Evidence map›Paper›PMID 18559914›Full record

ArticleThe Journal of clinical endocrinology and metabolism2008

Androstenedione up-regulation of endometrial aromatase expression via local conversion to estrogen: potential relevance to the pathogenesis of endometriosis.

Orhan Bukulmez, Daniel B Hardy, Bruce R Carr, Richard J Auchus, Tannaz Toloubeydokhti, R Ann Word, Carole R Mendelson

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2008. 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
5.4field-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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. DHEA supplementation improves endometrial HOXA-10 mRNA expression in poor responders.Journal of the Turkish German Gynecological Association · 2017
    Article
  4. Article
  5. Article
  6. CYP2C19 polymorphism increases the risk of endometriosis.Journal of assisted reproduction and genetics · 2015
    Article
  7. Article
  8. Article
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  10. Article
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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

7 authors at 3 institutions in 1 country.

Orhan BukulmezDepartment of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of Florida College of Medicine, 1600 SW Archer Road, Gainesville, Florida 32610-0294, USA. obukulmez@obgyn.ufl.edu
Daniel B Hardy
Bruce R Carr
Richard J Auchus
Tannaz Toloubeydokhti
R Ann Word
Carole R Mendelson
The University of Texas Southwestern Medical Center · USFlorida College · USUniversity of Florida · US

Funding

CELLULAR MECHANISMS IN THE INDUCTION OF AROMATASER01DK031206 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MENDELSON, CAROLE R · 1985 to 2015
$5.5M
NIDDK NIH HHS 5-R01-DK31206NIDDK NIH HHS R01 DK031206
6 · The paper itself

Abstract

contextUp-regulation of aromatase expression in endometrial cells disseminated into the peritoneal cavity may enhance their survival via local estrogen synthesis, which may lead to endometriosis. The factors that mediate induction of aromatase in the endometrium are not well defined, but increased expression of steroidogenic factor (SF)-1 may play a role.

objectiveThe objective of the study was to determine whether androstenedione (A4), the predominant sex steroid in peritoneal fluid, regulates endometrial aromatase expression.

designThis was a cell/tissue culture study.

settingThe study was conducted at an academic center.

methodsQuantitative real-time PCR, HPLC, and chromatin immunoprecipitation were used in this study.

resultsTreatment of cultured human endometrial explants and stromal cells with A4 (10 nm) significantly up-regulated expression of aromatase mRNA transcripts containing exon IIa at their 5'-ends. In endometrial stromal cells and the human endometrial surface epithelial (HES) cell line, induction of aromatase mRNA by A4 was associated with increased expression of SF-1. In HES cells, tritiated A4 was metabolized to estradiol, testosterone (T), dihydrotestosterone, and androstanediol. Both estradiol and T, but not nonaromatizable androgens, up-regulated aromatase and SF-1 mRNA in HES cells. Chromatin immunoprecipitation revealed that A4 enhanced recruitment of SF-1 to its response element (-136 bp) upstream of CYP19 exon IIa. This, together with the findings that both estrogen receptor antagonist, ICI 182,780, and aromatase inhibitor, fadrozole, suppressed A4 and T induction of aromatase and SF-1 mRNA, indicates that the inductive effects of A4 and T are mediated by their conversion to estrogens.

conclusionsExposure of endometrial cells to A4 may enhance CYP19 gene expression through its aromatization to estrogens.

Indexed as

AdultAndrostenedioneAromataseCells, CulturedCyclizationDihydrotestosteroneDose-Response Relationship, DrugEndometriosisEndometriumEstradiolFemaleGene Expression Regulation, EnzymologicHumansSteroidogenic Factor 1TestosteroneUp-RegulationAndrostenedioneAromataseDihydrotestosteroneEstradiolSteroidogenic Factor 1Testosterone

Identifiers

PMID18559914
PMCPMC2567859
OpenAlexW2112309922

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.