Molecular mechanisms of the remyelination in chronic phase of spinal cord injury

2016 Fiscal Year Final Research Report

• Project/Area Number: 26282159
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Rehabilitation science/Welfare engineering
• Research Institution: National Rehabilitation Center for Persons with Disabilities
• Principal Investigator: OGATA TORU 国立障害者リハビリテーションセンター(研究所), 病院(併任研究所)障者健康増進・運動医科学支援センター, センター長 (00392192)
• Co-Investigator(Kenkyū-buntansha): 長尾 元史 国立障害者リハビリテーションセンター(研究所), 研究所 運動機能系障害研究部, 研究室長 (00359671) ; 杉森 道也 富山大学, 大学院医学薬学研究部(医学), 助教 (20464026)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 再髄鞘化 / エピジェネティクス / オリゴデンドロサイト

Outline of Final Research Achievements

Oligodendrocyte precursor cells (OPCs) act as a reservoir of new oligodendrocytes (OLs) in homeostatic and pathological conditions. OPCs are activated in response to spinal cord injury (SCI), to generate myelinating OLs. This OPC activation is the first step in the process of remyelination, and proper control of OPC activation is important for tissue repair following SCI. However, the molecular mechanisms underlying OPC activation, especially its epigenetic regulation, remain mostly unknown. In this study, we demonstrate that chromodomain helicase DNA binding protein 7 (Chd7), which is a member of the Chd family of chromatin remodelers and is a causative gene for human CHARGE syndrome, collaborates with Sox2 and regulates OPC activation following SCI.

Free Research Field

リハビリテーション医学