2013 Fiscal Year Final Research Report
characterization of the laminin-dystroglycan interaction in neuropathy and its therapeutic application
| Project/Area Number |
23591256
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Teikyo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MASAKI Toshihiro 帝京科学大学, 医療科学部, 教授 (00585028)
HAGIWARA Hiroki 帝京科学大学, 医療科学部, 教授 (80276732)
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| Co-Investigator(Renkei-kenkyūsha) |
MATSUMURA Kiichiro 帝京大学, 医学部, 教授 (50260922)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 神経分子病態学 / ニューロパチー / ジストログリカン / 髄鞘形成 / 骨格筋再生 |
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| Research Abstract |
The interaction between dystroglycan in Schwann cell and laminin in the basement membrane is crucial for the myelination of peripheral nerve. We generated LARGE transgenic mice in which this interaction is greatly enhanced. In the peripheral nerves of these mice, the expression of some genes related to myelination was altered. We crossed LARGE transgenic mice with dy2J mice, which exhibit dysmyelination of the peripheral nerve, however the defects in myelination were not ameliorated. Since the peripheral nerve affects the regeneration of the skeletal muscle via neuromuscular junction, we examined the regeneration of dy2J mice skeletal muscles. We demonstrated that the muscle regeneration was suppressed by the overexpression of LARGE in these mice.
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[Journal Article] Overexpression of LARGE suppresses muscle regeneration via down-regulation of insulin-like growth factor 1 and aggravates muscular dystrophy in mice2014
Author(s)
Saito F, Kanagawa M, Ikeda M, Hagiwara H, Masaki T, Ohkuma H, Katanosaka Y, Shimizu T, Sonoo M, Toda T, Matsumura K
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Journal Title
Hum Mol Genet
Volume: (in press)
DOI
Peer Reviewed
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