Figure 8.

Schematic representation of the role of RGC-32 in astrocyte differentiation during EAE. Spinal cord astrocytes are generated from radial glia through a complex process involving cell lineage specification, migration, proliferation, terminal differentiation, and maturation. The presence of inflammatory infiltrate at the peak of EAE triggers astrocytes to become reactive and to upregulate their GFAP expression together with upregulating CTGF. Our results show that in the absence of RGC-32, astrocytes retain an elongated, bipolar shape and their elevated expression of progenitor markers such as vimentin and FABP7, but they are unable to undergo the morphological changes specific for reactive astrocytes and to upregulate their GFAP expression. It is currently not known whether RGC-32 also participates in adult radial glia-induced astrogliosis; these cells are an important source for reactive astrocytes in EAE.