Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Japan; Department of Molecular Pharmacology, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Japan; WPI Immunology Frontier Research Center, Osaka University, Suita, Japan
Harutoshi Fujimura
Toneyama National Hospital, Toyonaka, Japan
Hideki Mochizuki
Department of Neurology, Graduate School of Medicine, Osaka University, Suita, Japan
Hirotoshi Kataoka
Department of Neuro-Medical Science, Graduate School of Medicine, Osaka University, Suita, Japan
Toshihide Yamashita
Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Japan; WPI Immunology Frontier Research Center, Osaka University, Suita, Japan; Department of Neuro-Medical Science, Graduate School of Medicine, Osaka University, Suita, Japan; Graduate School of Frontier Biosciences, Osaka University, Suita, Japan
Oligodendrocyte maturation is necessary for functional regeneration in the CNS; however, the mechanisms by which the systemic environment regulates oligodendrocyte maturation is unclear. We found that Transforming growth factor (TGF)-β1, which is present in higher levels in the systemic environment, promotes oligodendrocyte maturation. Oligodendrocyte maturation was enhanced by adult mouse serum treatment via TGF-β type I receptor. Decrease in circulating TGF-β1 level prevented remyelination in the spinal cord after toxin-induced demyelination. TGF-β1 administration promoted remyelination and restored neurological function in a multiple sclerosis animal model. Furthermore, TGF-β1 treatment stimulated human oligodendrocyte maturation. These data provide the therapeutic possibility of TGF-β for demyelinating diseases.
