Adipocyte-derived molecules contribute to the proliferation of oligodendrocyte precursor cells (OPC)
Ken Matoba, Rieko Muramatsu, Toshihide Yamashita

Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Osaka, Japan

Multiple sclerosis (MS) is characterized by inflammation in the central nervous system (CNS), and is associated with chronic demyelination and neurological deficits. Signs of spontaneous remyelination are frequently observed in acute MS and are considered to contribute to recovery of neurological function. Remyelination is partially dependent on OPC proliferation; thus, molecular mechanism that promotes OPC proliferation is expected to contribute to restoration of neuronal function. In the present study, we explored the mechanism of OPC proliferation and found that adipocyte-derived molecules enhance OPC proliferation in vitro. We cultured OPC cell line FBD-102b, which was established from fetal brain of p53-deficient mice, in the presence or absence of conditioned medium from primary culture of white adipocytes. After culturing, we counted the number of OPC and found that conditioned medium from primary culture of mouse white adipocytes enhanced the number of OPCs compared with that of control. We examined the intracellular signal of adipocytes-induced proliferation of FBD-102b and found that adipocytes activated extracellular signal-regulated kinase (ERK) in FBD-102b cells. We also revealed that inhibition of ERK activation prevented adipocytes-mediated proliferation of FBD-102b cells. These finding suggest that adipocytes-derived molecule enhances OPC proliferation and may promote remyelination in the demyelinated lesions.