CNS-specific expression of C3a and C5a exacerbate demyelination severity in the cuprizone model.

ABSTRACT: Demyelination in the central nervous system (CNS) is known to involve several immune effector mechanisms, including complement proteins. Local production of complement by glial cells in the brain can be both harmful and protective. To investigate the roles of C3a and C5a in demyelination and remyelination pathology we utilized the cuprizone model. Transgenic mice expressing C3a or C5a under the control of the glial fibrillary acidic protein (GFAP) promoter had exacerbated demyelination and slightly delayed remyelination in the corpus callosum compared to WT mice. C3a and C5a transgenic mice had increased cellularity in the corpus callosum due to increase activation and/or migration of microglia. Oligodendrocytes migrated to the corpus callosum in higher numbers during early remyelination e

SUBMITTER: Ingersoll SA 

PROVIDER: S-EPMC2993815 | biostudies-literature | 2010 Nov-Dec

REPOSITORIES: biostudies-literature