PloS one, 2011-07, Vol.6 (7), p.e22419
2011
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- Autor(en) / Beteiligte
- Titel
- Glucocorticoid regulation of astrocytic fate and function
- Ist Teil von
- PloS one, 2011-07, Vol.6 (7), p.e22419
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2011
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- Glial loss in the hippocampus has been suggested as a factor in the pathogenesis of stress-related brain disorders that are characterized by dysregulated glucocorticoid (GC) secretion. However, little is known about the regulation of astrocytic fate by GC. Here, we show that astrocytes derived from the rat hippocampus undergo growth inhibition and display moderate activation of caspase 3 after exposure to GC. Importantly, the latter event, observed both in situ and in primary astrocytic cultures is not followed by either early- or late-stage apoptosis, as monitored by stage I or stage II DNA fragmentation. Thus, unlike hippocampal granule neurons, astrocytes are resistant to GC-induced apoptosis; this resistance is due to lower production of reactive oxygen species (ROS) and a greater buffering capacity against the cytotoxic actions of ROS. We also show that GC influence hippocampal cell fate by inducing the expression of astrocyte-derived growth factors implicated in the control of neural precursor cell proliferation. Together, our results suggest that GC instigate a hitherto unknown dialog between astrocytes and neural progenitors, adding a new facet to understanding how GC influence the cytoarchitecture of the hippocampus.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0022419Titel-ID: cdi_plos_journals_1306252859
- Format
- –
- Schlagworte
- Aging - drug effects, Animals, Animals, Newborn, Apoptosis, Apoptosis - drug effects, Astrocytes, Astrocytes - cytology, Astrocytes - drug effects, Astrocytes - enzymology, Astrocytes - metabolism, Biology, Bone marrow, Brain, Brain architecture, Caspase, Caspase 3 - metabolism, Caspase-3, Cell fate, Cell Lineage - drug effects, Cell proliferation, Cell Proliferation - drug effects, Cells, Cultured, Culture Media, Conditioned - pharmacology, Cytokines, Cytokines - metabolism, Cytotoxicity, Deoxyribonucleic acid, DNA, DNA fragmentation, Enzyme Activation - drug effects, Gene expression, Gene Expression Profiling, Gene Expression Regulation, Developmental - drug effects, Glucocorticoids, Glucocorticoids - pharmacology, Granule cells, Growth factors, Health sciences, Hippocampus, Hippocampus - cytology, Mediation, Medicine, Mental depression, Musculoskeletal system, Neural stem cells, Neurogenesis, Neurogenesis - drug effects, Neurons, Neurons - cytology, Neurons - drug effects, Neurons - metabolism, Oxygen, Pathogenesis, Phenotype, Psychiatry, Rats, Reactive oxygen species, Receptors, Glucocorticoid - metabolism, RNA, Messenger - genetics, RNA, Messenger - metabolism, Rodents, Secretion, Stem cells, Steroids (Organic compounds), Stress (Psychology)