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Fig. 1. Astrocytes are associated with non-cell autonomous motor neuronal damage in ALS. For example, cellular stresses elevate Bcl-xl gene expression in astrocytes, and the increase level of mitochondrial Bcl-xl prevents oxidative damage in astrocytes under ALS condition. Meanwhile, the increased iNOS/NOS2 expression and the decreased EAAT2/GLT-1/SLC1A2 expression in astrocytes lead to increased NO release and decreased glutamate uptake in the synaptic cleft of spinal cord. Consequently, elevation of glutamate and NO triggers motor neuronal damage and cell death via non-cell autonomous pathway.
Exp Neurobiol 2016;25:233~240
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