ArticleClinical science (London, England : 1979)2022
Stress signaler p38 mitogen-activated kinase activation: a cause for concern?
Article in Clinical science (London, England : 1979), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- 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
- A Review of the Potential Use of Antioxidants in Spinal Cord Injuries.Antioxidants (Basel, Switzerland) · 2025Review
- 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
- Acidosis-induced p38-kinase activation triggers an IL-6-mediated crosstalk of renal proximal tubule cells with fibroblasts leading to their inflammatory response.Cell communication and signaling : CCS · 2025Article
- Lead exposure at the feto-maternal interface: a cause for concern for fetal membrane trophoblasts.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- miR-548az-5p induces amniotic epithelial cell senescence by regulating KATNAL1 expression in labor.Scientific reports · 2024Article
- Histologic Evidence of Epithelial-Mesenchymal Transition and Autophagy in Human Fetal Membranes.The American journal of pathology · 2024Article
- Spatial transcriptomics of fetal membrane-Decidual interface reveals unique contributions by cell types in term and preterm births.PloS one · 2024Article
- The Potential of Senescence as a Target for Developing Anticancer Therapy.International journal of molecular sciences · 2023Review
- Review on new approach methods to gain insight into the feto-maternal interface physiology.Frontiers in medicine · 2023Review
- Significance of the p38MAPK-CRP2 axis in myofibroblastic phenotypic transition.Cell structure and function · 2023Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
Oxidative stress (OS) induced activation of p38 mitogen-activated kinase (MAPK) and cell fate from p38 signaling was tested using the human fetal membrane's amnion epithelial cells (AEC). We created p38 KO AEC using the CRISPR/Cas9 approach and tested cell fate in response to OS on an AEC-free fetal membrane extracellular matrix (ECM). Screening using image CyTOF indicated OS causing epithelial-mesenchymal transition (EMT). Further testing revealed p38 deficiency prevented AEC senescence, EMT, cell migration, and inflammation. To functionally validate in vitro findings, fetal membrane-specific conditional KO (cKO) mice were developed by injecting Cre-recombinase encoded exosomes intra-amniotically into p38αloxP/loxP mice. Amnion membranes from p38 cKO mice had reduced senescence, EMT, and increased anti-inflammatory IL-10 compared with WT animals. Our study suggested that overwhelming activation of p38 in response to OS inducing risk exposures can have an adverse impact on cells, cause cell invasion, inflammation, and ECM degradation detrimental to tissue homeostasis.
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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.