Oligodendrocyte-specific deletion of FGFR2 ameliorates MOG_35-55 -induced EAE through ERK and Akt signalling.

ABSTRACT: Fibroblast growth factors (FGFs) and their receptors (FGFRs) are involved in demyelinating pathologies including multiple sclerosis (MS). In our recent study, oligodendrocyte-specific deletion of FGFR1 resulted in a milder disease course, less inflammation, reduced myelin and axon damage in EAE. The objective of this study was to elucidate the role of oligodendroglial FGFR2 in MOG_35-55 -induced EAE. Oligodendrocyte-specific knockout of FGFR2 (Fgfr2^{ind -/-} ) was achieved by application of tamoxifen; EAE was induced using the MOG_35-55 peptide. EAE symptoms were monitored over 62 days. Spinal cord tissue was analysed by histology, immunohistochemistry and western blot. Fgfr2^{ind -/-} mice revealed a milder disease course, less my

SUBMITTER: Kamali S 

PROVIDER: S-EPMC8018040 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature