ArticleCell death & disease2010
Glucocorticoids induce long-lasting effects in neural stem cells resulting in senescence-related alterations.
Article in Cell death & disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 107 citations in OpenAlex.
- 'Glucocorticoids, Cushing's syndrome and cellular senescence: a mechanistic link to metabolic ageing'.Endocrine connections · 2026Review
- Inhibiting glucocorticoid receptors enhances adult spinal cord neural stem cell activity and improves outcomes in spinal cord injury.Communications biology · 2026Article
- The Etiological Role of Impaired Neurogenesis in Schizophrenia: Interactions with Inflammatory, Microbiome and Hormonal Signaling.International journal of molecular sciences · 2025Review
- Senolytic treatment for low back pain.Science advances · 2025Article
- Translational implications of circadian activity alterations in an experimental model of late-onset depression induced by prenatal excess of glucocorticoids.Frontiers in behavioral neuroscience · 2025Review
- Elevated glucocorticoid alters the developmental dynamics of hypothalamic neurogenesis in zebrafish.Communications biology · 2024Article
- Glucocorticoid effects on the brain: from adaptive developmental plasticity to allostatic overload.The Journal of experimental biology · 2024Review
- Emerging roles of mitochondrial functions and epigenetic changes in the modulation of stem cell fate.Cellular and molecular life sciences : CMLS · 2024Review
- Selenium suppressed the LPS-induced oxidative stress of bovine endometrial stromal cells through Nrf2 pathway with high cortisol background.Journal of animal science · 2024Article
- Review
- A Novel Methodology Using Dexamethasone to Induce Neuronal Differentiation in the CNS-Derived Catecholaminergic CAD Cells.Cellular and molecular neurobiology · 2022Article
- Glyphosate-based herbicide induces long-lasting impairment in neuronal and glial differentiation.Environmental toxicology · 2022Article
- Antenatal Dexamethasone Treatment Induces Sex-dependent Upregulation of NTPDase1/CD39 and Ecto-5'-nucleotidase/CD73 in the Rat Fetal Brain.Cellular and molecular neurobiology · 2022Article
- Protective Effect of Human Umbilical Cord Mesenchymal Stem Cells in Glucocorticoid-induced Osteonecrosis of Femoral Head.Current medical science · 2021Article
- Dermal Olfactory Receptor OR51B5 Is Essential for Survival and Collagen Synthesis in Human Dermal Fibroblast (Hs68 Cells).International journal of molecular sciences · 2021Article
- Glucocorticoid receptor triggers a reversible drug-tolerant dormancy state with acquired therapeutic vulnerabilities in lung cancer.Nature communications · 2021Article
- Sirt7-p21 Signaling Pathway Mediates Glucocorticoid-Induced Inhibition of Mouse Neural Stem Cell Proliferation.Neurotoxicity research · 2021Article
- Argentic staining reveals changes in cerebellar tissue organisation by prenatal glucocorticoid administration in rats.Histology and histopathology · 2021Article
- The Effects of Early Life Stress on the Brain and Behaviour: Insights From Zebrafish Models.Frontiers in cell and developmental biology · 2021Review
- The role of omega-3 fatty acids in preventing glucocorticoid-induced reduction in human hippocampal neurogenesis and increase in apoptosis.Translational psychiatry · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations in intrauterine programming occurring during critical periods of development have adverse consequences for whole-organ systems or individual tissue functions in later life. In this paper, we show that rat embryonic neural stem cells (NSCs) exposed to the synthetic glucocorticoid dexamethasone (Dex) undergo heritable alterations, possibly through epigenetic mechanisms. Exposure to Dex results in decreased NSC proliferation, with no effects on survival or differentiation, and changes in the expression of genes associated with cellular senescence and mitochondrial functions. Dex upregulates cell cycle-related genes p16 and p21 in a glucocorticoid receptor(GR)-dependent manner. The senescence-associated markers high mobility group (Hmg) A1 and heterochromatin protein 1 (HP1) are also upregulated in Dex-exposed NSCs, whereas Bmi1 (polycomb ring finger oncogene) and mitochondrial genes Nd3 (NADH dehydrogenase 3) and Cytb (cytochrome b) are downregulated. The concomitant decrease in global DNA methylation and DNA methyltransferases (Dnmts) suggests the occurrence of epigenetic changes. All these features are retained in daughter NSCs (never directly exposed to Dex) and are associated with a higher susceptibility to oxidative stress, as shown by the increased occurrence of apoptotic cell death on exposure to the redox-cycling reactive oxygen species (ROS) generator 2,3-dimethoxy-1-naphthoquinone (DMNQ). Our study provides novel evidence for programming effects induced by glucocorticoids (GCs) on NSCs and supports the idea that fetal exposure to endogenous or exogenous GCs is likely to result in long-term consequences that may predispose to neurodevelopmental and/or neurodegenerative disorders.
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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.