Metabolism in the Zebrafish Retina

被引:14
|
作者
Jaroszynska, Natalia [1 ]
Harding, Philippa [1 ]
Moosajee, Mariya [1 ,2 ,3 ,4 ]
机构
[1] UCL, Inst Ophthalmol, London EC1V 9EL, England
[2] Moorfields Eye Hosp NHS Fdn Trust, London EC1V 2PD, England
[3] Great Ormond St Hosp Children NHS Fdn Trust, London WC1N 3JH, England
[4] Francis Crick Inst, London NW1 1AT, England
基金
英国惠康基金;
关键词
metabolism; glucose; retina; photoreceptors; RPE; zebrafish; eye development; inherited retinal diseases; retinitis pigmentosa (RP); Leber congenital amaurosis (LCA); GLUCOSE-METABOLISM; ENERGY-METABOLISM; OXIDATIVE STRESS; INNER RETINA; OUTER RETINA; CELLS; CYCLE; PHOTORECEPTORS; DEGENERATION; MECHANISMS;
D O I
10.3390/jdb9010010
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
收藏
页数:18
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