Evidence map›Paper›PMID 27046120›Full record

ArticleInvestigative ophthalmology & visual science2016

Interphotoreceptor Retinoid-Binding Protein Mitigates Cellular Oxidative Stress and Mitochondrial Dysfunction Induced by All-trans-Retinal.

Minsup Lee, Songhua Li, Kota Sato, Minghao Jin

Open access · goldAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 31 citations in OpenAlex.

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  6. Ablation of Fatty Acid Transport Protein-4 Enhances Cone Survival, M-cone Vision, and Synthesis of Cone-Tropic 9-The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  7. Resilience to diabetic retinopathy.Progress in retinal and eye research · 2024
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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

4 authors at 2 institutions in 2 countries.

Minsup Lee
Songhua Li
Kota Sato
Minghao Jin
Louisiana State University Health Sciences Center New Orleans · USTohoku University · JP

Funding

Multiphoton ConfocalP30GM103340 · NIGMS · LSU HEALTH SCIENCES CENTER · PI SHELINE, CHRISTIAN THOMAS · 2012 to 2016
$5.1M
Regulation of normal and Leber congenital amaurosis-associated RPE65sR01EY021208 · NEI · LSU HEALTH SCIENCES CENTER · PI JIN, MINGHAO · 2011 to 2015
$1.7M
NEI NIH HHS EY021208NEI NIH HHS R01 EY021208NIGMS NIH HHS GM103340NIGMS NIH HHS P30 GM103340
6 · The paper itself

Abstract

purposePoint and null mutations in interphotoreceptor retinoid-binding protein (IRBP) cause retinal dystrophy in affected patients and IRBP-deficient mice with unknown mechanism. This study investigated whether IRBP protects cells from damages induced by all-trans-retinal (atRAL), which was increased in the Irbp(-/-) retina.

methodsWild-type and Irbp(-/-) mice retinal explants in buffer with or without purified IBRP were exposed to 800 lux light for different times and subjected to retinoid analysis by high-performance liquid chromatography. Purity of IRBP was determined by Coomassie Brilliant Blue staining and immunoblot analysis. Cellular damages induced by atRAL in the presence or absence of IRBP were evaluated in the mouse photoreceptor-derived 661W cells. Cell viability and death were measured by 3-(4,5-dimethyl-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) and TUNEL assays. Expression and modification levels of retinal proteins were determined by immunoblot analysis. Intracellular reactive oxygen species (ROS) and nitric oxide (NO) were detected with fluorogenic dyes and confocal microscopy. Mitochondrial membrane potential was analyzed by using JC-1 fluorescent probe and a flow cytometer.

resultsContent of atRAL in Irbp(-/-) retinal explants exposed to light for 40 minutes was significantly higher than that in wild-type retinas under the same light conditions. All-trans-retinal caused increase in cell death, tumor necrosis factor activation, and Adam17 upregulation in 661W cells. NADPH oxidase-1 (NOX1) upregulation, ROS generation, NO-mediated protein S-nitrosylation, and mitochondrial dysfunction were also observed in 661W cells treated with atRAL. These cytotoxic effects were significantly attenuated in the presence of IRBP.

conclusionsInterphotoreceptor retinoid-binding protein is required for preventing accumulation of retinal atRAL, which causes inflammation, oxidative stress, and mitochondrial dysfunction of the cells.

Indexed as

ADAM17 ProteinADAM ProteinsAnimalsCell SurvivalChromatography, High Pressure LiquidDark AdaptationEye ProteinsImmunoblottingIn Situ Nick-End LabelingLightMembrane Potential, MitochondrialMiceMicroscopy, ConfocalMitochondrial DiseasesNitric OxideOxidative StressADAM17 ProteinAdam17 protein, mouseADAM ProteinsEye ProteinsNitric OxideReactive Oxygen SpeciesRetinol-Binding ProteinsRetinol-Binding Proteins, InterstitialTumor Necrosis Factor-alphaVitamin A

Identifiers

PMID27046120
PMCPMC4824376
OpenAlexW2334607513

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.