Evidence map›Paper›PMID 25382630›Full record

ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2015

Type III transforming growth factor beta receptor regulates vascular and osteoblast development during palatogenesis.

Cynthia R Hill, Britni H Jacobs, Christopher B Brown, Joey V Barnett, Steven L Goudy

Open access · greenAbstract read
In one paragraph

Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  11. [Down-regulation of miR-381-3p inhibits osteogenic differentiation of mouse embryonic palatal mesenchymal cells in 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin-induced cleft palate of fetal mice].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2019
    Article
  12. Review
  13. Cellular and molecular mechanisms of cleft palate development.Laryngoscope investigative otolaryngology · 2019
    Review
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  15. Review
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  17. The pivotal role of CCN2 in mammalian palatogenesis.Journal of cell communication and signaling · 2017
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  19. 2,3,7,8-Tetrachlorodibenzo-p-dioxin andDose-response : a publication of International Hormesis Society
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  20. Article
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

5 authors at 1 institution in 1 country.

Cynthia R HillDepartment of Otolaryngology, Vanderbilt University Medical Center, Nashville, Tennessee.
Britni H Jacobs
Christopher B Brown
Joey V Barnett
Steven L Goudy
Vanderbilt University Medical Center · US

Funding

The Role of IRF6 During Craniofacial DevelopmentK08DE017953 · NIDCR · VANDERBILT UNIVERSITY · PI GOUDY, STEVEN L · 2008 to 2012
$604k
NIDCR NIH HHS 5K08DE17953-5NIDCR NIH HHS K08 DE017953
6 · The paper itself

Abstract

backgroundCleft palate occurs in up to 1:1,000 live births and is associated with mutations in multiple genes. Palatogenesis involves a complex choreography of palatal shelf elongation, elevation, and fusion. Transforming growth factor β (TGFβ) and bone morphogenetic protein 2 (BMP2) canonical signaling is required during each stage of palate development. The type III TGFβ receptor (TGFβR3) binds all three TGFβ ligands and BMP2, but its contribution to palatogenesis is unknown.

resultsThe role of TGFβR3 during palate formation was found to be during palatal shelf elongation and elevation. Tgfbr3(-) (/) (-) embryos displayed reduced palatal shelf width and height, changes in proliferation and apoptosis, and reduced vascular and osteoblast differentiation. Abnormal vascular plexus organization as well as aberrant expression of arterial (Notch1, Alk1), venous (EphB4), and lymphatic (Lyve1) markers was also observed. Decreased osteoblast differentiation factors (Runx2, alk phos, osteocalcin, col1A1, and col1A2) demonstrated poor mesenchymal cell commitment to the osteoblast lineage within the maxilla and palatal shelves in Tgfbr3(-) (/) (-) embryos. Additionally, in vitro bone mineralization induced by osteogenic medium (OM+BMP2) was insufficient in Tgfbr3(-) (/) (-) palatal mesenchyme, but mineralization was rescued by overexpression of TGFβR3.

conclusionsThese data reveal a critical, previously unrecognized role for TGFβR3 in vascular and osteoblast development during palatogenesis.

Indexed as

AnimalsAntigens, DifferentiationCalcification, PhysiologicGene Expression Regulation, DevelopmentalMesodermMiceMice, KnockoutNeovascularization, PhysiologicOrganogenesisOsteoblastsPalate, HardProteoglycansReceptors, Transforming Growth Factor betaAntigens, DifferentiationbetaglycanProteoglycansReceptors, Transforming Growth Factor betaBMPcleft palateosteogenesispalatogenesisTGFβvascularization

Identifiers

PMID25382630
PMCPMC4310801
OpenAlexW1757033803

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Registered trials

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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.