Evidence map›Paper›PMID 20026682›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010

Silencing of the JNK pathway maintains progesterone receptor activity in decidualizing human endometrial stromal cells exposed to oxidative stress signals.

Beatriz Leitao, Marius C Jones, Luca Fusi, Jenny Higham, Yun Lee, Masashi Takano, Tomoko Goto, Mark Christian, Eric W-F Lam, Jan J Brosens

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

49 citing papers in PubMed, 107 citations in OpenAlex.

  1. Article
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  12. Human embryo implantation.Development (Cambridge, England) · 2023
    Review
  13. Role of Placental Glucose Transporters in Determining Fetal Growth.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Review
  14. Co-option of stress mechanisms in the origin of evolutionary novelties.Evolution; international journal of organic evolution · 2022
    Article
  15. Review
  16. Embryo biosensing by uterine natural killer cells determines endometrial fate decisions at implantation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  17. Article
  18. 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

10 authors at 2 institutions in 1 country.

Beatriz LeitaoInstitute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Rd., London W12 0NN.
Marius C Jones
Luca Fusi
Jenny Higham
Yun Lee
Masashi Takano
Tomoko Goto
Mark Christian
Eric W-F Lam
Jan J Brosens
Hammersmith Hospital · GBImperial College London · GB

Funding

Cancer Research UK 12011Wellcome TrustWellcome Trust 084336
6 · The paper itself

Abstract

Survival of the conceptus is dependent on continuous progesterone signaling in the maternal decidua but how this is achieved under conditions of oxidative stress that characterize early pregnancy is unknown. Using primary cultures, we show that modest levels of reactive oxygen species (ROS) increase sumoylation in human endometrial stromal cells (HESCs), leading to enhanced modification and transcriptional inhibition of the progesterone receptor (PR). The ability of ROS to induce a sustained hypersumoylation response, or interfere with PR activity, was lost upon differentiation of HESCs into decidual cells. Hypersumoylation in response to modest levels of ROS requires activation of the JNK pathway. Although ROS-dependent JNK signaling is disabled on decidualization, the cells continue to mount a transcriptional response, albeit distinct from that observed in undifferentiated HESCs. We further show that attenuated JNK signaling in decidual cells is a direct consequence of altered expression of key pathway modulators, including induction of MAP kinase phosphatase 1 (MKP1). Overexpression of MKP1 dampens JNK signaling, prevents hypersumoylation, and maintains PR activity in undifferentiated HESCs exposed to ROS. Thus, JNK silencing uncouples ROS signaling from the SUMO conjugation pathway and maintains progesterone responses and cellular homeostasis in decidual cells under oxidative stress conditions imposed by pregnancy.

Indexed as

Oxidative StressCell DifferentiationDeciduaDual Specificity Phosphatase 1EndometriumFemaleGene Expression RegulationGene SilencingHumansHydrogen PeroxideMAP Kinase Kinase 4PregnancyReceptors, ProgesteroneRNA, Small InterferingSignal TransductionStromal CellsDual Specificity Phosphatase 1Hydrogen PeroxideMAP Kinase Kinase 4Receptors, ProgesteroneRNA, Small InterferingSUMO-1 ProteinSUMO1 protein, human

Identifiers

PMID20026682
PMCPMC2857868
OpenAlexW2011053249

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.