Evidence map›Paper›PMID 25377219›Full record

ArticleInvestigative ophthalmology & visual science2014

Eyelid closure in embryogenesis is required for ocular adnexa development.

Qinghang Meng, Maureen Mongan, Vinicius Carreira, Hisaka Kurita, Chia-Yang Liu, Winston W-Y Kao, Ying Xia

Open access · hybridAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.8field-weighted citation impact, top 9% 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, 46 citations in OpenAlex.

  1. Review
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  10. DNA-based eyelid trait prediction in Chinese Han population.International journal of legal medicine · 2021
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  19. Genetically modified laboratory mice with sebaceous glands abnormalities.Cellular and molecular life sciences : CMLS · 2016
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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

7 authors at 1 institution in 1 country.

Qinghang MengDepartment of Environmental Health, University of Cincinnati, College of Medicine, Cincinnati, Ohio, United States.
Maureen MonganDepartment of Environmental Health, University of Cincinnati, College of Medicine, Cincinnati, Ohio, United States.
Vinicius CarreiraDepartment of Environmental Health, University of Cincinnati, College of Medicine, Cincinnati, Ohio, United States.
Hisaka KuritaDepartment of Environmental Health, University of Cincinnati, College of Medicine, Cincinnati, Ohio, United States.
Chia-Yang LiuOphthalmology, University of Cincinnati, College of Medicine, Cincinnati, Ohio, United States.
Winston W-Y KaoOphthalmology, University of Cincinnati, College of Medicine, Cincinnati, Ohio, United States.
Ying XiaDepartment of Environmental Health, University of Cincinnati, College of Medicine, Cincinnati, Ohio, United States Ophthalmology, University of Cincinnati, College of Medicine, Cincinnati, Ohio, United States.
University of Cincinnati Medical Center · US

Funding

The Role of MAP 3 Kinase 1 in Ocular Surface MorphogenesisR01EY015227 · NEI · UNIVERSITY OF CINCINNATI · PI XIA, YING · 2004 to 2019
$5.4M
NEI NIH HHS EY15227NEI NIH HHS R01 EY015227
6 · The paper itself

Abstract

purposeMammalian eye development requires temporary fusion of the upper and lower eyelids in embryogenesis. Failure of lid closure in mice leads to an eye open at birth (EOB) phenotype. Many genetic mutant strains develop this phenotype and studies of the mutants lead to a better understanding of the signaling mechanisms of morphogenesis. The present study investigates the roles of lid closure in eye development.

methodsSeven mutant mouse strains were generated by different gene ablation strategies that inactivated distinct signaling pathways. These mice, including systemic ablation of Map3k1 and Dkk2, ocular surface epithelium (OSE) knockout of c-Jun and Egfr, conditional knockout of Shp2 in stratified epithelium (SE), as well as the Map3k1/Jnk1 and Map3k1/Rhoa compound mutants, all exhibited defective eyelid closure. The embryonic and postnatal eyes in these mice were characterized by histology and immunohistochemistry.

resultsSome eye abnormalities, such as smaller lens in the Map3k1-null mice and Harderian gland hypoplasia in the Dkk2-null mice, appeared to be mutant strain-specific, whereas other abnormalities were seen in all mutants examined. The common defects included corneal erosion/ulceration, meibomian gland hypoplasia, truncation of the eyelid tarsal muscles, failure of levator palpebrae superioris (LPS) extension into the upper eyelid and misplacement of the inferior oblique (IO) muscle and inferior rectus (IR) muscle. The muscle defects were traced to the prenatal fetuses.

conclusionsIn addition to providing a protective barrier for the ocular surface, eyelid closure in embryogenesis is required for the development of ocular adnexa, including eyelid and extraocular muscles.

Indexed as

Gene Expression Regulation, DevelopmentalPregnancy, AnimalAnimalsCell MovementCell ProliferationDNAEmbryonic DevelopmentEyelidsEye ProteinsFemaleImmunoblottingImmunohistochemistryMeibomian GlandsMiceMice, KnockoutPhenotypeDNAEye Proteinsembryonic eyelid closureextraocular musclesLPSocular adnexatarsal muscles

Identifiers

PMID25377219
PMCPMC4245069
OpenAlexW2074812660

What OpenQuestion holds

Textmetadata
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.