Glucocorticoid regulation of astrocytic fate and function
| Autor: | Yu, Shuang, Yang, Silei, Holsboer, F., Sousa, Nuno, Almeida, O. F. X. |
|---|---|
| Přispěvatelé: | Universidade do Minho |
| Rok vydání: | 2011 |
| Předmět: |
Aging
Neurogenesis lcsh:Medicine Apoptosis Hippocampus Receptors Glucocorticoid Molecular Cell Biology Neurobiology of Disease and Regeneration Animals Cell Lineage RNA Messenger lcsh:Science Glucocorticoids Biology Cells Cultured Cell Proliferation Cellular Stress Responses Neurons Psychiatry Science & Technology Cell Death Caspase 3 Mood Disorders Gene Expression Profiling lcsh:R Gene Expression Regulation Developmental Rats Enzyme Activation Phenotype Mental Health Animals Newborn Astrocytes Culture Media Conditioned Cytokines Medicine lcsh:Q Research Article Neuroscience |
| Zdroj: | PLoS ONE Repositório Científico de Acesso Aberto de Portugal Repositório Científico de Acesso Aberto de Portugal (RCAAP) instacron:RCAAP PLoS ONE, Vol 6, Iss 7, p e22419 (2011) |
| ISSN: | 1932-6203 |
| Popis: | 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. S. Yu was supported by a fellowship from the Max Planck Society. This study was supported by the Max Planck Institute of Psychiatry and by grants from the German Academic Exchange Service (DAAD) and the Portuguese Rectors' Conference (CRUP), and an Integrated Project grant from the European Commission (CRESCENDO, Contract No. LSHM-CT-2005-01852). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|