Evidence map›Paper›PMID 17118173›Full record

ArticleReproductive biology and endocrinology : RB&E2006

Estrogen receptor-alpha (ER-alpha) and defects in uterine receptivity in women.

Bruce A Lessey, Wilder A Palomino, K B C Apparao, Steven L Young, Ruth A Lininger

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Reproductive biology and endocrinology : RB&E, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04107129 (Predicting Endometrial Receptivity for Optimal Reproductive Management), which is not on this map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.5field-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.

NCT04107129 completednot on this mapstarted 2020, after this paper: background citation

Predicting Endometrial Receptivity for Optimal Reproductive Management (PERFORM)

TypeobservationalSponsorStanford UniversityRan2020 to 2024Enrolled76ConditionsInfertility, Female, EndometriosisArmsEndometrial Biopsy, Euploid embryo transfer, Blood sample
3 · Its place in the literature

Who cites it

64 citing papers in PubMed, 141 citations in OpenAlex.

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4 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Bruce A LesseyDivision of Reproductive Endocrinology and Infertility, University Medical Group, Department of Obstetrics and Gynecology, Greenville Hospital System, Greenville, SC, USA. blessey@ghs.org
Wilder A Palomino
K B C Apparao
Steven L Young
Ruth A Lininger
University of North Carolina at Chapel Hill · USPrisma Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is a disorder that affects 5% of the normal population but is present in up to 40% of women with pelvic pain and/or infertility. Recent evidence suggests that the endometrium of women with endometriosis exhibits progesterone insensitivity. One endometrial protein that fluctuates in response to progesterone is the estrogen receptor-alpha (ER alpha), being down-regulated at the time of peak progesterone secretion during the window of implantation. Here we demonstrate that the biomarker of uterine receptivity, beta 3 integrin subunit, is reduced or absent in some women with endometriosis and that such defects are accompanied by inappropriate over-expression of ER alpha during the mid-secretory phase. Using a well-differentiated endometrial cell line we showed that the beta 3 integrin protein is negatively regulated by estrogen and positively regulated by epidermal growth factor (EGF). By competing against estrogen with various selective estrogen receptor modulators (SERMs) and estrogen receptor agonists and antagonists, inhibition of expression of the beta 3 integrin by estrogen can be mitigated. In conclusion, we hypothesize that certain types of uterine receptivity defects may be caused by the loss of appropriate ER alpha down-regulation in the mid-secretory phase, leading to defects in uterine receptivity. Such changes might be effectively treated by timely administration of the appropriate anti-estrogens to artificially block ER alpha and restore normal patterns of gene expression. Such treatments will require further clinical studies.

Indexed as

Cells, CulturedEndometriosisEstradiolEstrogen Receptor alphaFemaleFulvestrantGene Expression RegulationHumansIntegrin beta3PregnancySelective Estrogen Receptor ModulatorsUterusEstradiolEstrogen Receptor alphaFulvestrantIntegrin beta3Selective Estrogen Receptor Modulators

Identifiers

PMID17118173
PMCPMC1679803
OpenAlexW1940579589

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.