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. Author manuscript; available in PMC: 2018 Aug 1.
Published in final edited form as: Curr Opin Neurobiol. 2017 May 29;45:113–120. doi: 10.1016/j.conb.2017.05.006

Figure 2.

Figure 2

Heterogeneity amongst reactive astrocytes. Following insult or injury, astrocytes enter a reactive state, characterized by changes in astrocyte morphology and gene expression. Depending on the stimulus, astrocytes can become neurotoxic A1 type reactive astrocytes, or neuroprotective A2 type reactive astrocytes. Neuroinflammatory stimuli, such as LPS, yield A1 reactive astrocytes, by activating microglia to secrete the inflammatory cytokines Il-1α, TNF, and C1q. A1 reactive astrocytes promote neurodegeneration and neurotoxicity, and are not synaptogenic. Interestingly, application of TGFβ and FGF can revert type A1 reactive astrocytes to a non-reactive state in vitro. Ischemia induces the formation of A2 reactive astrocytes, through an unknown mechanism. These astrocytes have a different gene signature from A1 reactive astrocytes, and secrete neurotrophic factors to promote neuroprotection and neural repair.