Evidence map›Paper›PMID 29941169›Full record

ArticlePlacenta2018

Oxidative stress induces p38MAPK-dependent senescence in the feto-maternal interface cells.

Jin Jin, Lauren Richardson, Samantha Sheller-Miller, Nanbert Zhong, Ramkumar Menon

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Placenta, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06280560 (Impact of Controlled Ovarian Stimulation and Luteal Phase Support on Endometrial Receptivity and Endometrial Senescent Cell Pathological Accumulation), which is not on this map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.6field-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.

NCT06280560 recruitingnot on this mapstarted 2024, after this paper: background citation

Impact of Controlled Ovarian Stimulation and Luteal Phase Support on Endometrial Receptivity and Endometrial Senescent Cell Pathological Accumulation: Pilot Study

Typeobservational_patient_registrySponsorFundación IVIRan2024 to 2025Enrolled60ConditionsEndometrial ReceptivityArmsControlled Ovarian Stimulation + Luteal Phase Support, Hormonal Replacement Therapy programmed artificial cycle, Natural Cycle (NC), Endometrial receptivity reference group
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
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  7. 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
    Article
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  9. Review
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  13. 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
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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

5 authors at 3 institutions in 2 countries.

Jin JinDepartment of Gynecology and Obstetrics, Nanfang Hospital, Southern Medical University, No.1838, North Guangzhou Avenue, Guangzhou, 510515, China; Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine and Perinatal Research, The University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Lauren RichardsonDepartment of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine and Perinatal Research, The University of Texas Medical Branch at Galveston, Galveston, TX, USA; Department of Neuroscience, Cell Biology, and Anatomy, The University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Samantha Sheller-MillerDepartment of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine and Perinatal Research, The University of Texas Medical Branch at Galveston, Galveston, TX, USA; Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch at Galveston, Galveston, TX, USA.
Nanbert ZhongNew York State Institute for Basic Research in Development Disabilities, New York, NY, 10314, USA.
Ramkumar MenonDepartment of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine and Perinatal Research, The University of Texas Medical Branch at Galveston, Galveston, TX, USA. Electronic address: ram.menon@utmb.edu.
The University of Texas Medical Branch at Galveston · USNanfang Hospital · CNNew York State Office for People With Developmental Disabilities · 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
ROS-Induced p38 MAPK activation: A Novel Pathway to Preterm BirthR03HD086354 · NICHD · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MENON, RAMKUMAR · 2016 to 2017
$155k
NICHD NIH HHS R01 HD084532NICHD NIH HHS R03 HD086354NIEHS NIH HHS T32 ES007254
6 · The paper itself

Abstract

objectiveThis study tested the mechanism of the oxidative stress (OS)-induced senescence pathway at the feto-maternal interface cells.

methodsPrimary amnion mesenchymal cells (AMCs), chorion and decidual cells isolated from the placental membranes of women at normal term (not in labor) were exposed to OS-inducing cigarette smoke extract (CSE) for 48 h. Reactive oxygen species (ROS) was measured using 2'7'-dichlorodihydrofluorescein. Western blot analysis determined phosphorylated (P) p38MAPK and p53 expression. Senescence-associated β-Galactosidase (SA-β-Gal) and matrix metallopeptidase 9 (MMP9) histochemistry were used to measure senescence and inflammation respectively. Cotreatment of cells with the antioxidant, N-acetyl cysteine (NAC), or the p38MAPK inhibitor, SB203580 (SB), verified the activation specificity.

resultsCSE increased ROS production from AMCs, chorion cells, and decidual cells (P < 0.05) compared to controls. Western blot analysis determined that CSE induced p38MAPK activation (P < 0.05) and cotreatment with NAC inhibited ROS production and p38MAPK activation (P < 0.05) in all cell types. CSE did not increase p53 phosphorylation in any of the cells; however, AMCs showed constitutive P-p53 expression. CSE increased senescence in AMCs and chorion cells compared to controls (P = 0.01 and P = 0.003, respectively); however, senescence was not observed in decidual cells. Senescence was significantly reduced following cotreatment with SB and NAC (AMCs; P = 0.01 and chorion; P = 0.009). CSE increased MMP9 in all cells that was reduced by NAC.

conclusionOS induced p38MAPK activation and inflammation in all cell types that was associated with senescence in fetal cells but not in maternal cells.

Indexed as

Cellular SenescenceAmnionCells, CulturedDeciduaEpithelial CellsFemaleHumansMaternal-Fetal RelationsNicotianaOxidative Stressp38 Mitogen-Activated Protein KinasesPlacentaPregnancyReactive Oxygen SpeciesSmokeStromal Cellsp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesSmokeAmnion mesenchymal cellsChorionDeciduaOxidative stressp38MAPKSenescence

Identifiers

PMID29941169
PMCPMC6023622
OpenAlexW2804972494

What OpenQuestion holds

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Registered trials

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.