ArticleBiology of reproduction2018
Oxidative stress-induced TGF-beta/TAB1-mediated p38MAPK activation in human amnion epithelial cells.
Article in Biology of reproduction, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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
40 citing papers in PubMed, 49 citations in OpenAlex.
- Correlation between hyperuricemia and coronary artery calcification.The Journal of international medical research · 2026Review
- Polystyrene nanoplastics promotes inflammation and aging in young mice through the oral-gut microbiome axis.Frontiers in immunology · 2026Article
- 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
- 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
- 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
- Oxidative stress on vessels at the maternal-fetal interface for female reproductive system disorders: Update.Frontiers in endocrinology · 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
- Epithelial to mesenchymal transition (EMT) of feto-maternal reproductive tissues generates inflammation: a detrimental factor for preterm birth.BMB reports · 2022Article
- Contemporary perspectives on heterotopic ossification.JCI insight · 2022Review
- Fetal membrane at the feto-maternal interface: An underappreciated and understudied intrauterine tissue.Placenta and reproductive medicine · 2022Article
- Single cell transcriptomic analysis of human amnion identifies cell-specific signatures associated with membrane rupture and parturition.Cell & bioscience · 2022Article
- Spontaneous preterm birth: Involvement of multiple feto-maternal tissues and organ systems, differing mechanisms, and pathways.Frontiers in endocrinology · 2022Review
- Fetal Lung-Derived Exosomes in Term Labor Amniotic Fluid Induce Amniotic Membrane Senescence.Frontiers in cell and developmental biology · 2022Article
- Platelet-Activating Factor Promotes the Development of Non-Alcoholic Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2022Review
- Discoidin domain receptor 2 activation of p38 mitogen-activated protein kinase as an important pathway for osteonectin-regulating osteoblast mineralization.Journal of orthopaedic surgery and research · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Term and preterm parturition are associated with oxidative stress (OS)-induced p38 mitogen-activated protein kinase (p38MAPK)-mediated fetal tissue (amniochorion) senescence. p38MAPK activation is a complex cell- and stimulant-dependent process. Two independent pathways of OS-induced p38MAPK activation were investigated in amnion epithelial cells (AECs) in response to cigarette smoke extract (CSE: a validated OS inducer in fetal cells): (1) the OS-mediated oxidation of apoptosis signal-regulating kinase (ASK)-1 bound Thioredoxin (Trx[SH]2) dissociates this complex, creating free and activated ASK1-signalosome and (2) transforming growth factor-mediated activation of (TGF)-beta-activated kinase (TAK)1 and TGF-beta-activated kinase 1-binding protein (TAB)1. AECs isolated from normal term, not-in-labor fetal membranes increased p38MAPK in response to CSE and downregulated it in response to antioxidant N-acetylcysteine. In AECs, both Trx and ASK1 were localized; however, they remained dissociated and not complexed, regardless of conditions. Silencing either ASK1 or its downstream effectors (MKK3/6) did not affect OS-induced p38MAPK activation. Conversely, OS increased TGF-beta's release from AECs and increased phosphorylation of both p38MAPK and TAB1. Silencing of TAB1, but not TAK1, prevented p38MAPK activation, which is indicative of TAB1-mediated autophosphorylation of p38MAPK, an activation mechanism seldom seen. OS-induced p38MAPK activation in AECs is ASK1-Trx signalosome-independent and is mediated by the TGF-beta pathway. This knowledge will help to design strategies to reduce p38MAPK activation-associated pregnancy risks.
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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 Socratic graph.