ArticlePlacenta2020
Stretch, scratch, and stress: Suppressors and supporters of senescence in human fetal membranes.
Article in Placenta, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- A call to standardize the nomenclature of human fetal membrane at the feto-maternal interface.Placenta · 2025Review
- Exposure to Extreme Heat Increases Preterm Birth Risk: Hypothetical Pathophysiological Mechanisms.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Microfluidic device successfully replaces traditional models of pregnancy associated drug pharmacokinetic studies.Pregnancy (Hoboken, N.J.) · 2025Article
- Modeling reproductive and pregnancy-associated tissues using organ-on-chip platforms: challenges, limitations, and the high throughput data frontier.Frontiers in bioengineering and biotechnology · 2025Review
- Role of Myofibroblasts in the Repair of Iatrogenic Preterm Membranes Subjected to Mechanical Stimulation.Prenatal diagnosis · 2025Article
- Modeling an ascending infection by Ureaplasma parvum and its cell signaling and inflammatory response at the feto-maternal interface.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- The role of extreme heat exposure on premature rupture of membranes in Southern California: A study from a large pregnancy cohort.Environment international · 2023Article
- Silencing P38 MAPK reduces cellular senescence in human fetal chorion trophoblast cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Microfluidic technology and simulation models in studying pharmacokinetics during pregnancy.Frontiers in pharmacology · 2023Article
- Adapting an organ-on-chip device to study the effect of fetal sex and maternal race/ethnicity on preterm birth related intraamniotic inflammation leading to fetal neuroinflammation.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022Article
- Testing of drugs using human feto-maternal interface organ-on-chips provide insights into pharmacokinetics and efficacy.Lab on a chip · 2022Article
- Epithelial to mesenchymal transition (EMT) of feto-maternal reproductive tissues generates inflammation: a detrimental factor for preterm birth.BMB reports · 2022Article
- Fetal membrane at the feto-maternal interface: An underappreciated and understudied intrauterine tissue.Placenta and reproductive medicine · 2022Article
- Generation and characterization of human Fetal membrane and Decidual cell lines for reproductive biology experiments†.Biology of reproduction · 2022Article
- Functional role and regulation of permeability-glycoprotein (P-gp) in the fetal membrane during drug transportation.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022Article
- The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Spontaneous preterm birth: Involvement of multiple feto-maternal tissues and organ systems, differing mechanisms, and pathways.Frontiers in endocrinology · 2022Review
- The Role of Innate Immune System in the Human Amniotic Membrane and Human Amniotic Fluid in Protection Against Intra-Amniotic Infections and Inflammation.Frontiers in immunology · 2021Review
- Modeling ascending infection with a feto-maternal interface organ-on-chip.Lab on a chip · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
introductionThroughout gestation, amnion membranes undergo mechanical and or physiological stretch, scratch, or stress which is withstood by repairing and remodeling processes to protect the growing fetus. At term, increased oxidative stress (OS) activates p38MAPK, induces senescence, and inflammation contributing to membrane dysfunction to promote labor. However, the signaling initiated by stretch and scratch is still unclear. This study compares the induction of p38MAPK mediated senescence by stretch, scratch, and stress in human amnion epithelial cells (AECs).
methodsPrimary AECs from term, not-in-labor, fetal membranes were cultured using the following conditions (N = 3); 1) CellFlex chambers with or without 20% biaxial stretch, 2) 8-well coverslips with or without scratch, and 3) cells exposed to cigarette smoke extract (CSE) inducing OS. p38MAPK (Western blot or immunocytochemistry), senescence activation, and inflammation (matrix metalloproteinases 9 [MMP9] activity-ELISA) were determined in cells exposed to various conditions. T-test and One-Way ANOVA was used to assess significance.
resultsBiological membrane extension, mimicked by 20% biaxial stretch of AEC, maintained an epithelial morphology and activated P-p38MAPK (P = 0.02) compared to the non-stretch controls, but did not induce senescence or MMP9 activation. AEC scratches were healed within 40-hrs, which included proliferation, migration, and cellular transitions aided by p38MAPK activation but not senescence. CSE induced OS increased p38MAPK (P = 0.018) activation, senescence (P = 0.019), and MMP9 (P = 0.02).
conclusionPhysiologic stretch and scratch experienced during gestation can cause p38MAPK activation without causing senescence or inflammation. This may be indicative of p38MAPK's role in tissue remodeling during pregnancy. Overwhelming OS, experienced at term, results in P-p38MAPK mediated senescence and inflammation to disrupt membrane remodeling.
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Registered trials
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