ArticleBiology of reproduction2019
Dexamethasone induces primary amnion epithelial cell senescence through telomere-P21 associated pathway†.
Article in Biology of reproduction, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Effect of Ethnicity on the Relationship Between Telomere Length and Metabolic Markers in Kuwait.The Journal of clinical endocrinology and metabolism · 2025Article
- Telomere shortening in middle-aged and elderly individuals with varying severities of obstructive sleep apnea.Scientific reports · 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 role of amniotic epithelial cells in preterm birth: mechanisms and clinical implications.Frontiers in cell and developmental biology · 2025Review
- Involvement of Inheritance in Determining Telomere Length beyond Environmental and Lifestyle Factors.Aging and disease · 2023Review
- 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
- Hormonal regulation of telomerase activity and hTERT expression in steroid-regulated tissues and cancer.Cancer cell international · 2022Review
- Cell Senescence and Central Regulators of Immune Response.International journal of molecular sciences · 2022Review
- Identification and validation of senescence-related genes in circulating endothelial cells of patients with acute myocardial infarction.Frontiers in cardiovascular medicine · 2022Article
- Influence of Glucocorticoids on Cellular Senescence Hallmarks in Osteoarthritic Fibroblast-like Synoviocytes.Journal of clinical medicine · 2021Article
- Article
- Editorial: The Role of the Fetal Membranes in Pregnancy and Birth.Frontiers in physiology · 2021Article
- Prolonged Glucocorticoid Exposure Does Not Accelerate Telomere Shortening in Cultured Human Fibroblasts.Genes · 2020Article
- Novel pathways of inflammation in human fetal membranes associated with preterm birth and preterm pre-labor rupture of the membranes.Seminars in immunopathology · 2020Review
- Cellular senescence mediates the detrimental effect of prenatal dexamethasone exposure on postnatal long bone growth in mouse offspring.Stem cell research & therapy · 2020Article
- Human geroprotector discovery by targeting the converging subnetworks of aging and age-related diseases.GeroScience · 2020Article
- Oxidative stress-induced downregulation of glycogen synthase kinase 3 beta in fetal membranes promotes cellular senescence†.Biology of reproduction · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Dexamethasone (Dex), a corticosteroid hormone, is used during the perinatal period to help fetal lung and other organ development. Conversely, Dex-induced cell proliferation has been associated with accelerated aging. Using primary amnion epithelial cells (AECs) from term, not in labor, fetal membranes, we tested the effects of Dex on cell proliferation, senescence, and inflammation. Primary AECs treated with Dex (100 and 200 nM) for 48 h were tested for cell viability (crystal violet dye exclusion), cell cycle progression and/or type of cell death (flow cytometry), expression patterns of steroid receptors (glucocorticoid receptor, progesterone receptor membrane component 1&2), inflammatory mediators (IL-6 and IL-8), and telomere length (quantitative RT-PCR). Mechanistic mediators of senescence (p38MAPK and p21) were determined by western blot analysis. Dex treatment did not induce AEC proliferation, cell cycle, influence viability, or morphology. However, Dex caused dependent telomere length reduction and p38MAPK-independent but p21-dependent (confirmed by treatment with p21 inhibitor UC2288). Senescence was not associated with an increase in inflammatory mediators, which is often associated with senescence. Co-treatment with RU486 produced DNA damage, cell cycle arrest, and cellular necrosis with an increase in inflammatory mediators. The effect of Dex was devoid of changes to steroid receptors, whereas RU486 increased GR expression. Dex treatment of AECs produced nonreplicative and noninflammatory senescence. Extensive use of Dex during the perinatal period may lead to cellular senescence, contributing to cellular aging associated pathologies during the perinatal and neonatal periods.
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Registered trials
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