tissue and inflammatory cells. This is usually found after a rapid, locally triggered inflammatory response to acute traumatic injury in the spinal cord and brain. In its extreme form, reactive astrogliosis can lead to the appearance of newly proliferated astrocytes and scar formation in response to severe tissue damage or inflammation. Molecular triggers that lead to this scar formation include epidermal growth factor (EGF), fibroblast growth factor (FGF), endothelin 1 and adenosine triphosphate (ATP). Mature astrocytes can re-enter the cell cycle and proliferate during scar formation. Some proliferating reactive astrocytes can derive from NG2 progenitor cells in the local parenchyma from ependymal cell progenitors after injury or stroke. There are also multipotent progenitors in subependymal tissue that express glial fibrillary acidic protein (GFAP) and generate progeny cells that migrate towards sites of injury after trauma or stroke. Regulation of inflammation Reactive astrocytes are related to the normal function of astrocytes. Astrocytes are involved in the complex regulation of CNS inflammation that is likely to be context-dependent and regulated by multimodal extra- and intracellular signaling events. They have the capacity to make different types of molecules with either pro- or anti-inflammatory potential in response to different types of stimulation. Astrocytes interact extensively with microglia and play a key role in CNS inflammation. Reactive astrocytes can then lead to abnormal function of astrocytes and affect their regulation and response to inflammation. Pertaining to anti-inflammatory effects, reactive scar-forming astrocytes help reduce the spread of inflammatory cells during locally initiated inflammatory responses to traumatic injury or during peripherally-initiated adaptive immune responses. In regard to pro-inflammatory potential, certain molecules in astrocytes are associated with an increase in inflammation after traumatic injury. At early stages after insults, astrocytes not only activate inflammation, but also form potent cell migration barriers over time. These barriers mark areas where intense inflammation is needed and restrict the spread of inflammatory cells and infectious agents to nearby healthy tissue. CNS injury responses have favored mechanisms that keep small injuries uninfected. Inhibition of the migration of inflammatory cells and infectious agents have led to the accidental byproduct of axon regeneration inhibition, owing to the redundancy between migration cues across cell types. Biological mechanisms Changes resulting from astrogliosis are regulated in a context-specific manner by specific signaling events that have the potential to modify both the nature and degree of these changes. Under different conditions of stimulation, astrocytes can produce intercellular effector molecules