Role of astrocyte elevated gene-1 (AEG-1) in reactive astrogliosis. Central nervous system (CNS) insults ranging from mild cellular disturbances to severe tissue damage and cell death lead to release of molecular mediators of reactive astrogliosis such as inflammatory cytokines interleukin 1β (IL-1β), tumor necrosis factor α (TNFα) and molecules of oxidative stress such as reactive oxygen species (ROS). These mediators in turn activate the local healthy astrocyte population by inducing a spectrum of changes in the microenvironment and intracellular signaling pathways resulting into reactive astrogliosis. Injury triggers increased AEG-1 localization to the cytoplasmic regions and the dense fibrillar nuclear regions of the astrocyte. This change in intracellular localization of AEG-1 in astrocytes undergoing reactive astrogliosis is a plausible mechanism of AEG-1-mediated regulation of astrocyte proliferation and migration during reactive astrogliosis.