Evidence map›Paper›PMID 28388726›Full record

ArticleThe Journal of clinical endocrinology and metabolism2017

The Role of Epithelial to Mesenchymal Transition in Human Amniotic Membrane Rupture.

Carla Janzen, Suvajit Sen, Margarida Y Y Lei, Marina Gagliardi de Assumpcao, John Challis, Gautam Chaudhuri

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Article
  6. Lead exposure at the feto-maternal interface: a cause for concern for fetal membrane trophoblasts.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  7. Review
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  15. Characterization of RAGE and CK2 Expressions in Human Fetal Membranes.International journal of molecular sciences · 2023
    Article
  16. Article
  17. Article
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  19. 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

6 authors at 3 institutions in 3 countries.

Carla JanzenDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California 90095, Los Angeles, Los Angeles, California.
Suvajit SenDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California 90095, Los Angeles, Los Angeles, California.
Margarida Y Y LeiDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California 90095, Los Angeles, Los Angeles, California.
Marina Gagliardi de AssumpcaoFaculty of Medical Sciences of Santa Casa de Sao Paulo, Sao Paulo, 01221-020, Brazil.
John ChallisUniversity of Western Australia and Curtin University, Crawley, Western Australia 6009, Australia.
Gautam ChaudhuriDepartment of Obstetrics and Gynecology, David Geffen School of Medicine, University of California 90095, Los Angeles, Los Angeles, California.
University of California, Los Angeles · USCurtin University · AUFaculdade de Ciências Médicas da Santa Casa de São Paulo · BR

Funding

Imaging Innovations for Placental Assessment in Response to Environmental PollutionU01HD087221 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEVASKAR, SHERIN U, JANZEN, CARLA · 2015 to 2015
$4.3M
NICHD NIH HHS U01 HD087221
6 · The paper itself

Abstract

Context: Biochemical weakening of the amnion is a major factor preceding preterm premature rupture of membranes (PPROMs), leading to preterm birth. Activation of matrix metalloproteinases (MMPs) is known to play a key role in collagen degradation of the amnion; however, epithelial to mesenchymal transition (EMT) that is also induced by MMP activation has not been investigated as a mechanism for amnion weakening. Objective: To measure amniotic EMT associated with vaginal delivery (VD) compared with unlabored cesarean sections (CSs), and to assess changes in amniotic mechanical strength with pharmacologic inhibitors and inducers of EMT, thus testing the hypothesis that EMT is a key biochemical event that promotes amniotic rupture. Findings: (1) Amnions taken from VD contained a significantly increased number of mesenchymal cells relative to epithelial cells compared with unlabored CS by fluorescence-activated cell sorting analysis (60% vs 10%); (2) tumor necrosis factor (TNF)-α stimulation of amniotic epithelial cells increased expression of the mesenchymal marker vimentin after 2 days; (3) EMT inhibitor, etodolac, significantly increased the time and mechanical pressure required to rupture the amnion; and (4) TNF-α and another pharmacologic EMT inducer, ethacridine, decreased the time and mechanical pressure required for amnion rupture, further confirming that the mesenchymal phenotype significantly weakens the amnion. Conclusions: This work demonstrated amniotic cell EMT was associated with labor and EMT decreased the tensile strength of the amnion. These findings suggest a role for EMT in the pathophysiology of PPROM and may provide a basis for development of therapies to prevent preterm labor.

Indexed as

AmnionCyclooxygenase 2 InhibitorsEpithelial-Mesenchymal TransitionEtodolacFemaleHumansMatrix MetalloproteinasesPregnancyPremature Rupture of Fetal MembranesTensile StrengthTumor Necrosis Factor-alphaCyclooxygenase 2 InhibitorsEtodolacMatrix MetalloproteinasesTumor Necrosis Factor-alpha

Identifiers

PMID28388726
PMCPMC5460731
OpenAlexW2560917706

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.