Evidence map›Paper›PMID 21270426›Full record

ArticleBiology of reproduction2011

Activation of the aryl hydrocarbon receptor during pregnancy in the mouse alters mammary development through direct effects on stromal and epithelial tissues.

Betina J Lew, Ravikumar Manickam, B Paige Lawrence

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

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  11. Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.International journal of molecular sciences · 2019
    Review
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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

3 authors at 1 institution in 1 country.

Betina J LewDepartment of Environmental Medicine, University of Rochester School of Medicine and Dentistry, New York, USA.
Ravikumar Manickam
B Paige Lawrence
University of Rochester · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Martha Susiarjo · 1985 to 2026
$42.8M
Training in Environment ToxicologyT32ES007026 · NIEHS · UNIVERSITY OF ROCHESTER · PI Alison Elder, Marissa Sobolewski Terry · 1985 to 2026
$20.2M
Ah receptor-mediated deregulation of lactogenesisR01ES013958 · NIEHS · WASHINGTON STATE UNIVERSITY · PI LAWRENCE, B PAIGE · 2005 to 2009
$1.7M
Mechanisms by which TCDD impairs immunological memoryK02ES012409 · NIEHS · WASHINGTON STATE UNIVERSITY · PI LAWRENCE, B PAIGE · 2005 to 2009
$619k
Exploring epigenetic mechanisms of developmental immunologyR21ES013863 · NIEHS · WASHINGTON STATE UNIVERSITY · PI LAWRENCE, B. PAIGE · 2005 to 2007
$436k
NIEHS NIH HHS K02 ES012409NIEHS NIH HHS K02-ES012409NIEHS NIH HHS P30 ES001247NIEHS NIH HHS P30-ES01247NIEHS NIH HHS R01 ES013958NIEHS NIH HHS R01-ES013958NIEHS NIH HHS R21 ES013863NIEHS NIH HHS R21-ES013863NIEHS NIH HHS T32 ES007026NIEHS NIH HHS T32-ES07026
6 · The paper itself

Abstract

Activation of the aryl hydrocarbon receptor (AHR), an environment-sensing transcription factor, causes profound impairment of mammary gland differentiation during pregnancy. Defects include decreased ductal branching, poorly formed alveolar structures, suppressed expression of milk proteins, and failure to nutritionally support offspring. AHR is activated by numerous environmental toxins, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and plays an as yet poorly understood role in development and reproduction. To better understand how AHR activation affects pregnancy-associated mammary gland differentiation, we used a combination of ex vivo differentiation, mammary epithelial transplantation, and AHR-deficient mice to determine whether AHR modulates mammary development through a direct effect on mammary epithelial cells (MECs) or by altering paracrine or systemic factors that drive pregnancy-associated differentiation. Studies using mutant mice that express an AHR protein lacking the DNA-binding domain show that defects in pregnancy-associated differentiation require AHR:DNA interactions. We then used fluorescence-based cell sorting to compare changes in gene expression in MECs and whole mammary tissue to gain insight into affected signaling pathways. Our data indicate that activation of the AHR during pregnancy directly affects mammary tissue development via both a direct effect on MECs and through changes in cells of the fat pad, and point to gene targets in MECs and stromal tissues as putative AHR targets.

Indexed as

AnimalsDNAEndocrine DisruptorsEnvironmental PollutantsFemaleGene Expression RegulationMammary Glands, AnimalMicePolychlorinated DibenzodioxinsPregnancyProtein BindingReceptors, Aryl Hydrocarbon1,2,7,8-tetrachlorodibenzo-p-dioxinDNAEndocrine DisruptorsEnvironmental PollutantsPolychlorinated DibenzodioxinsReceptors, Aryl Hydrocarbon

Identifiers

PMID21270426
PMCPMC3099582
OpenAlexW2099923540

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.