Evidence map›Paper›PMID 20068008›Full record

ArticleEndocrinology2010

The protein kinase A pathway-regulated transcriptome of endometrial stromal fibroblasts reveals compromised differentiation and persistent proliferative potential in endometriosis.

Lusine Aghajanova, Jose A Horcajadas, James L Weeks, Francisco J Esteban, Camran N Nezhat, Marco Conti, Linda C Giudice

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
10.4field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
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  11. New concepts on the etiology of endometriosis.The journal of obstetrics and gynaecology research · 2023
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Identification of hsa-miR-1275 as a Novel Biomarker TargetingMolecular therapy. Methods & clinical development · 2020
    Article
  17. Article
  18. Article
  19. Self-renewing endometrial epithelial organoids of the human uterus.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  20. Article
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 2 countries.

Lusine AghajanovaDepartment of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco, 505 Parnassus Avenue, San Francisco, California 94143-0132, USA.
Jose A Horcajadas
James L Weeks
Francisco J Esteban
Camran N Nezhat
Marco Conti
Linda C Giudice
University of California, San Francisco · USCenter for Special Minimally Invasive and Robotic Surgery · USUniversidad de Jaén · ES

Funding

Trophoblast Differentiation in In Vivo and In Vitro Fertilized EmbryosU54HD055764 · NICHD · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TRAN, NAM D · 2007 to 2013
$11.5M
NICHD NIH HHS U54 HD055764
6 · The paper itself

Abstract

Intrinsic abnormalities in transplanted eutopic endometrium are believed to contribute to the pathogenesis of pelvic endometriosis. Herein we investigated transcriptomic differences in human endometrial stromal fibroblasts (hESFs) from women with (hESF(endo)) vs. without (hESF(nonendo)) endometriosis, in response to activation of the protein kinase A (PKA) pathway with 8-bromoadenosine-cAMP (8-Br-cAMP). hESF(nonendo) (n = 4) and hESF(endo) (n = 4) were isolated from eutopic endometrium and treated +/- 0.5 mm 8-Br-cAMP for 96 h. Purified total RNA was subjected to microarray analysis using the whole-genome Gene 1.0 ST Affymetrix platform. A total of 691 genes were regulated in cAMP-treated hESF(nonendo) vs. 158 genes in hESF(endo), suggesting a blunted response to cAMP/PKA pathway activation in women with disease. Real-time PCR and ELISA validated the decreased expression of decidualization markers in hESF(endo) compared with hESF(nonendo). In the absence of disease, 8-Br-cAMP down-regulated progression through the cell cycle via a decrease in cyclin D1, cyclin-dependent kinase 6, and cell division cycle 2 and an increase in cyclin-dependent kinase inhibitor 1A. However, cell cycle components in hESF(endo) were not responsive to 8-Br-cAMP, resulting in persistence of a proliferative phenotype. hESF(endo) treated with 8-Br-cAMP exhibited altered expression of immune response, extracellular matrix, cytoskeleton, and apoptosis genes. Changes in phosphodiesterase expression and activity were not different among experimental groups. These data support that eutopic hESF(endo) with increased proliferative potential can seed the pelvic cavity via retrograde menstruation and promote establishment, survival, and proliferation of endometriosis lesions, independent of hydrolysis of cAMP and likely due to an inherent abnormality in the PKA pathway.

Indexed as

Cell CycleCell DifferentiationGene Expression ProfilingAdultCase-Control StudiesCell ProliferationCyclic AMP-Dependent Protein KinasesCyclinsCytoskeletal ProteinsEndometriosisEndometriumExtracellular Matrix ProteinsFemaleFibroblastsForkhead Transcription FactorsGene Expression RegulationCyclic AMP-Dependent Protein KinasesCyclinsCytoskeletal ProteinsExtracellular Matrix ProteinsForkhead Transcription FactorsPhosphoric Diester HydrolasesWnt Proteins

Identifiers

PMID20068008
PMCPMC2840687
OpenAlexW2031316279

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.