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Hyperglycemia Promotes Schwann Cell De-differentiation and De-myelination via Sorbitol Accumulation and Igf1 Protein Down-regulation

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Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/72270

Title: Hyperglycemia Promotes Schwann Cell De-differentiation and De-myelination via Sorbitol Accumulation and Igf1 Protein Down-regulation
Authors: Hao, W. Browse this author
Tashiro, S. Browse this author
Hasegawa, T. Browse this author →KAKEN DB
Sato, Y. Browse this author
Kobayashi, T. Browse this author
Tando, T. Browse this author
Katsuyama, E. Browse this author
Fujie, A. Browse this author
Watanabe, R. Browse this author
Morita, M. Browse this author
Miyamoto, K. Browse this author
Morioka, H. Browse this author
Nakamura, M. Browse this author
Matsumoto, M. Browse this author
Amizuka, N. Browse this author →KAKEN DB
Toyama, Y. Browse this author
Miyamoto, T Browse this author
Keywords: cell differentiation
cell metabolism
diabetes
differentiation
Schwann cells
vitamin D
Issue Date: 10-Jul-2015
Publisher: American Society for Biochemistry and Molecular Biology
Journal Title: The Journal of biological chemistry
Volume: 290
Issue: 28
Start Page: 17106
End Page: 17115
Publisher DOI: 10.1074/jbc.M114.631291
Abstract: Diabetes mellitus (DM) is frequently accompanied by complications, such as peripheral nerve neuropathy. Schwann cells play a pivotal role in regulating peripheral nerve function and conduction velocity; however, changes in Schwann cell differentiation status in DM are not fully understood. Here, we report that Schwann cells de-differentiate into immature cells under hyperglycemic conditions as a result of sorbitol accumulation and decreased Igf1 expression in those cells. We found that de-differentiated Schwann cells could be re-differentiated in vitro into mature cells by treatment with an aldose reductase inhibitor, to reduce sorbitol levels, or with vitamin D3, to elevate Igf1 expression. In vivo DM models exhibited significantly reduced nerve function and conduction, Schwann cell de-differentiation, peripheral nerve de-myelination, and all conditions were significantly rescued by aldose reductase inhibitor or vitamin D3 administration. These findings reveal mechanisms underlying pathological changes in Schwann cells seen in DM and suggest ways to treat neurological conditions associated with this condition.
Rights: This research was originally published in the Journal of Biological Chemistry. Wu Hao, Syoichi Tashiro, Tomoka Hasegawa, Yuiko Sato, Tami Kobayashi, Toshimi Tando, Eri Katsuyama, Atsuhiro Fujie, Ryuichi Watanabe, Mayu Morita, Kana Miyamoto, Hideo Morioka, Masaya Nakamura, Morio Matsumoto, Norio Amizuka, Yoshiaki Toyama, and Takeshi Miyamoto. Hyperglycemia Promotes Schwann Cell De-differentiation and De-myelination via Sorbitol Accumulation and Igf1 Protein Down-regulation. J. Biol. Chem. 2015; Vol 290(28): 17106-17115. © the American Society for Biochemistry and Molecular Biology.
Type: article
URI: http://hdl.handle.net/2115/72270
Appears in Collections:歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 長谷川 智香

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