Evidence map›Paper›PMID 18511503›Full record

ArticleEndocrinology2008

The androgen and progesterone receptors regulate distinct gene networks and cellular functions in decidualizing endometrium.

Brianna Cloke, Kaisa Huhtinen, Luca Fusi, Takeshi Kajihara, Maria Yliheikkilä, Ka-Kei Ho, Gijs Teklenburg, Stuart Lavery, Marius C Jones, Geoffrey Trew and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 162 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Androgens modulate endometrial function.Medical molecular morphology · 2025
    Review
  5. Review
  6. Article
  7. [Notch1/Akt/Foxo1 Pathway Regulated by Kisspeptin Is Involved in Endometrial Decidualization in Patients With Recurrent Spontaneous Abortion].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Strategies for modelling endometrial diseases.Nature reviews. Endocrinology · 2022
    Review
  12. Article
  13. Article
  14. Female Reproductive Systems: Hormone Dependence and Receptor Expression.Advances in experimental medicine and biology · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Endometrial Decidualization: The Primary Driver of Pregnancy Health.International journal of molecular sciences · 2020
    Review

14 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

15 authors at 7 institutions in 5 countries.

Brianna ClokeInstitute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, London W12 0NN, United Kingdom.
Kaisa Huhtinen
Luca Fusi
Takeshi Kajihara
Maria Yliheikkilä
Ka-Kei Ho
Gijs Teklenburg
Stuart Lavery
Marius C Jones
Geoffrey Trew
J Julie Kim
Eric W-F Lam
Judith E Cartwright
Matti Poutanen
Jan J Brosens
Imperial College London · GBUniversity of Turku · FICancer Research UK · GBHammersmith Hospital · GBNorthwestern University · USSt George's, University of London · GBUniversity Medical Center Utrecht · NL

Funding

Regulation of IGFBP-1 by FKHR and HOXA10 in pregnancyR01HD044715 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI KIM, JI-YONG JULIE · 2003 to 2010
$1.8M
NICHD NIH HHS R01 HD044715Wellcome Trust
6 · The paper itself

Abstract

Progesterone is indispensable for differentiation of human endometrial stromal cells (HESCs) into decidual cells, a process that critically controls embryo implantation. We now show an important role for androgen receptor (AR) signaling in this differentiation process. Decreased posttranslational modification of the AR by small ubiquitin-like modifier (SUMO)-1 in decidualizing cells accounted for increased responsiveness to androgen. By combining small interfering RNA technology with genome-wide expression profiling, we found that AR and progesterone receptor (PR) regulate the expression of distinct decidual gene networks. Ingenuity pathway analysis implicated a preponderance of AR-induced genes in cytoskeletal organization and cell motility, whereas analysis of AR-repressed genes suggested involvement in cell cycle regulation. Functionally, AR depletion prevented differentiation-dependent stress fiber formation and promoted motility and proliferation of decidualizing cells. In comparison, PR depletion perturbed the expression of many more genes, underscoring the importance of this nuclear receptor in diverse cellular functions. However, several PR-dependent genes encode for signaling intermediates, and knockdown of PR, but not AR, compromised activation of WNT/beta-catenin, TGFbeta/SMAD, and signal transducer and activator of transcription (STAT) pathways in decidualizing cells. Thus, the nonredundant function of the AR in decidualizing HESCs, centered on cytoskeletal organization and cell cycle regulation, implies an important role for androgens in modulating fetal-maternal interactions. Moreover, we show that PR regulates HESC differentiation, at least in part, by reprogramming growth factor and cytokine signal transduction.

Indexed as

Gene Expression RegulationGene Regulatory NetworksCells, CulturedDeciduaEndometriumFemaleGene Expression ProfilingHumansOligonucleotide Array Sequence AnalysisProtein Processing, Post-TranslationalReceptors, AndrogenReceptors, ProgesteroneSUMO-1 ProteinAR protein, humanReceptors, AndrogenReceptors, ProgesteroneSUMO-1 Protein

Identifiers

PMID18511503
PMCPMC5393297
OpenAlexW2055035644

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.