Evidence map›Paper›PMID 34495288›Full record

ArticleInvestigative ophthalmology & visual science2021

Genotype, Age, Genetic Background, and Sex Influence Epha2-Related Cataract Development in Mice.

Alpana Dave, Jamie E Craig, Mohammad Alamein, Karina Skrzypiec, Justin Beltz, Annalise Pfaff, Kathryn P Burdon, Nuran Ercal, Robb U de Iongh, Shiwani Sharma

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Investigative ophthalmology & visual science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Abnormal function ofInternational journal of ophthalmology · 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

10 authors at 3 institutions in 2 countries.

Alpana DaveDepartment of Ophthalmology, Flinders University, Bedford Park, South Australia, Australia.
Jamie E CraigDepartment of Ophthalmology, Flinders University, Bedford Park, South Australia, Australia.
Mohammad AlameinDepartment of Ophthalmology, Flinders University, Bedford Park, South Australia, Australia.
Karina SkrzypiecDepartment of Ophthalmology, Flinders University, Bedford Park, South Australia, Australia.
Justin BeltzDepartment of Chemistry, Missouri University of Science and Technology, Rolla, Missouri, United States.
Annalise PfaffDepartment of Chemistry, Missouri University of Science and Technology, Rolla, Missouri, United States.
Kathryn P BurdonDepartment of Ophthalmology, Flinders University, Bedford Park, South Australia, Australia.
Nuran ErcalDepartment of Chemistry, Missouri University of Science and Technology, Rolla, Missouri, United States.
Robb U de IonghOcular Development Laboratory, Anatomy & Neuroscience, University of Melbourne, Parkville, Australia.
Shiwani SharmaDepartment of Ophthalmology, Flinders University, Bedford Park, South Australia, Australia.
Flinders University · AUMissouri University of Science and Technology · USUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Age-related cataract is the leading cause of blindness worldwide. Variants in the EPHA2 gene increase the disease risk, and its knockout in mice causes cataract. We investigated whether age, sex, and genetic background, risk factors for age-related cataract, and Epha2 genotype influence Epha2-related cataract development in mice. Methods: Cataract development was monitored in Epha2+/+, Epha2+/-, and Epha2-/- mice (Epha2Gt(KST085)Byg) on C57BL/6J and FVB:C57BL/6J (50:50) backgrounds. Cellular architecture of lenses, endoplasmic reticulum (ER) stress, and redox state were determined using histological, molecular, and analytical techniques. Results: Epha2-/- and Epha2+/- mice on C57BL/6J background developed severe cortical cataracts by 18 and 38 weeks of age, respectively, compared to development of similar cataract significantly later in Epha2-/- mice and no cataract in Epha2+/- mice in this strain on FVB background, which was previously reported. On FVB:C57BL/6J background, Epha2-/- mice developed severe cortical cataract by 38 weeks and Epha2+/- mice exhibited mild cortical cataract up to 64 weeks of age. Progression of cataract in Epha2-/- and Epha2+/- female mice on C57BL/6J and mixed background, respectively, was slower than in matched male mice. N-cadherin and β-catenin immunolabeling showed disorganized lens fiber cells and disruption of lens architecture in Epha2-/- and Epha2+/- lenses, coinciding with development of severe cataracts. EPHA2 immunolabeling showed intracellular accumulation of the mutant EPHA2-β-galactosidase fusion protein that induced a cytoprotective ER stress response and in Epha2+/- lenses was also accompanied by glutathione redox imbalance. Conclusions: Both, Epha2-/- and Epha2+/- mice develop age-related cortical cataract; age as a function of Epha2 genotype, sex, and genetic background influence Epha2-related cataractogenesis in mice.

Indexed as

Gene Expression RegulationAnimalsCataractDisease Models, AnimalGenotypeLens, CrystallineMiceMice, Inbred C57BLMice, KnockoutReceptor, EphA2RNAReceptor, EphA2RNA

Identifiers

PMID34495288
PMCPMC8431977
OpenAlexW3196509842

What OpenQuestion holds

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LicenceCC BY
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.