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视网膜和视网膜色素上皮的生化适应支持脊椎动物眼睛中的代谢生态系统。

Biochemical adaptations of the retina and retinal pigment epithelium support a metabolic ecosystem in the vertebrate eye.

机构信息

Department of Biochemistry, University of Washington, Seattle, United States.

Department of Ophthalmology, University of Washington, Seattle, United States.

出版信息

Elife. 2017 Sep 13;6:e28899. doi: 10.7554/eLife.28899.

DOI:10.7554/eLife.28899
PMID:28901286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5617631/
Abstract

Here we report multiple lines of evidence for a comprehensive model of energy metabolism in the vertebrate eye. Metabolic flux, locations of key enzymes, and our finding that glucose enters mouse and zebrafish retinas mostly through photoreceptors support a conceptually new model for retinal metabolism. In this model, glucose from the choroidal blood passes through the retinal pigment epithelium to the retina where photoreceptors convert it to lactate. Photoreceptors then export the lactate as fuel for the retinal pigment epithelium and for neighboring Müller glial cells. We used human retinal epithelial cells to show that lactate can suppress consumption of glucose by the retinal pigment epithelium. Suppression of glucose consumption in the retinal pigment epithelium can increase the amount of glucose that reaches the retina. This framework for understanding metabolic relationships in the vertebrate retina provides new insights into the underlying causes of retinal disease and age-related vision loss.

摘要

在这里，我们报告了多种证据，证明了脊椎动物眼睛中能量代谢的综合模型。代谢通量、关键酶的位置，以及我们发现葡萄糖主要通过光感受器进入小鼠和斑马鱼的视网膜，支持了一种新的视网膜代谢概念模型。在这个模型中，脉络膜血液中的葡萄糖通过视网膜色素上皮进入视网膜，在那里光感受器将其转化为乳酸。然后，光感受器将乳酸输出作为视网膜色素上皮和相邻的 Muller 胶质细胞的燃料。我们使用人视网膜上皮细胞表明，乳酸可以抑制视网膜色素上皮对葡萄糖的消耗。抑制视网膜色素上皮对葡萄糖的消耗可以增加到达视网膜的葡萄糖量。这个理解脊椎动物视网膜代谢关系的框架为视网膜疾病和与年龄相关的视力丧失的根本原因提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/c5e5da1c39af/elife-28899-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/5ae219e730d1/elife-28899-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/10b656939ab3/elife-28899-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/4df81f869215/elife-28899-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/8ff235fb3dc1/elife-28899-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/06b93a1502d8/elife-28899-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/e3a1aa1ebf4e/elife-28899-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/0144e2ce3f07/elife-28899-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/7e21a39b1d4c/elife-28899-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/3248f4452060/elife-28899-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/c5e5da1c39af/elife-28899-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/5ae219e730d1/elife-28899-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/10b656939ab3/elife-28899-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/4df81f869215/elife-28899-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/8ff235fb3dc1/elife-28899-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/06b93a1502d8/elife-28899-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/e3a1aa1ebf4e/elife-28899-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/0144e2ce3f07/elife-28899-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/7e21a39b1d4c/elife-28899-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/3248f4452060/elife-28899-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75bc/5617631/c5e5da1c39af/elife-28899-fig10.jpg

相似文献

[1]
Biochemical adaptations of the retina and retinal pigment epithelium support a metabolic ecosystem in the vertebrate eye.

Elife. 2017-9-13

[2]
Modulating GLUT1 expression in retinal pigment epithelium decreases glucose levels in the retina: impact on photoreceptors and Müller glial cells.

Am J Physiol Cell Physiol. 2018-11-21

[3]
Microglia Activation and Inflammation During the Death of Mammalian Photoreceptors.

Annu Rev Vis Sci. 2020-9-15

[4]
Hypoxia-induced metabolic stress in retinal pigment epithelial cells is sufficient to induce photoreceptor degeneration.

Elife. 2016-3-15

[5]
Metabolic mapping in mammalian retina: a biochemical and 3H-2-deoxyglucose autoradiographic study.

Exp Eye Res. 2003-9

[6]
Lactate released by Müller glial cells is metabolized by photoreceptors from mammalian retina.

J Neurosci. 1995-7

[7]
Anisotropic Müller glial scaffolding supports a multiplex lattice mosaic of photoreceptors in zebrafish retina.

Neural Dev. 2017-11-15

[8]
Chemokine-mediated inflammation in the degenerating retina is coordinated by Müller cells, activated microglia, and retinal pigment epithelium.

J Neuroinflammation. 2015-1-17

[9]
Cultured retinal neuronal cells and Müller cells both show net production of lactate.

Neurochem Int. 2004

[10]
Trafficking of molecules and metabolic signals in the retina.

Prog Retin Eye Res. 1998-7

引用本文的文献

[1]
Metabolic dysfunction promoted by mitochondrial DNA mutation burden drives retinal degeneration.

bioRxiv. 2025-7-31

[2]
Regulation of RPE65 expression in human retinal pigment epithelium cells.

Sci Rep. 2025-7-25

[3]
Metabolic regulation of visual acuity.

Sci Adv. 2025-6-27

[4]
Feedback regulation between histone lactylation and ALKBH3-mediated glycolysis regulates age-related macular degeneration pathology.

Proc Natl Acad Sci U S A. 2025-6-17

[5]
Glutamine catabolism supports amino acid biosynthesis and suppresses the integrated stress response to promote photoreceptor survival.

Elife. 2025-5-21

[6]
Retinal Pigment Epithelium Specific Metabolic Phenotypes Are Regulated by High-Mobility Group Protein N1.

Invest Ophthalmol Vis Sci. 2025-4-1

[7]
Distinct metabolome and flux responses in the retinal pigment epithelium to cytokines associated with age-related macular degeneration: comparison of ARPE-19 cells and eyecups.

Sci Rep. 2025-4-15

[8]
RPE-specific MCT2 expression promotes cone survival in models of retinitis pigmentosa.

Proc Natl Acad Sci U S A. 2025-4-8

[9]
Pten Loss Triggers Progressive Photoreceptor Degeneration in an mTORC1-Independent Manner.

Invest Ophthalmol Vis Sci. 2025-3-3

[10]
Features that distinguish age-related macular degeneration from aging.

Exp Eye Res. 2025-5

本文引用的文献

[1]
Human retinal pigment epithelial cells prefer proline as a nutrient and transport metabolic intermediates to the retinal side.

J Biol Chem. 2017-8-4

[2]
Glycolytic reliance promotes anabolism in photoreceptors.

Elife. 2017-6-9

[3]
NNT reverse mode of operation mediates glucose control of mitochondrial NADPH and glutathione redox state in mouse pancreatic β-cells.

Mol Metab. 2017-4-21

[4]
Genetic rescue models refute nonautonomous rod cell death in retinitis pigmentosa.

Proc Natl Acad Sci U S A. 2017-5-3

[5]
Phagocytosis-dependent ketogenesis in retinal pigment epithelium.

J Biol Chem. 2017-5-12

[6]
Correction of Monogenic and Common Retinal Disorders with Gene Therapy.

Genes (Basel). 2017-1-27

[7]
Mitochondria Maintain Distinct Ca Pools in Cone Photoreceptors.

J Neurosci. 2017-2-22

[8]
Reductive carboxylation is a major metabolic pathway in the retinal pigment epithelium.

Proc Natl Acad Sci U S A. 2016-12-20

[9]
The Warburg Effect Mediator Pyruvate Kinase M2 Expression and Regulation in the Retina.

Sci Rep. 2016-11-24

[10]
Reprogramming metabolism by targeting sirtuin 6 attenuates retinal degeneration.

J Clin Invest. 2016-12-1

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