Evidence map›Paper›PMID 26073038›Full record

ArticleThe American journal of pathology2015

Estradiol is a critical mediator of macrophage-nerve cross talk in peritoneal endometriosis.

Erin Greaves, Julia Temp, Arantza Esnal-Zufiurre, Sylvia Mechsner, Andrew W Horne, Philippa T K Saunders

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 2 pooled it
13.5field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

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44 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

6 authors at 3 institutions in 3 countries.

Erin GreavesMedical Research Council Centre for Reproductive Health, The University of Edinburgh, Queen's Medical Research Institute, Edinburgh, United Kingdom. Electronic address: egreaves@ed.ac.uk.
Julia TempEndometriosis Centre Charité, Department of Gynecology, Charité, Campus Benjamin Franklin, Berlin, Germany; Department of Biology, Chemistry, and Pharmacy, Free University of Berlin, Berlin, Germany.
Arantza Esnal-ZufiurreMedical Research Council Centre for Reproductive Health, The University of Edinburgh, Queen's Medical Research Institute, Edinburgh, United Kingdom.
Sylvia MechsnerEndometriosis Centre Charité, Department of Gynecology, Charité, Campus Benjamin Franklin, Berlin, Germany.
Andrew W HorneMedical Research Council Centre for Reproductive Health, The University of Edinburgh, Queen's Medical Research Institute, Edinburgh, United Kingdom.
Philippa T K SaundersMedical Research Council Centre for Reproductive Health, The University of Edinburgh, Queen's Medical Research Institute, Edinburgh, United Kingdom.
MRC Centre for Reproductive Health · GBCharité - Universitätsmedizin Berlin · DEFranklin University · US

Funding

Medical Research Council G1100356Medical Research Council G1100356/1
6 · The paper itself

Abstract

Endometriosis occurs in approximately 10% of women and is associated with persistent pelvic pain. It is defined by the presence of endometrial tissue (lesions) outside the uterus, most commonly on the peritoneum. Peripheral neuroinflammation, a process characterized by the infiltration of nerve fibers and macrophages into lesions, plays a pivotal role in endometriosis-associated pain. Our objective was to determine the role of estradiol (E2) in regulating the interaction between macrophages and nerves in peritoneal endometriosis. By using human tissues and a mouse model of endometriosis, we demonstrate that macrophages in lesions recovered from women and mice are immunopositive for estrogen receptor β, with up to 20% being estrogen receptor α positive. In mice, treatment with E2 increased the number of macrophages in lesions as well as concentrations of mRNAs encoded by Csf1, Nt3, and the tyrosine kinase neurotrophin receptor, TrkB. By using in vitro models, we determined that the treatment of rat dorsal root ganglia neurons with E2 increased mRNA concentrations of the chemokine C-C motif ligand 2 that stimulated migration of colony-stimulating factor 1-differentiated macrophages. Conversely, incubation of colony-stimulating factor 1 macrophages with E2 increased concentrations of brain-derived neurotrophic factor and neurotrophin 3, which stimulated neurite outgrowth from ganglia explants. In summary, we demonstrate a key role for E2 in stimulating macrophage-nerve interactions, providing novel evidence that endometriosis is an estrogen-dependent neuroinflammatory disorder.

Indexed as

AdultAnimalsCell CommunicationCell DifferentiationCell MovementDisease Models, AnimalEndometriosisEstradiolEstrogen Receptor betaFemaleGanglia, SpinalHumansMacrophage Colony-Stimulating FactorMacrophagesMiceMiddle AgedEstradiolEstrogen Receptor betaMacrophage Colony-Stimulating Factor

Identifiers

PMID26073038
PMCPMC4530129
OpenAlexW2121381144

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.