Evidence map›Paper›PMID 21803694›Full record

ArticleEnvironmental health perspectives2011

A mutant Ahr allele protects the embryonic kidney from hydrocarbon-induced deficits in fetal programming.

Adrian Nanez, Irma N Ramos, Kenneth S Ramos

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. AHR regulates WT1 genetic programming during murine nephrogenesis.Molecular medicine (Cambridge, Mass.) · 2011
    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 2 institutions in 1 country.

Adrian NanezDepartment of Biochemistry and Molecular Biology, University of Louisville, Louisville, Kentucky 40292, USA.
Irma N Ramos
Kenneth S Ramos
University of Louisville · USUniversity of Louisville Hospital · US

Funding

Strategic Vision & Impact on Environmental HealthP30ES014443 · NIEHS · UNIVERSITY OF LOUISVILLE · PI PROUGH, RUSSELL ALLEN · 2007 to 2010
$4.4M
MOLECULAR MECHANISMS OF VASCULAR TOXICITYR01ES004849 · NIEHS · UNIVERSITY OF LOUISVILLE · PI RAMOS, KENNETH S · 1988 to 2005
$1.3M
NIEHS NIH HHS ES014443NIEHS NIH HHS ES04849NIEHS NIH HHS P30 ES014443NIEHS NIH HHS R01 ES004849
6 · The paper itself

Abstract

backgroundThe use of experimental model systems has expedited the elucidation of pathogenetic mechanisms of renal developmental disease in humans and the identification of genes that orchestrate developmental programming during nephrogenesis.

objectivesWe conducted studies to evaluate the role of AHR polymorphisms in the disruption of renal developmental programming by benzo(a)pyrene (BaP).

methodsWe used metanephric cultures of C57BL/6J (C57) mice expressing the Ahr(b-1) allele and B6.D2N-Ahr(d)/J (D2N) mice expressing a mutant allele deficient in ligand binding (Ahr(d)) to investigate molecular mechanisms of renal development. Deficits in fetal programming were evaluated in the offspring of pregnant mice treated with BaP during nephrogenesis.

resultsHydrocarbon challenge of metanephri from C57 mice altered Wilms' tumor suppressor gene (Wt1) mRNA splice variant ratios and reduced mRNAs of the Wt1 transcriptional targets syndecan-1 (Sdc1) paired box gene 2 (Pax2), epidermal growth factor receptor (Egfr), and retinoic acid receptor, alpha (Rarα). These changes correlated with down-regulation of effectors of differentiation [secreted frizzled-related sequence protein 1 (Sfrp1), insulin-like growth factor 1 receptor (Igf1r), wingless-related MMTV-integration site 4 (Wnt4), Lim homeobox protein 1 (Lhx1), E-cadherin]. In contrast, metanephri from D2N mice were spared hydrocarbon-induced changes in Wt1 splice variant ratios and deficits of differentiation. We observed similar patterns of dysmorphogenesis and progressive loss of renal function at postnatal weeks 7 and 52 in the offspring of pregnant C57 but not D2N mice gavaged with 0.1 or 0.5 mg/kg BaP on gestation days 10-13.

conclusionsThese findings support a functional link between AHR and WT1 in the regulation of renal morphogenesis and raise important questions about the contribution of human AHR polymorphisms to the fetal origins of adult-onset kidney disease.

Indexed as

Analysis of VarianceAnimalsBasic Helix-Loop-Helix ProteinsBenzo(a)pyreneBlotting, WesternCells, CulturedDNA PrimersErbB ReceptorsFemaleGene Expression Regulation, DevelopmentalHistological TechniquesImmunohistochemistryKidneyMaternal ExposureMiceMice, Inbred C57BLAhr protein, mouseBasic Helix-Loop-Helix ProteinsBenzo(a)pyreneDNA PrimersErbB ReceptorsPax2 protein, mousePAX2 Transcription FactorProtein IsoformsRARA protein, humanRara protein, mouseReceptors, Aryl HydrocarbonReceptors, Retinoic AcidRetinoic Acid Receptor alphaSdc1 protein, mouseSyndecan-1WT1 Proteins

Identifiers

PMID21803694
PMCPMC3261986
OpenAlexW2021129053

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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.