Evidence map›Paper›PMID 27776183›Full record

ArticlePloS one2016

Progesterone Alleviates Endometriosis via Inhibition of Uterine Cell Proliferation, Inflammation and Angiogenesis in an Immunocompetent Mouse Model.

Yanfen Li, Malavika K Adur, Athilakshmi Kannan, Juanmahel Davila, Yuechao Zhao, Romana A Nowak, Milan K Bagchi, Indrani C Bagchi, Quanxi Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 3 pooled it
7.9field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 3 syntheses or guidelines pooled it, 81 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Endometriosis and the Hallmarks of Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Induction of Endometriosis in a Menstruating Mouse Model (Mus musculus): A Translational Animal Disease Model.Journal of the American Association for Laboratory Animal Science : JAALAS · 2025
    Article
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  16. Review
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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

9 authors at 1 institution in 1 country.

Yanfen LiDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Malavika K AdurDepartment of Animal Science, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Athilakshmi KannanDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Juanmahel DavilaDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Yuechao ZhaoDepartment of Molecular & Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Romana A NowakDepartment of Animal Science, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Milan K BagchiDepartment of Molecular & Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Indrani C BagchiDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
Quanxi LiDepartment of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, Illinois, United States of America.
University of Illinois Urbana-Champaign · US

Funding

Tissue Procurement and Cell CultureU54HD040093 · NICHD · UNIVERSITY OF ILLINOIS AT CHICAGO · PI HALES, DALE B · 2002 to 2011
$13.1M
Role of C/EBPb in Uterine Decidualization and ImplantationU54HD055787 · NICHD · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI BAGCHI, MILAN K · 2008 to 2012
$6.8M
Bisphenol A, Phthalate, and Endometriosis: Mechanisms and PathogenesisR21ES024198 · NIEHS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI LI, QUANXI · 2014 to 2015
$436k
NICHD NIH HHS U54 HD040093NICHD NIH HHS U54 HD055787NIEHS NIH HHS R21 ES024198
6 · The paper itself

Abstract

Endometriosis, defined as growth of the endometrial cells outside the uterus, is an inflammatory disorder that is associated with chronic pelvic pain and infertility in women of childbearing age. Although the estrogen-dependence of endometriosis is well known, the role of progesterone in development of this disease remains poorly understood. In this study, we developed a disease model in which endometriosis was induced in the peritoneal cavities of immunocompetent female mice, and maintained with exogenous estrogen. The endometriosis-like lesions that were identified at a variety of ectopic locations exhibited abundant blood supply and extensive adhesions. Histological examination revealed that these lesions had a well-organized endometrial architecture and fibrotic response, resembling those recovered from clinical patients. In addition, an extensive proliferation, inflammatory response, and loss of estrogen receptor alpha (ERα) and progesterone receptor (PR) expression were also observed in these lesions. Interestingly, administration of progesterone before, but not after, lesion induction suppressed lesion expansion and maintained ERα and PR expressions. These progesterone-pretreated lesions exhibited attenuation in KI67, CD31, and pro-inflammatory cytokine expression as well as macrophage infiltration, indicating that progesterone ameliorates endometriosis progression by inhibiting cell proliferation, inflammation and neovascularization. Our studies further showed that suppression of global DNA methylation by application of DNA methyltransferase inhibitor to female mice bearing ectopic lesions restrained lesion expansion and restored ERα and PR expression in eutopic endometrium and ectopic lesions. These results indicate that epigenetic regulation of target gene expression via DNA methylation contributes, at least in part, to progesterone resistance in endometriosis.

Indexed as

ImmunocompetenceAnimalsCell ProliferationDisease ProgressionDNA MethylationEndometriosisEpigenesis, GeneticEstradiolEstrogen Receptor alphaFemaleMiceOvariectomyProgesteroneReceptors, ProgesteroneSignal TransductionUterusEstradiolEstrogen Receptor alphaProgesteroneReceptors, Progesterone

Identifiers

PMID27776183
PMCPMC5077092
OpenAlexW2536189867

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.