Astrocytes are one of the first responders to central nervous system (CNS) injuries such as spinal cord injury (SCI). They are thought to repress injury-induced CNS inflammation as well as… Click to show full abstract
Astrocytes are one of the first responders to central nervous system (CNS) injuries such as spinal cord injury (SCI). They are thought to repress injury-induced CNS inflammation as well as inhibit axonal regeneration. While reactive astrocytes migrate and accumulate around the lesion core, the mechanism of astrocyte migration towards the lesion site remains unclear. Here, we examined possible involvement of acidification of the lesion site and expression of proton-sensing receptors in astrocyte migration, both in mice models and in vitro. We found that the expression of several proton-sensing receptors was increased at the lesion site after SCI. Among these receptors, Gpr132 was expressed in primary cultured astrocytes and exhibited significant enhanced expression in acidic conditions in vitro. Furthermore, astrocyte motility was enhanced in acidic media and by Gpr132 activation. These results suggest that acidification of the lesion site facilitates astrocyte migration via the proton-sensing receptor Gpr132.
               
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