Evidence map›Paper›PMID 26862745›Full record

ArticleEnvironmental health perspectives2016

Transgenic Overexpression of Aryl Hydrocarbon Receptor Repressor (AhRR) and AhR-Mediated Induction of CYP1A1, Cytokines, and Acute Toxicity.

Christoph F A Vogel, W L William Chang, Sarah Kado, Kelly McCulloh, Helena Vogel, Dalei Wu, Thomas Haarmann-Stemmann, GuoXiang Yang, Patrick S C Leung, Fumio Matsumura and 1 more

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  4. The aryl hydrocarbon receptor: a new frontier in male reproductive system.Reproductive biology and endocrinology : RB&E · 2025
    Review
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  18. Aryl-Hydrocarbon Receptor Repressor Gene in Primary Graft Dysfunction after Lung Transplantation.American journal of respiratory cell and molecular biology · 2019
    Article
  19. Article
  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

11 authors at 3 institutions in 2 countries.

Christoph F A VogelDepartment of Environmental Toxicology, University of California, Davis, Davis, California, USA.
W L William Chang
Sarah Kado
Kelly McCulloh
Helena Vogel
Dalei Wu
Thomas Haarmann-Stemmann
GuoXiang Yang
Patrick S C Leung
Fumio Matsumura
M Eric Gershwin
University of California, Davis · USSociety of Environmental Toxicology and Chemistry · USLeibniz Institute of Environmental Medicine · DE

Funding

Importance of AhR for the cellular function and communication of dendritic cellsR01ES019898 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI VOGEL, CHRISTOPH F A · 2012 to 2016
$1.7M
NIEHS NIH HHS R01 ES019898
6 · The paper itself

Abstract

backgroundThe aryl hydrocarbon receptor repressor (AhRR) is known to repress aryl hydrocarbon receptor (AhR) signaling, but very little is known regarding the role of the AhRR in vivo.

objectiveThis study tested the role of AhRR in vivo in AhRR overexpressing mice on molecular and toxic end points mediated through a prototypical AhR ligand.

methodsWe generated AhRR-transgenic mice (AhRR Tg) based on the genetic background of C57BL/6J wild type (wt) mice. We tested the effect of the prototypical AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the expression of cytochrome P450 (CYP)1A1 and cytokines in various tissues of mice. We next analyzed the infiltration of immune cells in adipose tissue of mice after treatment with TCDD using flow cytometry.

resultsAhRR Tg mice express significantly higher levels of AhRR compared to wt mice. Activation of AhR by TCDD caused a significant increase of the inflammatory cytokines Interleukin (IL)-1β, IL-6 and IL-10, and CXCL chemokines in white epididymal adipose tissue from both wt and AhRR Tg mice. However, the expression of IL-1β, CXCL2 and CXCL3 were significantly lower in AhRR Tg versus wt mice following TCDD treatment. Exposure to TCDD caused a rapid accumulation of neutrophils and macrophages in white adipose tissue of wt and AhRR Tg mice. Furthermore we found that male AhRR Tg mice were protected from high-dose TCDD-induced lethality associated with a reduced inflammatory response and liver damage as indicated by lower levels of TCDD-induced alanine aminotransferase and hepatic triglycerides. Females from both wt and AhRR Tg mice were less sensitive than male mice to acute toxicity induced by TCDD.

conclusionIn conclusion, the current study identifies AhRR as a previously uncharacterized regulator of specific inflammatory cytokines, which may protect from acute toxicity induced by TCDD. CITATION: Vogel CF, Chang WL, Kado S, McCulloh K, Vogel H, Wu D, Haarmann-Stemmann T, Yang GX, Leung PS, Matsumura F, Gershwin ME. 2016. Transgenic overexpression of aryl hydrocarbon receptor repressor (AhRR) and AhR-mediated induction of CYP1A1, cytokines, and acute toxicity. Environ Health Perspect 124:1071-1083; http://dx.doi.org/10.1289/ehp.1510194.

Indexed as

Toxicity Tests, AcuteAnimalsAnimals, Genetically ModifiedCytochrome P-450 CYP1A1CytokinesInterleukin-10Interleukin-6MiceMice, Inbred C57BLPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRepressor ProteinsCytochrome P-450 CYP1A1CytokinesInterleukin-10Interleukin-6Polychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonRepressor Proteins

Identifiers

PMID26862745
PMCPMC4937866
OpenAlexW2410181542

What OpenQuestion holds

Textmetadata
LicenceCC0
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.