Evidence map›Paper›PMID 23429912›Full record

ArticleToxicological sciences : an official journal of the Society of Toxicology2013

TCDD inhibition of canonical Wnt signaling disrupts prostatic bud formation in mouse urogenital sinus.

Amanda M Branam, Nicole M Davis, Robert W Moore, Andrew J Schneider, Chad M Vezina, Richard E Peterson

Open access · bronzeAbstract read
In one paragraph

Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. 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
2.4field-weighted citation impact, top 11% 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, 21 citations in OpenAlex.

  1. Article
  2. AhR and Wnt/β-Catenin Signaling Pathways and Their Interplay.Current issues in molecular biology · 2023
    Review
  3. TCDD alters essential transcriptional regulators of osteogenic differentiation in multipotent mesenchymal stem cells.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Intersection of AHR and Wnt signaling in development, health, and disease.International journal of molecular sciences · 2014
    Review
  13. Article
  14. Article
  15. Review
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

6 authors at 2 institutions in 1 country.

Amanda M BranamSchool of Pharmacy, University of Wisconsin, Madison, Wisconsin 53705, USA.
Nicole M Davis
Robert W Moore
Andrew J Schneider
Chad M Vezina
Richard E Peterson
University of Wisconsin–Madison · USSociety of Environmental Toxicology and Chemistry · US

Funding

Molecular & Environmental Toxicology Pre-& Postdoctoral Training ProgramT32ES007015 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI CHRISTOPHER A BRADFIELD · 1985 to 2026
$11.5M
REPRODUCTIVE AND DEVELOPMENTAL TOXICITY OF DIOXINR01ES001332 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI PETERSON, RICHARD EUGENE, VEZINA, CHAD M. · 1985 to 2021
$5.3M
REPRODUCTIVE AND DEVELOPMENTAL TOXICITY OF DIOXINR37ES001332 · NIEHS · UNIVERSITY OF WISCONSIN-MADISON · PI PETERSON, RICHARD EUGENE · 2000 to 2009
$3.9M
NIEHS NIH HHS ES01332NIEHS NIH HHS R01 ES001332NIEHS NIH HHS T32 ES007015
6 · The paper itself

Abstract

In mice, in utero exposure to 2,3,7,8-tetrachlorodibenzo-p- dioxin (TCDD) reduces the number of dorsolateral prostatic buds resulting in a smaller dorsolateral prostate and prevents formation of ventral buds culminating in ventral prostate agenesis. The genes and signaling pathways affected by TCDD that are responsible for disrupting prostate development are largely unknown. Here we show that treatment of urogenital sinus (UGS) organ cultures with known inhibitors of canonical Wnt signaling also inhibits prostatic bud formation. In support of the hypothesis that TCDD decreases canonical Wnt signaling, we identify inhibitory effects of TCDD on multiple components of the canonical Wnt signaling pathway in the UGS that temporally coincide with the inhibitory effect of TCDD on prostatic bud formation: (1) expression of R-spondins (Rspo2 and Rspo3) that promote canonical Wnt signaling is reduced; (2) expression of Lef1, Tcf1, and Wif1, established canonical Wnt target genes, is decreased; (3) expression of Lgr5, a RSPO receptor that activates canonical Wnt signaling, is reduced; and (4) expression of Dickkopfs (Dkks), inhibitors of canonical Wnt signaling, is not increased by TCDD. Thus, the TCDD-induced reduction in canonical Wnt signaling is associated with a decrease in activators (Rspo2 and Rspo3) rather than an increase in inhibitors (Dkk1 and Dkk2) of the pathway. This study focuses on determining whether treatment of TCDD-exposed UGS organ cultures with RSPO2 and/or RSPO3 is capable of rescuing the inhibitory effects of TCDD on canonical Wnt signaling and prostatic bud formation. We discovered that each RSPO alone or in combination partially rescues TCDD inhibition of both canonical Wnt signaling and prostatic bud formation.

Indexed as

AnimalsFemaleGene Expression Regulation, DevelopmentalGestational AgeImmunohistochemistryIn Situ HybridizationMaleMaternal ExposureMiceMice, Inbred C57BLOrgan Culture TechniquesOrganogenesisPolychlorinated DibenzodioxinsPregnancyProstateReverse Transcriptase Polymerase Chain ReactionPolychlorinated DibenzodioxinsWnt Proteins

Identifiers

PMID23429912
PMCPMC3627553
OpenAlexW2144614276

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.