Evidence map›Paper›PMID 32047115›Full record

ArticleScience signaling2020

Reversible EMT and MET mediate amnion remodeling during pregnancy and labor.

Lauren S Richardson, Robert N Taylor, Ramkumar Menon

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
9.1field-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

82 citing papers in PubMed, 103 citations in OpenAlex.

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  11. Exposure to Extreme Heat Increases Preterm Birth Risk: Hypothetical Pathophysiological Mechanisms.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
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  18. Review
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  20. Article

22 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

3 authors at 2 institutions in 1 country.

Lauren S RichardsonDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, Galveston, TX, USA.ORCID 0000-0001-8392-2833
Robert N TaylorDivision of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of Utah, Salt Lake City, UT, USA.ORCID 0000-0002-1423-6351
Ramkumar MenonDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, University of Texas Medical Branch at Galveston, Galveston, TX, USA. ram.menon@utmb.edu.ORCID 0000-0001-9213-6105
The University of Texas Medical Branch at Galveston · USUniversity of Utah · US

Funding

Molecular Mechanisms of Environmental InjuryT32ES007254 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI AMEREDES, BILL T · 1990 to 2022
$6.6M
Static state of epithelial mesenchymal transition in fetal membrane cells: a novel inflammatory pathway to parturitionR03HD098469 · NICHD · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MENON, RAMKUMAR · 2019 to 2020
$158k
NICHD NIH HHS R03 HD098469NIEHS NIH HHS T32 ES007254
6 · The paper itself

Abstract

The amnion is remodeled during pregnancy to protect the growing fetus it contains, and it is particularly dynamic just before and during labor. By combining ultrastructural, immunohistochemical, and Western blotting analyses, we found that human and mouse amnion membranes during labor were subject to epithelial-to-mesenchymal transition (EMT), mediated, in part, by the p38 mitogen-activated protein kinase (MAPK) pathway responding to oxidative stress. Primary human amnion epithelial cell cultures established from amnion membranes from nonlaboring, cesarean section deliveries exhibited EMT after exposure to oxidative stress, and the pregnancy maintenance hormone progesterone (P4) reversed this process. Oxidative stress or transforming growth factor-β (TGF-β) stimulated EMT in a manner that depended on TGF-β-activated kinase 1 binding protein 1 (TAB1) and p38 MAPK. P4 stimulated the reverse transition, MET, in primary human amnion mesenchymal cells (AMCs) through progesterone receptor membrane component 2 (PGRMC2) and c-MYC. Our results indicate that amnion membrane cells dynamically transition between epithelial and mesenchymal states to maintain amnion integrity and repair membrane damage, as well as in response to inflammation and mechanical damage to protect the fetus until parturition. An irreversible EMT and the accumulation of AMCs characterize the amnion membranes at parturition.

Indexed as

Epithelial-Mesenchymal TransitionAdaptor Proteins, Signal TransducingAmnionAnimalsCells, CulturedEpithelial CellsFemaleGene ExpressionHumansMembrane ProteinsMesenchymal Stem CellsMiceMicroscopy, Electron, TransmissionOxidative Stressp38 Mitogen-Activated Protein KinasesParturitionAdaptor Proteins, Signal TransducingMembrane Proteinsp38 Mitogen-Activated Protein KinasesPGRMC2 protein, humanReceptors, ProgesteroneTAB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID32047115
PMCPMC7092701
OpenAlexW3006044154

What OpenQuestion holds

Textmetadata
LicenceTDM
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.