Evidence map›Paper›PMID 26490843›Full record

ArticleBiology of reproduction2015

Bisphenol A and Related Alkylphenols Exert Nongenomic Estrogenic Actions Through a G Protein-Coupled Estrogen Receptor 1 (Gper)/Epidermal Growth Factor Receptor (Egfr) Pathway to Inhibit Meiotic Maturation of Zebrafish Oocytes.

Amanda C Fitzgerald, Candace Peyton, Jing Dong, Peter Thomas

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.6field-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

26 citing papers in PubMed, 72 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Amanda C FitzgeraldUniversity of Texas at Austin Marine Science Institute, Port Aransas, Texas.
Candace PeytonUniversity of Texas at Austin Marine Science Institute, Port Aransas, Texas.
Jing DongUniversity of Texas at Austin Marine Science Institute, Port Aransas, Texas.
Peter ThomasUniversity of Texas at Austin Marine Science Institute, Port Aransas, Texas peter.thomas@utexas.edu.
The University of Texas at Austin · US

Funding

Characteristics of a putative steroid membrane receptorR01ES012961 · NIEHS · UNIVERSITY OF TEXAS AT AUSTIN · PI THOMAS, PETER · 2006 to 2010
$1.6M
NIEHS NIH HHS ES012961
6 · The paper itself

Abstract

Xenobiotic estrogens, such as bisphenol A (BPA), disrupt a wide variety of genomic estrogen actions, but their nongenomic estrogen actions remain poorly understood. We investigated nongenomic estrogenic effects of low concentrations of BPA and three related alkylphenols on the inhibition of zebrafish oocye maturation (OM) mediated through a G protein-coupled estrogen receptor 1 (Gper)-dependent epidermal growth factor receptor (Egfr) pathway. BPA (10-100 nM) treatment for 3 h mimicked the effects of estradiol-17beta (E2) and EGF, decreasing spontaneous maturation of defolliculated zebrafish oocytes, an effect not blocked by coincubation with actinomycin D, but blocked by coincubation with a Gper antibody. BPA displayed relatively high binding affinity (15.8% that of E2) for recombinant zebrafish Gper. The inhibitory effects of BPA were attenuated by inhibition of upstream regulators of Egfr, intracellular tyrosine kinase (Src) with PP2, and matrix metalloproteinase with ilomastat. Treatment with an inhibitor of Egfr transactivation, AG1478, and an inhibitor of the mitogen-activated protein kinase (MAPK) 3/1 pathway, U0126, increased spontaneous OM and blocked the inhibitory effects of BPA, E2, and the selective GPER agonist, G-1. Western blot analysis showed that BPA (10-200 nM) mimicked the stimulatory effects of E2 and EGF on Mapk3/1 phosphorylation. Tetrabromobisphenol A, 4-nonylphenol, and tetrachlorobisphenol A (5-100 nM) also inhibited OM, an effect blocked by cotreatment with AG1478, as well as with the GPER antagonist, G-15, and displayed similar binding affinities as BPA to zebrafish Gper. The results suggest that BPA and related alkylphenols disrupt zebrafish OM by a novel nongenomic estrogenic mechanism involving activation of the Gper/Egfr/Mapk3/1 pathway.

Indexed as

AnimalsBenzhydryl CompoundsBisphenol A CompoundsChlorophenolsEpidermal Growth FactorErbB ReceptorsEstradiolMeiosisMitogen-Activated Protein KinasesOocytesPhenolsPhosphorylationPolybrominated BiphenylsReceptors, G-Protein-CoupledSignal TransductionZebrafish4-nonylphenolBenzhydryl Compoundsbisphenol ABisphenol A CompoundsChlorophenolsEpidermal Growth FactorErbB ReceptorsEstradiolgper1 protein, zebrafishMitogen-Activated Protein KinasesPhenolsPolybrominated BiphenylsReceptors, G-Protein-Coupledtetrabromobisphenol AtetrachlorodianZebrafish Proteinsbisphenol AEGFRendocrine disruptorsGPERGPR30MAPkinasemeiotic arrestnonylphenoloocyte maturationtetrabromobisphenol Atetrachorobisphenol Azebrafish

Identifiers

PMID26490843
PMCPMC4712694
OpenAlexW2283703569

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.