Evidence map›Paper›PMID 26215528›Full record

ArticleExperimental eye research2015

Loss of DJ-1 elicits retinal abnormalities, visual dysfunction, and increased oxidative stress in mice.

Vera L Bonilha, Brent A Bell, Mary E Rayborn, Xiaoping Yang, Charlie Kaul, Gregory H Grossman, Ivy S Samuels, Joe G Hollyfield, Chengsong Xie, Huaibin Cai and 1 more

Abstract read
In one paragraph

Article in Experimental eye research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

39 citing papers in PubMed, 54 citations in OpenAlex.

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  14. Microsomal triglyceride transfer protein is necessary to maintain lipid homeostasis and retinal function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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  18. Park7 protects retinal ganglion cells and promotes functional preservation after optic nerve crush via regulation of the Nrf2 signaling pathway.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2023
    Article
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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

11 authors at 2 institutions in 1 country.

Vera L BonilhaDepartment of Ophthalmology, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Cleveland, OH, USA; Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA. Electronic address: bonilhav@ccf.org.
Brent A BellDepartment of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA.
Mary E RaybornDepartment of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA.
Xiaoping YangDepartment of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA.
Charlie KaulDepartment of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA.
Gregory H GrossmanDepartment of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA.
Ivy S SamuelsDepartment of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA; Research Service, Louis Stokes Cleveland Veterans Affairs Medical Center, Cleveland, OH, USA.
Joe G HollyfieldDepartment of Ophthalmology, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University, Cleveland, OH, USA; Department of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA.
Chengsong XieLaboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA.
Huaibin CaiLaboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA.
Karen G ShadrachDepartment of Ophthalmic Research, Cole Eye Institute, Cleveland Clinic, Cleveland, OH, USA.
Cleveland Clinic · USNational Institute on Aging · US

Funding

Molecular and Pathophysiological Study of Parkinson's DiseaseZIAAG000928 · NIA · NATIONAL INSTITUTE ON AGING · PI CAI, HUAIBIN · 2011 to 2025
$15.8M
The Pathogenic Mechanism of ALS-related VAPB MutationZIAAG000943 · NIA · NATIONAL INSTITUTE ON AGING · PI CAI, HUAIBIN · 2009 to 2025
$6.8M
Striatal Projection Neuron Changes in Dopamine Depletion and Parkinsons DiseaseZIAAG000945 · NIA · NATIONAL INSTITUTE ON AGING · PI CAI, HUAIBIN · 2009 to 2025
$5.4M
Age-related Changes in Epithelial MicrovilliR21EY017153 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI BONILHA, VERA L · 2007 to 2010
$532k
Generation and Characterization of Novel Mouse Models of Parkinson's DiseaseZ01AG000945 · NIA · NATIONAL INSTITUTE ON AGING · PI CAI, HUAIBIN · 2008 to 2008
$299k
Intramural NIH HHS Z01 AG000945NEI NIH HHS EY017153NEI NIH HHS R21 EY017153
6 · The paper itself

Abstract

DJ-1/PARK7 mutations or deletions cause autosomal recessive early onset Parkinson's disease (PD). Thus, DJ-1 protein has been extensively studied in brain and neurons. PD patients display visual symptoms; however, the visual symptoms specifically attributed to PD patients carrying DJ-1/PARK7 mutations are not known. In this study, we analyzed the structure and physiology of retinas of 3- and 6-month-old DJ-1 knockout (KO) mice to determine how loss of function of DJ-1 specifically contributes to the phenotypes observed in PD patients. As compared to controls, the DJ-1 KO mice displayed an increase in the amplitude of the scotopic ERG b-wave and cone ERG, while the amplitude of a subset of the dc-ERG components was decreased. The main structural changes in the DJ-1 KO retinas were found in the outer plexiform layer (OPL), photoreceptors and retinal pigment epithelium (RPE), which were observed at 3 months and progressively increased at 6 months. RPE thinning and structural changes within the OPL were observed in the retinas in DJ-1 KO mice. DJ-1 KO retinas also exhibited disorganized outer segments, central decrease in red/green cone opsin staining, decreased labeling of ezrin, broader distribution of ribeye labeling, decreased tyrosine hydroxylase in dopaminergic neurons, and increased 7,8-dihydro-8-oxoguanine-labeled DNA oxidation. Accelerated outer retinal atrophy was observed in DJ-1 KO mice after selective oxidative damage induced by a single tail vein injection of NaIO3, exposing increased susceptibility to oxidative stress. Our data indicate that DJ-1-deficient retinas exhibit signs of morphological abnormalities and physiological dysfunction in association with increased oxidative stress. Degeneration of RPE cells in association with oxidative stress is a key hallmark of age-related macular degeneration (AMD). Therefore, in addition to detailing the visual defects that occur as a result of the absence of DJ-1, our data is also relevant to AMD pathogenesis.

Indexed as

MutationAnimalsBlotting, WesternDisease Models, AnimalDNADNA Mutational AnalysisElectroretinographyFemaleGenotypeImmunohistochemistryMaleMiceMice, Inbred C57BLMice, KnockoutMicroscopy, Electron, TransmissionOncogene ProteinsDNAOncogene ProteinsPARK7 protein, mousePeroxiredoxinsProtein Deglycase DJ-1BiochemistryDJ-1 knockoutHistologyImmunohistologyMorphologyOxidationPhysiologyRetina

Identifiers

PMID26215528
PMCPMC4573318
OpenAlexW2153064445

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Registered trials

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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.