ArticlePloS one2013
Senescence of primary amniotic cells via oxidative DNA damage.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 111 citations in OpenAlex.
- 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 · 2020Pooled it
- Systematic review of p38 mitogen-activated kinase and its functional role in reproductive tissues.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018Pooled it
- MicroRNA-548 regulates high mobility group box 1 expression in patients with preterm birth and chorioamnionitis.Scientific reports · 2019Trial
- From Stress to Survival: Trophoblast-Derived Extracellular Vesicle Proteome Captures Aspirin-Driven Cellular Reprogramming in a Preeclampsia Model.Pharmaceutics · 2026Article
- Heat-Induced Pathophysiological and Metabolic Changes at the Feto-Maternal Interface Predisposing to Preterm Birth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Fetal response to maternal exposures of environmental chemicals: Utility of a four-cell human feto-maternal interface organ-on-chip.Chemico-biological interactions · 2025Article
- Regulatory Interplay of p53, AMPK, and mTOR in Decidualization: Implications for Reproductive Competence and Cancer Biology.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- Exposure to Extreme Heat Increases Preterm Birth Risk: Hypothetical Pathophysiological Mechanisms.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Do progesterone receptor membrane components (PGRMC)s play a role in the chorions refractoriness to epithelial-to-mesenchymal transition (EMT)?Journal of reproductive immunology · 2025Article
- The effect of Polybrominated diphenyl ethers at the fetal blood-brain-barrier: evaluation using a microphysiological system.Frontiers in cell and developmental biology · 2025Article
- A dynamic flow fetal membrane organ-on-a-chip system for modeling the effects of amniotic fluid motion.Biomedical microdevices · 2024Article
- A Dynamic Flow Fetal Membrane Organ-on-a-Chip System for Modeling the Effects of Amniotic Fluid Motion.Research square · 2024Article
- Histologic Evidence of Epithelial-Mesenchymal Transition and Autophagy in Human Fetal Membranes.The American journal of pathology · 2024Article
- Frontiers in the Etiology and Treatment of Preterm Premature Rupture of Membrane: From Molecular Mechanisms to Innovative Therapeutic Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Autophagy Determines Distinct Cell Fates in Human Amnion and Chorion Cells.Autophagy reports · 2024Article
- Mitigating Oxidative Stress in Perinatal Cells: A Critical Step toward an Optimal Therapeutic Use in Regenerative Medicine.Biomolecules · 2023Review
- Measuring DNA modifications with the comet assay: a compendium of protocols.Nature protocols · 2023Review
- The Role of Fetal Membranes during Gestation, at Term, and Preterm Labor.Placenta and reproductive medicine · 2023Article
- Silencing P38 MAPK reduces cellular senescence in human fetal chorion trophoblast cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Recommendations from the COST action CA17116 (SPRINT) for the standardization of perinatal derivative preparation andFrontiers in bioengineering and biotechnology · 2023Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOxidative stress is a postulated etiology of spontaneous preterm birth (PTB) and preterm prelabor rupture of the membranes (pPROM); however, the precise mechanistic role of reactive oxygen species (ROS) in these complications is unclear. The objective of this study is to examine impact of a water soluble cigarette smoke extract (wsCSE), a predicted cause of pregnancy complications, on human amnion epithelial cells.
methodsAmnion cells isolated from fetal membranes were exposed to wsCSE prepared in cell culture medium and changes in ROS levels, DNA base and strand damage was determined by using 2'7'-dichlorodihydro-fluorescein and comet assays as well as Fragment Length Analysis using Repair Enzymes (FLARE) assays, respectively. Western blot analyses were used to determine the changes in mass and post-translational modification of apoptosis signal-regulating kinase (ASK1), phospho-p38 (P-p38 MAPK), and p19(arf). Expression of senescence-associated β-galectosidase (SAβ-gal) was used to confirm cell ageing in situ.
resultsROS levels in wsCSE-exposed amnion cells increased rapidly (within 2 min) and significantly (p<0.01) at all-time points, and DNA strand and base damage was evidenced by comet and FLARE assays. Activation of ASK1, P-p38 MAPK and p19(Arf) correlated with percentage of SAβ-gal expressing cells after wsCSE treatment. The antioxidant N-acetyl-L-cysteine (NAC) prevented ROS-induced DNA damage and phosphorylation of p38 MAPK, whereas activation of ASK1 and increased expression of p19(Arf) were not significantly affected by NAC.
conclusionsThe findings support the hypothesis that compounds in wsCSE induces amnion cell senescence via a mechanism involving ROS and DNA damage. Both pathways may contribute to PTB and pPROM. Our results imply that antioxidant interventions that control ROS may interrupt pathways leading to pPROM and other causes of PTB.
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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.