Evidence map›Paper›PMID 28664994›Full record

ArticlePrenatal diagnosis2017

Trauma induces overexpression of Cx43 in human fetal membrane defects.

David W Barrett, Aumie Kethees, Christopher Thrasivoulou, Alvaro Mata, Alex Virasami, Neil J Sebire, Alex C Engels, Jan A Deprest, David L Becker, Anna L David and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Prenatal diagnosis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. 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

11 authors at 6 institutions in 3 countries.

David W BarrettInstitute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.
Aumie KetheesInstitute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.
Christopher ThrasivoulouDepartment of Cell and Developmental Biology, University College London, London, UK.
Alvaro MataInstitute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.
Alex VirasamiHistopathology Department, Camelia Botnar Laboratories, Great Ormond Street Hospital for Children NHS Trust, London, UK.
Neil J SebireHistopathology Department, Camelia Botnar Laboratories, Great Ormond Street Hospital for Children NHS Trust, London, UK.
Alex C EngelsDepartment of Obstetrics and Gynaecology, University Hospitals Leuven, Leuven, Belgium.ORCID http://orcid.org/0000-0002-8478-5831
Jan A DeprestDepartment of Obstetrics and Gynaecology, University Hospitals Leuven, Leuven, Belgium.
David L BeckerLee Kong Chian School of Medicine, Nanyang Technological University, Singapore.
Anna L DavidInstitute for Women's Health, University College London, London, UK.
Tina T ChowdhuryInstitute of Bioengineering, School of Engineering and Materials Science, Queen Mary University of London, London, UK.ORCID http://orcid.org/0000-0003-4167-7782
Queen Mary University of London · GBGreat Ormond Street Hospital · GBKU Leuven · BELondon Women's Clinic · GBNanyang Technological University · SGUniversity College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWe developed an in vitro model to examine whether trauma induces connexin 43 (Cx43) expression and collagen organisation in the amniotic membrane (AM) of fetal membrane (FM) defects.

methodTerm human FM was traumatised in vitro. Cell morphology and Cx43 were examined in the wound edge AM by immunofluorescence (IMF) confocal microscopy and compared to control AM. Collagen microstructure was examined by second harmonic generation (SHG) imaging. Cell viability was assessed with calcein and ethidium staining.

resultsAfter trauma, the AM showed a dense region of cells, which had migrated towards the wound edge. In wound edge AM, Cx43 puncta was preferentially distributed in mesenchymal cells compared to epithelial cells with significant expression in the fibroblast layer than epithelial layer (p < 0.001). In the fibroblast layer, the collagen fibres were highly polarised and aligned in parallel to the axis of the wound edge AM. There was an absence of cell migration across the defect with no healing after 168 h. Cell viability of the FM after trauma was maintained during culture.

conclusionCx43 overexpression in wounded AM drives structural changes in collagen that slows down efficacy of cell migration across the FM defect. © 2017 The Authors. Prenatal Diagnosis published by John Wiley & Sons, Ltd.

Indexed as

AmnionCell SurvivalCollagenConnexin 43Epithelial CellsExtraembryonic MembranesFemaleFluorescent Antibody TechniqueHumansMesenchymal Stem CellsMicroscopy, ConfocalPregnancyPremature Rupture of Fetal MembranesWounds and InjuriesCollagenConnexin 43

Identifiers

PMID28664994
PMCPMC5638101
OpenAlexW2726939948

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.