Stress-induced senescence in human and rodent astrocytes.

There is an increasing awareness that astrocytes, the most abundant cell type in the central nervous system, are critical mediators of brain homeostasis, playing multifunctional roles including buffering potassium ions, maintaining the blood–brain barrier, releasing growth factors, and regulating neurotransmitter levels. Defects in astrocyte function have been implicated in a variety of diseases including age-related diseases such Alzheimer's disease and Parkinson's disease. However, little is known about the age-related changes that occur in astrocytes and if these cells are able to generate a senescent phenotype in response to stress. In this report we have examined whether astrocytes can initiate a senescence program similar to that described in other cell types in response to a variety of stresses. Our results indicate that after oxidative stress, proteasome inhibition, or exhausted replication, human and mouse astrocytes show changes in several established markers of cellular senescence. Astrocytes appear to be more sensitive to oxidative stress than fibroblasts, suggesting that stress-induced senescence may be more pronounced in the brain than in other tissues.