Evidence map›Paper›PMID 26283861›Full record

ArticleMolecular vision2015

Disruption of eyelid and cornea morphogenesis by epithelial β-catenin gain-of-function.

Shin Mizoguchi, Kentaro Suzuki, Jianhua Zhang, Osamu Yamanaka, Chia-Yang Liu, Yuka Okada, Masayasu Miyajima, Masahide Kokado, Winston W Y Kao, Gen Yamada and 1 more

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

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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 2 countries.

Shin MizoguchiDepartment of Ophthalmology, Wakayama Medical University School of Medicine, Wakayama, Japan.
Kentaro SuzukiDepartment of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.
Jianhua ZhangDepartment of Ophthalmology, University of Cincinnati School of Medicine, Cincinnati, Ohio.
Osamu YamanakaDepartment of Ophthalmology, Wakayama Medical University School of Medicine, Wakayama, Japan.
Chia-Yang LiuDepartment of Ophthalmology, University of Cincinnati School of Medicine, Cincinnati, Ohio.
Yuka OkadaDepartment of Ophthalmology, Wakayama Medical University School of Medicine, Wakayama, Japan.
Masayasu MiyajimaLaboratory Animal Center, Wakayama Medical University, Wakayama, Japan.
Masahide KokadoDepartment of Ophthalmology, Wakayama Medical University School of Medicine, Wakayama, Japan.
Winston W Y KaoDepartment of Ophthalmology, University of Cincinnati School of Medicine, Cincinnati, Ohio.
Gen YamadaDepartment of Developmental Genetics, Institute of Advanced Medicine, Wakayama Medical University, Wakayama, Japan.
Shizuya SaikaDepartment of Ophthalmology, Wakayama Medical University School of Medicine, Wakayama, Japan.
Wakayama Medical University · JPUniversity of Cincinnati · US

Funding

New Insights into the Ocular Surface in Health and DiseaseR01EY023680 · NEI · TRUSTEES OF INDIANA UNIVERSITY · PI LIU, CHIA-YANG · 2015 to 2017
$1.3M
NEI NIH HHS R01 EY023680
6 · The paper itself

Abstract

purposeTo examine the developmental pathobiology of the eyelid and the cornea caused by epithelial β-catenin gain-of-function (gof) during mouse embryogenesis.

methodsCompound mutant mice (Ctnnb1(GOFOSE) , gof of β-catenin in the epidermis and the ocular surface epithelium) were generated by time-mating keratin 5-promoter-Cre recombinase (Krt5-Cre) and Ctnnb1(fE3/WT) (floxed exon 3 of Ctnnb1) mice. Eyes obtained from wild-type (WT) and mutant embryos at various gestation stages until E18.5 were examined with histology and immunohistochemistry. The ultrastructure of the ocular tissues of the E18.5 embryos was also examined.

resultsExpression of the gof-β-catenin mutant protein in the epidermis severely impaired eyelid morphogenesis at E15.5, E17.5, and E18.5. The mutant stroma exhibited impaired keratocyte differentiation with accelerated cell proliferation and reduction in the accumulation of collagen type I. The mutant embryos also showed hyperproliferative nodules in the ocular surface epithelia with anomaly of cornea-type epithelial differentiation and the absence of the epithelial basement membrane.

conclusionsExpression of the gof-β-catenin mutant protein in basal epithelial cells disrupts eyelid and cornea morphogenesis during mouse embryonic development due to the perturbation of cell proliferation and differentiation of the epithelium and the neural crest-derived mesenchyme.

Indexed as

MutationAnimalsbeta CateninCell DifferentiationCell ProliferationCorneaEpithelial-Mesenchymal TransitionEpitheliumEyelidsFemaleGestational AgeKeratin-5MiceMice, Mutant StrainsMice, TransgenicMorphogenesisbeta CateninCTNNB1 protein, mouseKeratin-5

Identifiers

PMID26283861
PMCPMC4522241
OpenAlexW1801310573

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.