol to 3H-retinyl ester was determined by HPLC in mutant and normal mice at 3 and 9 weeks. RESULTS: Retinyl ester levels were elevated significantly in the mutant RPE as early as postnatal week 2 and were four-fold greater by 8 weeks. The esterification assay indicated no significant differences between mutants and controls at 3 weeks. At 9 weeks, the esterification activity of the mutant RPE was significantly reduced compared to controls rather than elevated. CONCLUSIONS: The data suggest that the accumulation of retinyl esters is not due to increased LRAT activity. Alternative explanations for the retinyl ester accumulation are discussed.

AB - PURPOSE: Mice homozygous for the vitiligo mutation of the microphthalmia (Mitf) gene have a retinal degeneration characterized by slow loss of photoreceptor cells and compromised retinal pigment epithelial (RPE) structure and function. The levels of retinyl esters, which are essential for generation of 11-cis-retinaldehyde for the formation of rhodopsin, were reported previously to be elevated by 6 weeks postnatally in the RPE of vitiligo mutant mice. The purpose of the present study was to determine whether this elevation was due to increased activity of lecithin:retinol acyl transferase (LRAT) the enzyme that converts all-trans-retinol to retinyl esters. METHODS: Retinoids extracted from the RPE and neural retina of mutant and normal mice ages 2, 4, 6 and 8 weeks were analyzed by reversed-phase HPLC. The esterification capacity of the RPE to convert 3H-retinol to 3H-retinyl ester was determined by HPLC in mutant and normal mice at 3 and 9 weeks. RESULTS: Retinyl ester levels were elevated significantly in the mutant RPE as early as postnatal week 2 and were four-fold greater by 8 weeks. The esterification assay indicated no significant differences between mutants and controls at 3 weeks. At 9 weeks, the esterification activity of the mutant RPE was significantly reduced compared to controls rather than elevated. CONCLUSIONS: The data suggest that the accumulation of retinyl esters is not due to increased LRAT activity. Alternative explanations for the retinyl ester accumulation are discussed.

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