Evidence map›Paper›PMID 27312807›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2016

Preferential epigenetic programming of estrogen response after in utero xenoestrogen (bisphenol-A) exposure.

Elisa M Jorgensen, Myles H Alderman, Hugh S Taylor

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

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
5.5field-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

30 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. Article
  3. Postnatal maternal care impacts hypothalamicbioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
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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.

Elisa M JorgensenYale University School of Medicine, New Haven, Connecticut, USA.
Myles H AldermanYale University School of Medicine, New Haven, Connecticut, USA.
Hugh S TaylorYale University School of Medicine, New Haven, Connecticut, USA hugh.taylor@yale.edu.
Yale University · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
HOX Gene Expression by Endocrine Disrupting ChemicalsR01ES010610 · NIEHS · YALE UNIVERSITY · PI TAYLOR, HUGH SMITH · 2001 to 2011
$2.9M
Environmental Estrogen Induced Epigenetic Alteration of Uterine Stem CellsR01HD076422 · NICHD · YALE UNIVERSITY · PI TAYLOR, HUGH SMITH · 2012 to 2016
$2.0M
NCATS NIH HHS UL1 TR001863NICHD NIH HHS R01 HD076422NIEHS NIH HHS R01 ES010610
6 · The paper itself

Abstract

Bisphenol-A (BPA) is an environmentally ubiquitous estrogen-like endocrine-disrupting compound. Exposure to BPA in utero has been linked to female reproductive disorders, including endometrial hyperplasia and breast cancer. Estrogens are an etiological factor in many of these conditions. We sought to determine whether in utero exposure to BPA altered the global CpG methylation pattern of the uterine genome, subsequent gene expression, and estrogen response. Pregnant mice were exposed to an environmentally relevant dose of BPA or DMSO control. Uterine DNA and RNA were examined by using methylated DNA immunoprecipitation methylation microarray, expression microarray, and quantitative PCR. In utero BPA exposure altered the global CpG methylation profile of the uterine genome and subsequent gene expression. The effect on gene expression was not apparent until sexual maturation, which suggested that estrogen response was the primary alteration. Indeed, prenatal BPA exposure preferentially altered adult estrogen-responsive gene expression. Changes in estrogen response were accompanied by altered methylation that preferentially affected estrogen receptor-α (ERα)-binding genes. The majority of genes that demonstrated both altered expression and ERα binding had decreased methylation. BPA selectively altered the normal developmental programming of estrogen-responsive genes via modification of the genes that bind ERα. Gene-environment interactions driven by early life xenoestrogen exposure likely contributes to increased risk of estrogen-related disease in adults.-Jorgensen, E. M., Alderman, M. H., III, Taylor, H. S. Preferential epigenetic programming of estrogen response after in utero xenoestrogen (bisphenol-A) exposure.

Indexed as

AnimalsBenzhydryl CompoundsBisphenol A CompoundsEpigenesis, GeneticEstrogen Receptor alphaEstrogensFemaleGene Expression RegulationHomeobox A10 ProteinsHomeodomain ProteinsMicePhenolsPregnancyPrenatal Exposure Delayed EffectsPromoter Regions, GeneticProtein BindingBenzhydryl Compoundsbisphenol ABisphenol A CompoundsEstrogen Receptor alphaEstrogensHomeobox A10 ProteinsHomeodomain ProteinsHoxa10 protein, mousePhenolsendocrine disruptorERα bindingmethylationuterus

Identifiers

PMID27312807
PMCPMC5001514
OpenAlexW2420401258

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.