Evidence map›Paper›PMID 22020769›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2012

TCDD disrupts hypural skeletogenesis during medaka embryonic development.

Wu Dong, David E Hinton, Seth W Kullman

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Evidence for Aryl hydrocarbon Receptor-Mediated Inhibition of Osteoblast Differentiation in Human Mesenchymal Stem Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
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  13. Article
  14. Cardiac myocyte-specific AHR activation phenocopies TCDD-induced toxicity in zebrafish.Toxicological sciences : an official journal of the Society of Toxicology · 2014
    Article
  15. Sensitivity to dioxin decreases as zebrafish mature.Toxicological sciences : an official journal of the Society of Toxicology · 2012
    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

3 authors at 3 institutions in 2 countries.

Wu DongDepartment of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, North Carolina 27695, USA.
David E Hinton
Seth W Kullman
Duke University · USInner Mongolia University for Nationalities · CNNorth Carolina State University · US

Funding

Comparative Medicine and Translational Research Training ProgramT32OD011130 · OD · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Lauren Virginia Schnabel · 2012 to 2026
$7.8M
TRAINING IN BIOCHEMICAL AND ENVIRONMENTAL TOXICOLOGYT32ES007046 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI Seth William Kullman · 1985 to 2026
$5.1M
NIEHS NIH HHS T32 ES007046NIH HHS T32 OD011130
6 · The paper itself

Abstract

Defective bone and cartilage development account for a large number of human birth defects annually. Normal skeletogenesis involves cartilage development in early morphogenesis through a highly coordinated and orchestrated series of events involving commitment and differentiation of mesenchymal cells to chondrocytes followed by a highly programmed process of structural maturation. Recent developmental studies with laboratory model fish demonstrate that exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) results in cartilage and skeletal abnormalities. In this study, we exposed embryonic medaka to TCDD to induce developmental modification(s) of both cartilage and bone formation. Emphasis is placed on cell-rich hyaline cartilage of the hypural plate where both chondrogenesis and osteogenesis are impaired by TCDD exposure. In this model, TCDD exposure results in a concentration-dependent impairment of mesenchymal cell recruitment, chondrocyte cell proliferation, differentiation, and progression to hypertrophy. Gene expression of ColA2, a marker of chondrocyte terminal differentiation in hypural structures, is markedly attenuated consistent with hypural dysmorphogenesis. Assessment of hypural structure using a transgenic medaka expressing mCherry under control of the osterix promoter illustrated significant attenuation in expression of the osteoblast gene marker and lack of formation of a calcified perichondral sheath surrounding hypural anlage. Overall, these studies illustrate that TCDD impacts terminal differentiation and growth of cartilage and bone in axial structures not likely derived from neural crest progenitors in medaka hypurals.

Indexed as

AnimalsCartilageCell DifferentiationCell ProliferationChondrocytesCollagen Type IIDose-Response Relationship, DrugEmbryo, NonmammalianGene ExpressionMesenchymal Stem CellsMicroscopy, Electron, TransmissionMusculoskeletal AbnormalitiesOryziasOsteogenesisPolychlorinated DibenzodioxinsReal-Time Polymerase Chain ReactionCollagen Type IIPolychlorinated Dibenzodioxins

Identifiers

PMID22020769
PMCPMC7904101
OpenAlexW2097256926

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.