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Metabolism in the Zebrafish Retina
Retinal photoreceptors are amongst the most metabolically active cells in the body, consuming more glucose as a metabolic substrate than even the brain. This ensures that there is sufficient energy to establish and maintain photoreceptor functions during and after their differentiation. Such high de...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8006245/ https://www.ncbi.nlm.nih.gov/pubmed/33804189 http://dx.doi.org/10.3390/jdb9010010 |
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author | Jaroszynska, Natalia Harding, Philippa Moosajee, Mariya |
author_facet | Jaroszynska, Natalia Harding, Philippa Moosajee, Mariya |
author_sort | Jaroszynska, Natalia |
collection | PubMed |
description | Retinal photoreceptors are amongst the most metabolically active cells in the body, consuming more glucose as a metabolic substrate than even the brain. This ensures that there is sufficient energy to establish and maintain photoreceptor functions during and after their differentiation. Such high dependence on glucose metabolism is conserved across vertebrates, including zebrafish from early larval through to adult retinal stages. As the zebrafish retina develops rapidly, reaching an adult-like structure by 72 hours post fertilisation, zebrafish larvae can be used to study metabolism not only during retinogenesis, but also in functionally mature retinae. The interplay between rod and cone photoreceptors and the neighbouring retinal pigment epithelium (RPE) cells establishes a metabolic ecosystem that provides essential control of their individual functions, overall maintaining healthy vision. The RPE facilitates efficient supply of glucose from the choroidal vasculature to the photoreceptors, which produce metabolic products that in turn fuel RPE metabolism. Many inherited retinal diseases (IRDs) result in photoreceptor degeneration, either directly arising from photoreceptor-specific mutations or secondary to RPE loss, leading to sight loss. Evidence from a number of vertebrate studies suggests that the imbalance of the metabolic ecosystem in the outer retina contributes to metabolic failure and disease pathogenesis. The use of larval zebrafish mutants with disease-specific mutations that mirror those seen in human patients allows us to uncover mechanisms of such dysregulation and disease pathology with progression from embryonic to adult stages, as well as providing a means of testing novel therapeutic approaches. |
format | Online Article Text |
id | pubmed-8006245 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-80062452021-03-30 Metabolism in the Zebrafish Retina Jaroszynska, Natalia Harding, Philippa Moosajee, Mariya J Dev Biol Review Retinal photoreceptors are amongst the most metabolically active cells in the body, consuming more glucose as a metabolic substrate than even the brain. This ensures that there is sufficient energy to establish and maintain photoreceptor functions during and after their differentiation. Such high dependence on glucose metabolism is conserved across vertebrates, including zebrafish from early larval through to adult retinal stages. As the zebrafish retina develops rapidly, reaching an adult-like structure by 72 hours post fertilisation, zebrafish larvae can be used to study metabolism not only during retinogenesis, but also in functionally mature retinae. The interplay between rod and cone photoreceptors and the neighbouring retinal pigment epithelium (RPE) cells establishes a metabolic ecosystem that provides essential control of their individual functions, overall maintaining healthy vision. The RPE facilitates efficient supply of glucose from the choroidal vasculature to the photoreceptors, which produce metabolic products that in turn fuel RPE metabolism. Many inherited retinal diseases (IRDs) result in photoreceptor degeneration, either directly arising from photoreceptor-specific mutations or secondary to RPE loss, leading to sight loss. Evidence from a number of vertebrate studies suggests that the imbalance of the metabolic ecosystem in the outer retina contributes to metabolic failure and disease pathogenesis. The use of larval zebrafish mutants with disease-specific mutations that mirror those seen in human patients allows us to uncover mechanisms of such dysregulation and disease pathology with progression from embryonic to adult stages, as well as providing a means of testing novel therapeutic approaches. MDPI 2021-03-15 /pmc/articles/PMC8006245/ /pubmed/33804189 http://dx.doi.org/10.3390/jdb9010010 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Jaroszynska, Natalia Harding, Philippa Moosajee, Mariya Metabolism in the Zebrafish Retina |
title | Metabolism in the Zebrafish Retina |
title_full | Metabolism in the Zebrafish Retina |
title_fullStr | Metabolism in the Zebrafish Retina |
title_full_unstemmed | Metabolism in the Zebrafish Retina |
title_short | Metabolism in the Zebrafish Retina |
title_sort | metabolism in the zebrafish retina |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8006245/ https://www.ncbi.nlm.nih.gov/pubmed/33804189 http://dx.doi.org/10.3390/jdb9010010 |
work_keys_str_mv | AT jaroszynskanatalia metabolisminthezebrafishretina AT hardingphilippa metabolisminthezebrafishretina AT moosajeemariya metabolisminthezebrafishretina |