ArticleAmerican journal of reproductive immunology (New York, N.Y. : 1989)2023
Silencing P38 MAPK reduces cellular senescence in human fetal chorion trophoblast cells.
Article in American journal of reproductive immunology (New York, N.Y. : 1989), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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
18 citing papers in PubMed, 18 citations in OpenAlex.
- Mitochondrial dysfunction and cellular senescence drive accelerated gestational aging in spontaneous preterm birth: a narrative review.Apoptosis : an international journal on programmed cell death · 2026Review
- Heterogeneity in inflammatory responses to endotoxin at the fetomaternal interface.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Dasatinib and quercetin mitigate radiation-induced lung injury by eliminating senescent cells in a rat model.Frontiers in pharmacology · 2026Article
- A call to standardize the nomenclature of human fetal membrane at the feto-maternal interface.Placenta · 2025Review
- Cell cycle regulation by the ribotoxic stress response.Trends in cell biology · 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
- Nuclear Translocation of S100A9 Triggers Senescence of Human Amnion Fibroblasts by De-Repressing LINE1 Via Heterochromatin Erosion at Parturition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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
- 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
- Chorionic trophoblast cells demonstrate functionally different phenotypes from placental trophoblasts†.Biology of reproduction · 2025Article
- Determining Sex-Specific Gene Expression Differences in Human Chorion Trophoblast Cells.International journal of molecular sciences · 2025Article
- miR-548az-5p induces amniotic epithelial cell senescence by regulating KATNAL1 expression in labor.Scientific reports · 2024Article
- PGRMC2 and HLA-G regulate immune homeostasis in a microphysiological model of human maternal-fetal membrane interface.Communications biology · 2024Article
- Enhancing adipose tissue functionality in obesity: senotherapeutics, autophagy and cellular senescence as a target.Biological research · 2024Review
- Establishment and comparison of human term placenta-derived trophoblast cells†.Biology of reproduction · 2024Article
- Histologic Evidence of Epithelial-Mesenchymal Transition and Autophagy in Human Fetal Membranes.The American journal of pathology · 2024Article
- Review
- Autophagy Determines Distinct Cell Fates in Human Amnion and Chorion Cells.Autophagy reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
problemAmniochorion senescence generates mechanistic signals to initiate parturition. Activation of p38 mitogen-activated kinase (MAPK) in fetal amnion cells is a key mediator of senescence as well as epithelial-mesenchymal transition (EMT) of amnion cells. However, the impact of p38 MAPK in chorion trophoblast cells (CTCs) is unclear. We tested if eliminating p38 will reduce oxidative stress (OS) induced cell fates like cellular senescence, EMT, and inflammation induced by these processes in CTCs.
methodsp38MAPK in CTCs was silenced using CRISPR/Cas9. OS was evoked by cigarette smoke extract (CSE) exposure. EMT was evoked by transforming growth factor (TGF)-ß treatment. Cell cycle, senescence, EMT, and inflammation were analyzed.
resultsCSE-induced changes in the cell cycle were not seen in p38KO CTCs compared to WT cells. OS induced by CSE evoked senescence and senescence-associated secretory phenotype (SASP as indicated by IL-6 and IL-8 increase) in WT but not in p38MAPK KO CTCs. No changes were noted in HLA-G expression regardless of the status of p38MAPK. Neither CSE nor TGF-ß evoked EMT in either WT or p38 KO CTCs.
conclusionSenescence and senescence-associated inflammation in human fetal CTCs are mediated by p38MAPK. Compared to amnion epithelial cells, CTCs are resistant to EMT. This refractoriness may help them to maintain the barrier functions at the choriodecidual interface.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.