The Effects of Insulin on Immortalized Rat Schwann Cells,IFRS1 |
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Authors: | Tomokazu Saiki Nobuhisa Nakamura Megumi Miyabe Mizuho Ito Tomomi Minato Kazunori Sango Tatsuaki Matsubara Keiko Naruse |
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Affiliation: | 1.Department of Pharmacy, Aichi Gakuin University Dental Hospital, Nagoya 464-8651, Japan;2.Department of Internal Medicine, School of Dentistry, Aichi Gakuin University, Nagoya 464-8651, Japan; (M.M.); (M.I.); (T.M.); (K.N.);3.Department of Clinical Laboratory, Aichi Gakuin University Dental Hospital, Nagoya 464-8651, Japan;4.Diabetic Neuropathy Project, Department of Diseases and Infection, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan; |
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Abstract: | Schwann cells play an important role in peripheral nerve function, and their dysfunction has been implicated in the pathogenesis of diabetic neuropathy and other demyelinating diseases. The physiological functions of insulin in Schwann cells remain unclear and therefore define the aim of this study. By using immortalized adult Fischer rat Schwann cells (IFRS1), we investigated the mechanism of the stimulating effects of insulin on the cell proliferation and expression of myelin proteins (myelin protein zero (MPZ) and myelin basic protein (MBP). The application of insulin to IFRS1 cells increased the proliferative activity and induced phosphorylation of Akt and ERK, but not P38-MAPK. The proliferative potential of insulin-stimulated IFRS1 was significantly suppressed by the addition of LY294002, a PI3 kinase inhibitor. The insulin-stimulated increase in MPZ expression was significantly suppressed by the addition of PD98059, a MEK inhibitor. Furthermore, insulin-increased MBP expression was significantly suppressed by the addition of LY294002. These findings suggest that both PI3-K/Akt and ERK/MEK pathways are involved in insulin-induced cell growth and upregulation of MPZ and MBP in IFRS1 Schwann cells. |
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Keywords: | Schwann cells insulin myelin protein zero myelin basic protein myelin associated glycoprotein Akt extracellular-signal-regulated kinase (ERK) |
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