Evidence map›Paper›PMID 35421560›Full record

ArticleReproductive toxicology (Elmsford, N.Y.)2022

Phthalate monoesters act through peroxisome proliferator-activated receptors in the mouse ovary.

Daryl D Meling, Kathy M De La Torre, Andres S Arango, Andressa Gonsioroski, Ashley R K Deviney, Alison M Neff, Mary J Laws, Genoa R Warner, Emad Tajkhorshid, Jodi A Flaws

Open access · greenAbstract read
In one paragraph

Article in Reproductive toxicology (Elmsford, N.Y.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Single-cell RNA-seq reveals that granulosa cells are a target of phthalate toxicity in the ovary.Toxicological sciences : an official journal of the Society of Toxicology · 2025
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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

10 authors at 1 institution in 1 country.

Daryl D MelingDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Kathy M De La TorreDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Andres S ArangoCenter for Biophysics and Quantitative Biology, Department of Biochemistry, University of Illinois at Urbana-Champaign, Urbana, IL, USA; Theoretical and Computational Biophysics Group, NIH Center for Macromolecular Modeling and Bioinformatics, Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Andressa GonsioroskiDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Ashley R K DevineyDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Alison M NeffDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Mary J LawsDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Genoa R WarnerDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Emad TajkhorshidCenter for Biophysics and Quantitative Biology, Department of Biochemistry, University of Illinois at Urbana-Champaign, Urbana, IL, USA; Theoretical and Computational Biophysics Group, NIH Center for Macromolecular Modeling and Bioinformatics, Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Jodi A FlawsDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA. Electronic address: jflaws@illinois.edu.
University of Illinois Urbana-Champaign · US

Funding

WHOLE CELL SIMULATIONP41GM104601 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI SCHULTEN, KLAUS · 2012 to 2021
$19.0M
Research Training Program in Toxicology and Environmental HealthT32ES007326 · NIEHS · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI Jodi A. Flaws · 2000 to 2026
$8.7M
Resource for Macromolecular Modeling and VisualizationR24GM145965 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI Emad Tajkhorshid · 2022 to 2026
$6.2M
Phthalates and Ovarian ToxicityR01ES028661 · NIEHS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI FLAWS, JODI A. · 2018 to 2022
$1.8M
Mechanisms of Phthalate Toxicity in the OvaryR00ES031150 · NIEHS · NEW JERSEY INSTITUTE OF TECHNOLOGY · PI WARNER, GENOA R · 2022 to 2024
$1.1M
Mechanisms of Phthalate Toxicity in the OvaryK99ES031150 · NIEHS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI WARNER, GENOA R · 2020 to 2021
$194k
NIEHS NIH HHS K99 ES031150NIEHS NIH HHS R00 ES031150NIEHS NIH HHS R01 ES028661NIEHS NIH HHS T32 ES007326NIGMS NIH HHS P41 GM104601NIGMS NIH HHS R24 GM145965
6 · The paper itself

Abstract

Widespread use of phthalates as solvents and plasticizers leads to everyday human exposure. The mechanisms by which phthalate metabolites act as ovarian toxicants are not fully understood. Thus, this study tested the hypothesis that the phthalate metabolites monononyl phthalate (MNP), monoisononyl phthalate (MiNP), mono(2-ethylhexyl) phthalate (MEHP), monobenzyl phthalate (MBzP), monobutyl phthalate (MBP), monoisobutyl phthalate (MiBP), and monoethyl phthalate (MEP) act through peroxisome proliferator-activated receptors (PPARs) in mouse granulosa cells. Primary granulosa cells were isolated from CD-1 mice and cultured with vehicle control (dimethyl sulfoxide) or MNP, MiNP, MEHP, MBzP, MBP, MiBP, or MEP (0.4-400 μM) for 24 h. Following culture, qPCR was performed for known PPAR targets, Fabp4 and Cd36. Treatment with the phthalate metabolites led to significant changes in Fabp4 and Cd36 expression relative to control in dose-dependent or nonmonotonic fashion. Primary granulosa cell cultures were also transfected with a DNA plasmid containing luciferase expressed under the control of a consensus PPAR response element. MNP, MiNP, MEHP, and MBzP caused dose-dependent changes in expression of luciferase, indicating the presence of functional endogenous PPAR receptors in the granulosa cells that respond to phthalate metabolites. The effects of phthalate metabolites on PPAR target genes were inhibited in most of the cultures by co-treatment with the PPAR-γ inhibitor, T0070907, or with the PPAR-α inhibitor, GW6471. Collectively, these data suggest that some phthalate metabolites may act through endogenous PPAR nuclear receptors in the ovary and that the differing structures of the phthalates result in different levels of activity.

Indexed as

Environmental PollutantsPhthalic AcidsAnimalsEnvironmental ExposureFemaleMiceOvaryPlasticizersPPAR alphaPPAR gammaEnvironmental Pollutantsphthalic acidPhthalic AcidsPlasticizersPPAR alphaPPAR gammaGranulosa cellsNuclear receptorOvaryPhthalatesPPARToxicants

Identifiers

PMID35421560
PMCPMC9749796
OpenAlexW4223553195

What OpenQuestion holds

Textmetadata
LicenceTDM
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.