ArticleThe American journal of pathology2024
Histologic Evidence of Epithelial-Mesenchymal Transition and Autophagy in Human Fetal Membranes.
Article in The American journal of pathology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Identification of cell senescence-related genes in spontaneous preterm birth based on bioinformatics analysis and machine learning.PloS one · 2026Article
- 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
- IL-1β stimulates ADAMTS9 expression and contributes to preterm prelabor rupture of membranes.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
- The role of amniotic epithelial cells in preterm birth: mechanisms and clinical implications.Frontiers in cell and developmental biology · 2025Review
- Acute exposure to electronic cigarette components alters mRNA expression of pre-osteoblasts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Identification of circRNA Expression Profile and Potential Systemic Immune Imbalance Modulation in Premature Rupture of Membranes.Analytical cellular pathology (Amsterdam) · 2024Article
- Spatial transcriptomics of fetal membrane-Decidual interface reveals unique contributions by cell types in term and preterm births.PloS one · 2024Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
Abstract
Preterm, prelabor rupture of the human fetal membranes (pPROM) is involved in 40% of spontaneous preterm births worldwide. Cellular-level disturbances and inflammation are effectors of membrane degradation, weakening, and rupture. Maternal risk factors induce oxidative stress (OS), senescence, and senescence-associated inflammation of the fetal membranes as reported mechanisms related to pPROM. Inflammation can also arise in fetal membrane cells (amnion/chorion) due to OS-induced autophagy and epithelial-mesenchymal transition (EMT). Autophagy, EMT, and their correlation in pPROM, along with OS-induced autophagy-related changes in amnion and chorion cells in vitro, were investigated. Immunocytochemistry staining of cytokeratin-18 (epithelial marker)/vimentin (mesenchymal marker) and proautophagy-inducing factor LC3B were performed in fetal membranes from pPROM, term not in labor, and term labor. Ultrastructural changes associated with autophagy were verified by transmission electron microscopy of the fetal membranes and in cells exposed to cigarette smoke extract (an OS inducer). EMT and LC3B staining was compared in the chorion from pPROM versus term not in labor. Transmission electron microscopy confirmed autophagosome formation in pPROM amnion and chorion. In cell culture, autophagosomes were formed in the amnion with OS treatment, while autophagosomes were accumulated in both cell types with autophagy inhibition. This study documents the association between pPROMs and amniochorion autophagy and EMT, and supports a role for OS in inducing dysfunctional cells that increase inflammation, predisposing membranes to rupture.
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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.