Evidence map›Paper›PMID 25159211›Full record

ArticleInvestigative ophthalmology & visual science2014

Deletion of aryl hydrocarbon receptor AHR in mice leads to subretinal accumulation of microglia and RPE atrophy.

Soo-Young Kim, Hyun-Jin Yang, Yi-Sheng Chang, Jung-Woong Kim, Matthew Brooks, Emily Y Chew, Wai T Wong, Robert N Fariss, Rivka A Rachel, Tiziana Cogliati and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.4field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 70 citations in OpenAlex.

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  13. Prph2 disease mutations lead to structural and functional defects in the RPE.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
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  16. A mouse model of cone photoreceptor function lossFrontiers in molecular neuroscience · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 2 countries.

Soo-Young KimNeurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Hyun-Jin YangNeurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Yi-Sheng ChangNeurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States Department of Ophthalmology, National Cheng Kung University and Hospital, Tainan, Taiwan.
Jung-Woong KimNeurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Matthew BrooksNeurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Emily Y ChewDivision of Epidemiology and Clinical Application, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Wai T WongSection on Neuron-Glia Interactions in Retinal Disease, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Robert N FarissImaging Core, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Rivka A RachelNeurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Tiziana CogliatiNeurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Haohua QianVisual Function Core, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
Anand SwaroopNeurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, United States.
National Institutes of Health · USNational Eye Institute · US

Funding

Mechanisms, modeling and therapies of retinal and macular neurodegenerationZIAEY000546 · NEI · NATIONAL EYE INSTITUTE · PI SWAROOP, ANAND · 2015 to 2025
$36.3M
Imaging Core UnitZICEY000459 · NEI · NATIONAL EYE INSTITUTE · PI FARISS, ROBERT · 2009 to 2025
$13.1M
Visual Function CoreZICEY000503 · NEI · NATIONAL EYE INSTITUTE · PI QIAN, HAOHUA · 2011 to 2025
$12.3M
Genetic susceptibility and common multi-factorial retinal/macular diseasesZIAEY000475 · NEI · NATIONAL EYE INSTITUTE · PI SWAROOP, ANAND · 2009 to 2014
$6.9M
Role of Microglia in the Retina in Retinal DiseasesZIAEY000541 · NEI · NATIONAL EYE INSTITUTE · PI WONG, WAI · 2014 to 2020
$5.2M
The Age-Related Eye Disease Study 2 (AREDS2)ZIAEY000485 · NEI · NATIONAL EYE INSTITUTE · PI CHEW, EMILY Y · 2009 to 2015
$990k
Intramural NIH HHS
6 · The paper itself

Abstract

purposeThe aryl hydrocarbon receptor (AHR) is a ligand-activated nuclear receptor that regulates cellular response to environmental signals, including UV and blue wavelength light. This study was undertaken to elucidate AHR function in retinal homeostasis.

methodsRNA-seq data sets were examined for Ahr expression in the mouse retina and rod photoreceptors. The Ahr(-/-) mice were evaluated by fundus imaging, optical coherence tomography, histology, immunohistochemistry, and ERG. For light damage experiments, adult mice were exposed to 14,000 to 15,000 lux of diffuse white light for 2 hours.

resultsIn mouse retina, Ahr transcripts were upregulated during development, with continued increase in aging rod photoreceptors. Fundus examination of 3-month-old Ahr(-/-) mice revealed subretinal autofluorescent spots, which increased in number with age and following acute light exposure. Ahr(-/-) retina also showed subretinal microglia accumulation that correlated with autofluorescence changes, RPE abnormalities, and reactivity against immunoglobulin, complement factor H, and glial fibrillary acidic protein. Functionally, Ahr(-/-) mice displayed reduced ERG c-wave amplitudes.

conclusionsThe Ahr(-/-) mice exhibited subretinal accumulation of microglia and focal RPE atrophy, phenotypes observed in AMD. Together with a recently published report on another Ahr(-/-) mouse model, our study suggests that AHR has a protective role in the retina as an environmental stress sensor. As such, its altered function may contribute to human AMD progression and provide a target for pharmacological intervention.

Indexed as

AnimalsAtrophyBasic Helix-Loop-Helix ProteinsDisease Models, AnimalFundus OculiGene DeletionMiceMice, Inbred C57BLMice, KnockoutMicrogliaReceptors, Aryl HydrocarbonRetinal DegenerationRetinal Pigment EpitheliumRetinal Rod Photoreceptor CellsRetinitisTomography, Optical CoherenceAhr protein, mouseBasic Helix-Loop-Helix ProteinsReceptors, Aryl Hydrocarbonmicrogliaorphan nuclear receptorretinal degenerationRPE atrophysubretinal deposits

Identifiers

PMID25159211
PMCPMC4176417
OpenAlexW2069765448

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.