Evidence map›Paper›PMID 25469638›Full record

ArticlePloS one2014

HMGB1 promotes a p38MAPK associated non-infectious inflammatory response pathway in human fetal membranes.

Sarah Bredeson, John Papaconstantinou, James H Deford, Talar Kechichian, Tariq A Syed, George R Saade, Ramkumar Menon

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
6.5field-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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 122 citations in OpenAlex.

  1. Glycogen synthase kinase (GSK) 3 in pregnancy and parturition: a systematic review of literature.The journal of maternal-fetal & neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians · 2020
    Pooled it
  2. Systematic review of p38 mitogen-activated kinase and its functional role in reproductive tissues.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018
    Pooled it
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  6. Decidual Cells Induce Release of Free and Exosome-Bound Interferon Epsilon From Vaginal Epithelial Cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025
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  20. Characterization of RAGE and CK2 Expressions in Human Fetal Membranes.International journal of molecular sciences · 2023
    Article

18 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

7 authors at 1 institution in 1 country.

Sarah BredesonDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.
John PapaconstantinouDepartment of Biochemistry and Molecular Biology, NHLBI Proteomics Center on Airway Inflammation and UTMB Biomolecular Resource Facility, University of Texas Medical Branch, Galveston, Texas, United States of America.
James H DefordDepartment of Biochemistry and Molecular Biology, NHLBI Proteomics Center on Airway Inflammation and UTMB Biomolecular Resource Facility, University of Texas Medical Branch, Galveston, Texas, United States of America.
Talar KechichianDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.
Tariq A SyedDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.
George R SaadeDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.
Ramkumar MenonDivision of Maternal-Fetal Medicine and Perinatal Research, Department of Obstetrics and Gynecology, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States of America.
The University of Texas Medical Branch at Galveston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSpontaneous preterm birth (PTB) and preterm prelabor rupture of membranes (pPROM) are major pregnancy complications often associated with a fetal inflammatory response. Biomolecular markers of this fetal inflammatory response to both infectious and non-infectious risk factors and their contribution to PTB and pPROM mechanism are still unclear. This study examined fetal membrane production, activation and mechanistic properties of high mobility group box 1 (HMGB1) as a contributor of the non-infectious fetal inflammatory response. MATERIALS AND

methodsHMGB1 transcripts and active HMGB1 were profiled in fetal membranes and amniotic fluids collected from PTB and normal term birth. In vitro, normal term not in labor fetal membranes were exposed to lipopolysaccharide (LPS) and water soluble cigarette smoke extract (CSE). HMGB1-transcripts and its protein concentrations were documented by RT-PCR and ELISA. Recombinant HMGB1 treated membranes and media were subjected to RT-PCR for HMGB1 receptors, mitogen activated protein kinase pathway analysis, cytokine levels, and Western blot for p38MAPK.

resultsHMGB1 expression and its active forms were higher in PTB and pPROM than normal term membranes and amniotic fluid samples. Both LPS and CSE enhanced HMGB1 expression and release in vitro. Fetal membrane exposure to HMGB1 resulted in increased expression of TLR2 and 4 and dose-dependent activation of p38MAPK-mediated inflammation.

conclusionsHMGB1 increase by fetal membrane cells in response to either oxidative stress or infection can provide a positive feedback loop generating non-infectious inflammatory activation. Activation of p38MAPK by HMGB1 promotes development of the senescence phenotype and senescence associated sterile inflammation. HMGB1 activity is an important regulator of the fetal inflammatory response regardless of infection.

Indexed as

Signal TransductionAmniotic FluidBlotting, WesternCells, CulturedCytokinesExtraembryonic MembranesFemaleGene Expression Regulation, DevelopmentalHMGB1 ProteinHumansInfant, NewbornInflammation MediatorsLipopolysaccharidesNF-kappa BObstetric Labor Complicationsp38 Mitogen-Activated Protein KinasesCytokinesHMGB1 ProteinInflammation MediatorsLipopolysaccharidesNF-kappa Bp38 Mitogen-Activated Protein KinasesReceptor for Advanced Glycation End ProductsReceptors, ImmunologicToll-Like Receptor 4

Identifiers

PMID25469638
PMCPMC4254744
OpenAlexW2033797039

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.