Evidence map›Paper›PMID 27535957›Full record

ArticleBiology of reproduction2016

Developmental Toxicant Exposure Is Associated with Transgenerational Adenomyosis in a Murine Model.

Kaylon L Bruner-Tran, Antoni J Duleba, Hugh S Taylor, Kevin G Osteen

Open access · bronzeAbstract read
In one paragraph

Article in Biology of reproduction, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

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  15. Adenomyosis: Mechanisms and Pathogenesis.Seminars in reproductive medicine · 2020
    Review
  16. Animal Models of Adenomyosis.Seminars in reproductive medicine · 2020
    Review
  17. Environmental Endocrine Disruptors and Endometriosis.Advances in anatomy, embryology, and cell biology · 2020
    Review
  18. Review
  19. Article
  20. Review
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 3 institutions in 1 country.

Kaylon L Bruner-Tran
Antoni J Duleba
Hugh S Taylor
Kevin G Osteen
Vanderbilt University Medical Center · USUniversity of California, San Diego · USYale University · US

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STACIE B DUSETZINA · 1995 to 2026
$172.8M
Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Dioxin Exposure and the Invasive Pathogenesis of EndometriosisR01ES014942 · NIEHS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI BRUNER-TRAN, KAYLON L, OSTEEN, KEVIN G · 2006 to 2016
$3.5M
Paternal Toxicant Exposure Impacts Testicular-Placental CrosstalkI01BX002853 · VA · VETERANS HEALTH ADMINISTRATION · PI OSTEEN, KEVIN G · 2016 to 2020
–
BLRD VA I01 BX002853NCATS NIH HHS UL1 TR001863NCI NIH HHS P30 CA068485NIDDK NIH HHS U24 DK059637NIEHS NIH HHS R01 ES014942
6 · The paper itself

Abstract

The common environmental toxicant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or, commonly, dioxin) is a known endocrine disruptor that has been linked to the development of endometriosis in experimental models. Using a murine model, we previously demonstrated that in utero TCDD exposure promotes the transgenerational development of an "endometriosis-like" uterine phenotype consisting of reduced responsiveness to progesterone, subfertility and an increased risk of preterm birth. Since adenomyosis is frequently observed as a comorbidity in women with endometriosis, herein, we sought to determine the incidence of adenomyosis in non-pregnant mice with a history of direct or indirect TCDD exposure. Using histologic assessment and immunohistochemical staining, we analyzed murine uteri for adenomyosis, microvessel density and expression of estrogen receptors alpha and beta (ESR1 and ESR2). Our studies revealed that unexposed control mice did not exhibit adenomyosis while this disease was frequently observed in mice with a history of early life TCDD exposure. A transgenerational impact of developmental TCDD exposure was demonstrated since a subset of mice with only an indirect exposure (F3) also exhibited adenomyosis. Microvessel density within the uterus was significantly higher in all groups of TCDD exposed mice compared to control animals, with density correlated to the severity of disease. Both ESR1 and ESR2 protein exhibited alterations in expression in experimental mice compared to controls. Similar to women with endometriosis, we observed a significant reduction in the ratio of Esr1/Esr2 mRNA in all F1 mice compared to controls. Although this retrospective study was not designed to specifically address mechanisms associated with development of adenomyosis, our data suggest that developmental TCDD exposure permanently alters adult steroid responses which may contribute to the transgenerational development of adenomyosis.

Indexed as

adenomyosisDevelopmental origins of health and diseaseEndometriosisEnvironmental contaminants and toxicantstransgenerational

Identifiers

PMID27535957
PMCPMC5333937
OpenAlexW2517712760

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.