Evidence map›Paper›PMID 27886516›Full record

ArticleEndocrinology2017

Inflammatory Stimuli Increase Progesterone Receptor-A Stability and Transrepressive Activity in Myometrial Cells.

Gregory A Peters, Lijuan Yi, Yelenna Skomorovska-Prokvolit, Bansari Patel, Peyvand Amini, Huiqing Tan, Sam Mesiano

Abstract read
In one paragraph

Article in Endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

40 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. An Ex Vivo Model for the Onset of Human Labor.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Article
  4. Observational
  5. Article
  6. Article
  7. Review
  8. The hormonal control of parturition.Physiological reviews · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Next generation strategies for preventing preterm birth.Advanced drug delivery reviews · 2021
    Review
  17. TBX2, a Novel Regulator of Labour.Medicina (Kaunas, Lithuania) · 2021
    Article
  18. Review
  19. Progesterone receptor isoform B regulates theProceedings of the National Academy of Sciences of the United States of America · 2021
    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.

Gregory A PetersDepartments of Reproductive Biology and.
Lijuan YiDepartments of Reproductive Biology and.
Yelenna Skomorovska-ProkvolitDepartments of Reproductive Biology and.
Bansari PatelDepartments of Reproductive Biology and.
Peyvand AminiPhysiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106; and.
Huiqing TanDepartments of Reproductive Biology and.
Sam MesianoDepartments of Reproductive Biology and.

Funding

Role of nuclear progesterone receptors in the control of human parturitionR01HD069819 · NICHD · CASE WESTERN RESERVE UNIVERSITY · PI MESIANO, SAM ANTONIO · 2012 to 2016
$1.6M
NICHD NIH HHS R01 HD069819
6 · The paper itself

Abstract

The steroid hormone progesterone acting via the nuclear progesterone receptor (PR) isoforms, progesterone receptor A (PR-A) and progesterone receptor B (PR-B), is essential for the maintenance of uterine quiescence during pregnancy. Inhibition of PR signaling augments uterine contractility and induces labor. Human parturition is thought to be triggered by modulation of PR signaling in myometrial cells to induce a functional progesterone withdrawal. One mechanism for functional progesterone withdrawal is increased abundance of PR-A, which decreases progesterone responsiveness by inhibiting the transcriptional activity of PR-B. Human parturition also involves tissue-level inflammation within the myometrium. This study examined the control of PR-A abundance and transrepressive activity in myometrial cells and the role of the inflammatory stimuli in the form of interleukin-1β (IL-1β) and lipopolysaccharide (LPS) in these processes. We found that abundance of PR-A was markedly increased by progesterone and by exposure to IL-1β and LPS via posttranslational mechanisms involving increased PR-A protein stability. In contrast, progesterone decreased abundance of PR-B by increasing its rate of degradation. Together, progesterone and proinflammatory stimuli induced a PR-A-dominant state in myometrial cells similar to that observed in term laboring myometrium. IL-1β and LPS also increased the capacity for PR-A to inhibit the transcriptional activity of PR-B. Taken together, our data suggest that proinflammatory stimuli increase the steady-state levels of PR-A and its transrepressive activity in myometrial cells and support the hypothesis that tissue-level inflammation triggers parturition by inducing PR-A-mediated functional progesterone withdrawal.

Indexed as

Uterine ContractionCell LineFemaleHumansInflammationMyometriumPregnancyProgesteroneReceptors, ProgesteroneTissue Culture TechniquesProgesteroneprogesterone receptor Aprogesterone receptor BReceptors, Progesterone

Identifiers

PMID27886516
PMCPMC5412979

What OpenQuestion holds

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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.