Evidence map›Paper›PMID 28648759›Full record

ArticleExperimental eye research2017

EphA2 and ephrin-A5 are not a receptor-ligand pair in the ocular lens.

Catherine Cheng, Velia M Fowler, Xiaohua Gong

Open access · greenAbstract read
In one paragraph

Article in Experimental eye research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 39% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 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

3 authors at 2 institutions in 1 country.

Catherine ChengSchool of Optometry and Vision Science Program, University of California, Berkeley, CA 94720, United States.
Velia M FowlerDepartment of Molecular Medicine, The Scripps Research Institute, La Jolla, CA 92037, United States.
Xiaohua GongSchool of Optometry and Vision Science Program, University of California, Berkeley, CA 94720, United States.
University of California, Berkeley · USScripps Research Institute · US

Funding

Cataracts, Connexin Mutants and Genetic ModifiersR01EY013849 · NEI · UNIVERSITY OF CALIFORNIA BERKELEY · PI Xiaohua Gong · 2002 to 2026
$8.2M
Membrane Skeleton Regulation of Cell Shape and Interactions in Lens DevelopmentR01EY017724 · NEI · UNIVERSITY OF DELAWARE · PI FOWLER, VELIA M · 2008 to 2024
$6.9M
Eph-ephrin signaling in the lensR21EY027389 · NEI · TRUSTEES OF INDIANA UNIVERSITY · PI CHENG, CATHERINE KEHSIN · 2017 to 2018
$493k
NEI NIH HHS R01 EY013849NEI NIH HHS R01 EY017724NEI NIH HHS R21 EY027389
6 · The paper itself

Abstract

Eph-ephrin bidirectional signaling is essential for eye lens transparency in humans and mice. Our previous studies in mouse lenses demonstrate that ephrin-A5 is mainly expressed in the anterior epithelium, where it is required for maintaining the anterior epithelial monolayer. In contrast, EphA2 is localized in equatorial epithelial and fiber cells where it is essential for equatorial epithelial and fiber cell organization and hexagonal cell shape. Immunostaining of lens epithelial and fiber cells reveals that EphA2 and ephrin-A5 are also co-expressed in anterior fiber cell tips, equatorial epithelial cells and newly formed lens fibers, although they are not precisely colocalized. Due to this complex expression pattern and the promiscuous interactions between Eph receptors and ephrin ligands, as well as their complex bidirectional signaling pathways, cataracts in ephrin-A5(-/-) or EphA2(-/-) lenses may arise from loss of function or abnormal signaling mechanisms. To test whether abnormal signaling mechanisms may play a role in cataractogenesis in ephrin-A5(-/-) or EphA2(-/-) lenses, we generated EphA2 and ephrin-A5 double knockout (DKO) mice. We compared the phenotypes of EphA2(-/-) and ephrin-A5(-/-) lenses to that of DKO lenses. DKO lenses displayed an additive lens phenotype that was not significantly different from the two single KO lens phenotypes. Similar to ephrin-A5(-/-) lenses, DKO lenses had abnormal anterior epithelial cells leading to a large mass of epithelial cells that invade into the underlying fiber cell layer, directly resulting in anterior cataracts in ephrin-A5(-/-) and DKO lenses. Yet, similar to EphA2(-/-) lenses, DKO lenses also had abnormal packing of equatorial epithelial cells with disorganized meridional rows, lack of a lens fulcrum and disrupted fiber cells. The DKO lens phenotype rules out abnormal signaling by EphA2 in ephrin-A5(-/-) lenses or by ephrin-A5 in EphA2(-/-) lenses as possible cataract mechanisms. Thus, these results indicate that EphA2 and ephrin-A5 do not form a lens receptor-ligand pair, and that EphA2 and ephrin-A5 have other binding partners in the lens to help align differentiating equatorial epithelial cells or maintain the anterior epithelium, respectively.

Indexed as

AnimalsEphrin-A5Imaging, Three-DimensionalLens, CrystallineMiceMice, Inbred C57BLMicroscopy, ConfocalModels, AnimalProtein BindingReceptor, EphA2Signal TransductionEphrin-A5Receptor, EphA2

Identifiers

PMID28648759
PMCPMC5554726
OpenAlexW2637699177

What OpenQuestion holds

Textmetadata
LicenceTDM
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.