Evidence map›Paper›PMID 22521153›Full record

ArticleFertility and sterility2012

Activated glucocorticoid and eicosanoid pathways in endometriosis.

Diana Monsivais, Jeffrey D Bray, Emily Su, Mary Ellen Pavone, Matthew T Dyson, Antonia Navarro, Toshiyuki Kakinuma, Serdar E Bulun

Open access · greenAbstract read
In one paragraph

Article in Fertility and sterility, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.8field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 36 citations in OpenAlex.

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  13. Endometriosis: pathogenesis and treatment.Nature reviews. Endocrinology · 2014
    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

8 authors at 2 institutions in 1 country.

Diana MonsivaisDivision of Reproductive Biology Research, Northwestern University, Chicago, Illinois 60611, USA.
Jeffrey D Bray
Emily Su
Mary Ellen Pavone
Matthew T Dyson
Antonia Navarro
Toshiyuki Kakinuma
Serdar E Bulun
Northwestern University · USGlaxoSmithKline (United States) · US

Funding

TRAINING IN METABOLISM, DIABETES AND ENDOCRINOLOGYT32DK007169 · NIDDK · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Joseph Bass · 1988 to 2026
$6.6M
Mentoring For Success: Developing Fundamental Skills For Biomedical ResearchR25GM079300 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MCGEE, RICHARD · 2007 to 2020
$6.6M
Endometriosis and RetinoidsR37HD038691 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BULUN, SERDAR E. · 2010 to 2019
$4.5M
NICHD NIH HHS R37 HD038691NICHD NIH HHS R37HD038691NIDDK NIH HHS T32 DK007169NIDDK NIH HHS T32DK007169NIGMS NIH HHS R25 GM079300
6 · The paper itself

Abstract

objectiveTo define altered gene expression networks in endometriosis.

designExperiments using endometriotic tissues and primary cells.

settingDivision of Reproductive Biology Research, Northwestern University. PATIENT(S): Premenopausal women. INTERVENTION(S): Matched samples of eutopic endometrium and ovarian endometriosis (n = 8 patients) were analyzed by microarray and verified in a separate set of tissues (n = 6 patients). Experiments to define signaling pathways were performed in primary endometriotic stromal cells (n = 12 patients). MAIN OUTCOMES MEASURE(S): Using a genome-wide in vivo approach, we identified 1,366 differentially expressed genes and a new gene network favoring increased glucocorticoid levels and action in endometriosis. RESULT(S): Transcript and protein levels of 11β-hydroxysteroid dehydrogenase (HSD11B1), which produces cortisol, the biologically active glucocorticoid, were strikingly higher, whereas messenger RNA (mRNA) levels of the cortisol-degrading HSD11B2 enzyme were significantly lower in endometriotic tissue. Glucocorticoid receptor mRNA and protein levels were significantly higher in endometriosis. The inflammatory cytokine tumor necrosis factor robustly induced mRNA and protein levels of HSD11B1 and glucocorticoid receptor but suppressed HSD11B2 mRNA in primary endometriotic stromal cells, suggesting that tumor necrosis factor stimulates cortisol production and action. We also uncovered a subset of genes critical for prostaglandin synthesis and degradation, which favor high eicosanoid levels and activity in endometriosis. CONCLUSION(S): The proinflammatory milieu of the endometriotic lesion stimulates cortisol synthesis and action in endometriotic lesions.

Indexed as

AdultCase-Control StudiesCells, CulturedEicosanoidsEndometriosisEndometriumFemaleGene Expression ProfilingGlucocorticoidsHumansMetabolic Networks and PathwaysMicroarray AnalysisMiddle AgedOvarian DiseasesUp-RegulationYoung AdultEicosanoidsGlucocorticoids

Identifiers

PMID22521153
PMCPMC3389283
OpenAlexW2005159615

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.