Energy Metabolism in the Vertebrate Retina

Hurley, James B.; Chertov, Andrei O.; Lindsay, Ken J.; Giamarco, Michelle; Cleghorn, Whitney M.; Du, Jianhai; Brockerhoff, Susan E.

doi:10.1007/978-4-431-54880-5_5

Cited by 6 publications

(4 citation statements)

References 240 publications

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“…Müller glia are involved in glucose metabolism and secrete ATP, 30 and photoreceptors are highly metabolic cells requiring constant supply of cellular energy. 31 Müller glia secrete numerous factors that may be required for photoreceptor neuroprotection, including CNTF, bFGF, PEDF, IGF-1, GDNF, VEGF, LIF, NGF, and BDNF. 32 The structural contribution of Müller glia to retinal architecture may be required for photoreceptor survival, as their processes form the external limiting membrane, a key boundary between photoreceptor nuclei and their inner and outer segments.…”

Section: Discussionmentioning

confidence: 99%

Arap1 Deficiency Causes Photoreceptor Degeneration in Mice

Moshiri

Humpal

Leonard

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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PurposeSmall guanosine triphosphatase (GTPase) ADP-ribosylation factors (Arfs) regulate membrane traffic and actin reorganization under the control of GTPase-activating proteins (GAPs). Arap1 is an Arf-directed GAP that inhibits the trafficking of epidermal growth factor receptor (EGFR) to the early endosome, but the diversity of its functions is incompletely understood. The aim of this study was to determine the role of Arap1 in the mammalian retina.MethodsGenetically engineered Arap1 knockout mice were screened for ocular abnormalities in the National Institutes of Health Knockout Mouse Production and Phenotyping (KOMP2) Project. Arap1 knockout and wild-type eyes were imaged using optical coherence tomography and fundus photography, and analyzed by immunohistochemistry.ResultsArap1−/− mice develop a normal appearing retina, but undergo photoreceptor degeneration starting at 4 weeks postnatal age. The fundus appearance of mutants is notable for pigmentary changes, optic nerve pallor, vascular attenuation, and outer retinal thinning, reminiscent of retinitis pigmentosa in humans. Immunohistochemical studies suggest the cell death is predominantly in the outer nuclear layer. Functional evaluation of the retina by electroretinography reveals amplitudes are reduced. Arap1 is detected most notably in Müller glia, and not in photoreceptors, implicating a role for Müller glia in photoreceptor survival.ConclusionsArap1 is necessary for normal photoreceptor survival in mice, and may be a novel gene relevant to human retinal degenerative processes, although its mechanism is unknown. Further studies in this mouse model of retinal degeneration will give insights into the cellular functions and signaling pathways in which Arap1 participates.

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Section: Discussionmentioning

confidence: 99%

Arap1 Deficiency Causes Photoreceptor Degeneration in Mice

Moshiri

Humpal

Leonard

et al. 2017

Invest. Ophthalmol. Vis. Sci.

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“…This substantially diminishes the ATP consumption required to maintain ion gradients across the plasma membrane. The metabolism of the cell shifts away from energy production to more anabolic activities (Hurley et al, ). The cell hyperpolarizes, which slows the rate at which it releases glutamate into the synapse.…”

Section: Functions Of the Vertebrate Retina And Their Relationships Tmentioning

confidence: 99%

Glucose, lactate, and shuttling of metabolites in vertebrate retinas

Hurley

Lindsay

2015

J of Neuroscience Research

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211

188

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The vertebrate retina has specific functions and structures that give it a unique set of constraints on the way in which it can produce and use metabolic energy. The retina’s response to illumination influences its energy requirements, and the retina’s laminated structure influences the extent to which neurons and glia can access metabolic fuels. There are fundamental differences between energy metabolism in retina and that in brain. The retina relies on aerobic glycolysis much more than the brain does, and morphological differences between retina and brain limit the types of metabolic relationships that are possible between neurons and glia. This Mini-Review summarizes the unique metabolic features of the retina with a focus on the role of lactate shuttling.

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“…1 ). 13 14 In light, however, consumption of O 2 by rods was shown to decrease by approximately 30% in macaques and approximately 50–70% in cats, 10 11 12 indicating a marked reduction in oxidative phosphory-lation in light compared with that in darkness ( Fig. 1 ).…”

Section: Introductionmentioning

confidence: 93%

“…1 ). In light, there is increased anabolic activity 14 ; mRNA levels are increased four to 10 times, 15 16 and outer segments appear to follow a circadian pattern, in which discs are shed more at the onset of light in a 12–hour light–dark cycle irrespective of whether the lights are turned on or not, which is accompanied by an increase in outer segment renewal, 17 18 presumably fueled by increased lipid and protein production.…”

Section: Introductionmentioning

confidence: 99%

Rod metabolic demand drives progression in retinopathies

Lin

Kim

Zhang

et al. 2015

Taiwan Journal of Ophthalmology

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Various factors are thought to cause the development and progression of disease in macular degeneration, diabetic retinopathy, and retinitis pigmentosa. Some of the deleterious processes include oxidative stress, hypoxia, metabolic derangement, genetics, and vasculopathy. In this review, we present a unified theory for the pathophysiology of several retinopathies based on the unique and intense metabolism of rod photoreceptors.

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Energy Metabolism in the Vertebrate Retina

Cited by 6 publications

References 240 publications

Arap1 Deficiency Causes Photoreceptor Degeneration in Mice

Arap1 Deficiency Causes Photoreceptor Degeneration in Mice

Glucose, lactate, and shuttling of metabolites in vertebrate retinas

Rod metabolic demand drives progression in retinopathies

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