Roles of oligodendrocytic connexins in the pathogenesis of ALS
| Project/Area Number |
26893184
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurology
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Project Period (FY) |
2014-08-29 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 筋萎縮性側索硬化症 / コネキシン / オリゴデンドロサイト / 変異SOD1マウス |
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| Outline of Final Research Achievements |
Connexins (Cxs) are transmembrane-type proteins, they form gap junctions between cells and allow direct intercellular communications. In nervous system, gilal Cxs especially play a key role in energy supply to neurons. We previously reported that expression of oligodedrocytic Cxs are impaired in ALS model mice at late disease stage. We used cultured oligodendrocyte precursor cell (OPC) from wild-type and mutant SOD1 Tg mice, and examined differentiation to oligodendrocyte and expression of Cxs. There were no difference between wild-type and mutant SOD1 Tg mice. Zonula occludens-1 (ZO-1) protein is scaffolding proteins providing the structural basis for the gap junction. In mutant SOD1 Tg mice at early disease stage, expression of Cx47 was maintained but ZO-1 expression was decreased. Our result suggest that disruption of ZO-1 might lead to impaired expression of Cx47 and associate with motor neuron degeneration in ALS.
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Report
(3 results)
Research Products
(3 results)
