Evidence map›Paper›PMID 27122169›Full record

ArticleDevelopment (Cambridge, England)2016

Primary cilia maintain corneal epithelial homeostasis by regulation of the Notch signaling pathway.

Laura Grisanti, Ekaterina Revenkova, Ronald E Gordon, Carlo Iomini

Open access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
7.5field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 73 citations in OpenAlex.

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  14. Morphological Observation and Transcriptome Analysis of Ciliogenesis inInternational journal of molecular sciences · 2023
    Article
  15. Article
  16. Article
  17. The role of primary cilia in thyroid diseases.Frontiers in endocrinology · 2023
    Review
  18. Article
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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 1 country.

Laura GrisantiDepartment of Ophthalmology and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Ekaterina RevenkovaDepartment of Ophthalmology and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Ronald E GordonDepartment of Pathology, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA.
Carlo IominiDepartment of Ophthalmology and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA Department of Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029, USA carlo.iomini@mssm.edu.ORCID 0000-0001-6483-9540
Allen Institute for Brain Science · USIcahn School of Medicine at Mount Sinai · US

Funding

UAB Recessive PKD Research and Translational Core CenterP30DK074038 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI YODER, BRADLEY K. · 2005 to 2019
$16.6M
Role of primary cilia in corneal development and repairR01EY022639 · NEI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI IOMINI, CARLO · 2012 to 2016
$2.1M
NEI NIH HHS R01 EY022639NIDDK NIH HHS P30 DK074038
6 · The paper itself

Abstract

Primary cilia have been linked to signaling pathways involved in cell proliferation, cell motility and cell polarity. Defects in ciliary function result in developmental abnormalities and multiple ciliopathies. Patients affected by severe ciliopathies, such as Meckel syndrome, present several ocular surface disease conditions of unclear pathogenesis. Here, we show that primary cilia are predominantly present on basal cells of the mouse corneal epithelium (CE) throughout development and in the adult. Conditional ablation of cilia in the CE leads to an increase in proliferation and vertical migration of basal corneal epithelial cells (CECs). A consequent increase in cell density of suprabasal layers results in a thicker than normal CE. Surprisingly, in cilia-deficient CE, cilia-mediated signaling pathways, including Hh and Wnt pathways, were not affected but the intensity of Notch signaling was severely diminished. Although Notch1 and Notch2 receptors were expressed normally, nuclear Notch1 intracellular domain (N1ICD) expression was severely reduced. Postnatal development analysis revealed that in cilia-deficient CECs downregulation of the Notch pathway precedes cell proliferation defects. Thus, we have uncovered a function of the primary cilium in maintaining homeostasis of the CE by balancing proliferation and vertical migration of basal CECs through modulation of Notch signaling.

Indexed as

HomeostasisSignal TransductionAnimalsAnimals, NewbornCell MovementCell ProliferationCiliaEpithelial CellsEpithelium, CornealMice, Inbred C57BLMice, KnockoutMutationReceptor, Notch1Receptor, Notch2Tumor Suppressor ProteinsWound HealingReceptor, Notch1Receptor, Notch2Tg737Rpw protein, mouseTumor Suppressor ProteinsCorneaEpitheliumMouseNotch signalingOcular surfacePrimary ciliaWound healing

Identifiers

PMID27122169
PMCPMC4920172
OpenAlexW2345231977

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.