Evidence map›Paper›PMID 29981743›Full record

ArticleThe American journal of pathology2018

Proliferative, Migratory, and Transition Properties Reveal Metastate of Human Amnion Cells.

Lauren Richardson, Ramkumar Menon

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.2field-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

40 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  5. Amniotic miracle: Investigating the unique development and applications of amniotic membrane in wound healing.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024
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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

2 authors at 1 institution in 1 country.

Lauren RichardsonDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, Texas; Department of Neuroscience, Cell Biology and Anatomy, The University of Texas Medical Branch at Galveston, Galveston, Texas.
Ramkumar MenonDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, Texas. Electronic address: ra2menon@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

Molecular Mechanisms of Environmental InjuryT32ES007254 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI AMEREDES, BILL T · 1990 to 2022
$6.6M
Fetal Cell Senescence Signals Initiation of ParturitionR01HD084532 · NICHD · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MENON, RAMKUMAR · 2016 to 2020
$695k
NICHD NIH HHS R01 HD084532NIEHS NIH HHS T32 ES007254
6 · The paper itself

Abstract

Amnion epithelial cell (AEC) shedding causes microfractures in human placental membranes during gestation. However, microfractures are healed to maintain membrane integrity. To better understand the cellular mechanisms of healing and tissue remodeling, scratch assays were performed using primary AECs derived from normal term not in labor membranes. AECs were grown under different conditions: i) normal cultures (control), ii) oxidative stress (OS) induction by cigarette smoke extract (CSE), iii) co-treatment of CSE and antioxidant N-acetyl-l-cysteine, and iv) treatment with amniotic fluid (AF). Cell migration time and distance, changes in intermediate filament (cytokeratin-18 and vimentin) expressions, and cellular senescence were determined. Control AECs in culture exhibited a metastate with the expression of both cytokeratin-18 and vimentin. During healing, AECs proliferated, migrated, and transitioned from epithelial to mesenchymal phenotype with increased vimentin. Wound healing was associated with mesenchymal to epithelial transition (MET). CSE-induced OS and senescence prevented wound healing in which cells sustained mesenchymal state. N-acetyl-l-cysteine reversed CSE's effect to aid wound closure through MET. AF accelerated cellular transitions and healing. Our data suggest that AECs undergo epithelial to mesenchymal transition during proliferation and migration and MET at the injury site to promote healing. AF accelerated whereas OS diminished cellular transitions and healing. OS-inducing pregnancy risk factors may diminish remodeling capacity contributing to membrane dysfunction, leading to preterm birth.

Indexed as

Cell MovementCell ProliferationCellular SenescenceEpithelial-Mesenchymal TransitionAmnionCells, CulturedEpithelial CellsFemaleHumansInflammationOxidative StressPregnancyWound Healing

Identifiers

PMID29981743
PMCPMC6119821
OpenAlexW2814869992

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.