ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2018
A distinct mechanism of senescence activation in amnion epithelial cells by infection, inflammation, and oxidative stress.
Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- 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
- P-glycoprotein exofection between fetal and maternal cells as a mechanism of intercellular material transfer at the feto maternal interface.bioRxiv : the preprint server for biology · 2026Article
- 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) · 2025Article
- Cell cycle regulation by the ribotoxic stress response.Trends in cell biology · 2025Review
- Placental Inflammation in Preterm Premature Rupture of Membranes and Risk of Neurodevelopmental Disorders.Cells · 2025Review
- The Profile of Selected Protein Markers of Senescence in the Placentas of Cows During Early-Mid-Pregnancy and Parturition with and Without the Retention of Fetal Membranes: A Preliminary Study.International journal of molecular sciences · 2025Article
- The Impacts of TNF-α-Induced Inflammation on Amnion Epithelial Cells: Exploring Stem Cell Gene Expression, Senescence, Inflammatory Responses, and Cellular Transition.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Article
- The role of amniotic epithelial cells in preterm birth: mechanisms and clinical implications.Frontiers in cell and developmental biology · 2025Review
- miR-548az-5p induces amniotic epithelial cell senescence by regulating KATNAL1 expression in labor.Scientific reports · 2024Article
- A multi-organ, feto-maternal interface organ-on-chip, models pregnancy pathology and is a useful preclinical extracellular vesicle drug trial platform.Extracellular vesicle · 2024Article
- Copper and zinc deficiency to the risk of preterm labor in pregnant women: a case-control study.BMC pregnancy and childbirth · 2023Article
- A Microphysiological Device to Model the Choriodecidual Interface Immune Status during Pregnancy.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Chlamydia trachomatis antigen induces TLR4-TAB1-mediated inflammation, but not cell death, in maternal decidua cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Silencing P38 MAPK reduces cellular senescence in human fetal chorion trophoblast cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2023Article
- Review on new approach methods to gain insight into the feto-maternal interface physiology.Frontiers in medicine · 2023Review
- 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
- Stress signaler p38 mitogen-activated kinase activation: a cause for concern?Clinical science (London, England : 1979) · 2022Article
- Propofol protects against lipopolysaccharide-induced inflammatory response in human amnion-derived WISH cells.Journal of dental anesthesia and pain medicine · 2022Article
- New approaches suggest term and preterm human fetal membranes may have distinct biomechanical properties.Scientific reports · 2022Article
- Differences in cord blood extracellular vesicle cargo in preterm and term births.American journal of reproductive immunology (New York, N.Y. : 1989) · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
problemWe investigated p38MAPK activation-induced fetal membrane cell senescence in response to inflammation (tumour necrosis factor-alpha [TNF-α]) and infection (lipopolysaccharide [LPS]), factors associated with spontaneous preterm birth. METHOD OF STUDY: Primary amnion epithelial cells (AECs) were exposed to TNF-α, 50 ng/mL and LPS, 100 ng/mL. Cigarette smoke extract (CSE), a known OS inducer, was used as positive control. AECs were cotreated with the antioxidant N-acetyl cysteine (NAC) and p38MAPK inhibitor SB203580 to determine the effect of OS and p38MAPK. Western blot analysis was performed for active (Phospho-p38MAPK) and total p38MAPK. Senescence was determined by flow cytometry, and culture supernatants were tested for IL-6 using ELISA.
resultsTNF-α, but not LPS, increased p38MAPK activation compared to untreated cells (P = .01). The number of senescent cells and senescence-associated IL-6 was higher in both TNF-α and LPS-treated cells compared to control (P = .001, P = .01, respectively). Antioxidant NAC inhibited p38MAPK activation by TNF-α. p38MAPK inhibitor SB203580 reduced the development of senescence and IL-6 by TNF-α and LPS. CSE treatment validated our current data.
conclusionTNF-α caused OS-mediated p38MAPK induction, senescence, and IL-6 increase from AECs. LPS also induced senescence and IL-6 increase. Inflammatory and infectious factors may cause premature fetal cell senescence contributing to preterm birth pathophysiology.
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