2012 Fiscal Year Final Research Report
In vivo mechanism of neuronal injury by DRP1
| Project/Area Number |
22590956
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurology
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
SHIINO Akihiko 滋賀医科大学, MR 医学総合研究センター, 准教授 (50215935)
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| Co-Investigator(Kenkyū-buntansha) |
INUBUSHI Toshirou 滋賀医科大学, MR 医学総合研究センター, 教授 (20213142)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 臨床神経生理学 / アルツハイマー病 / ミトコンドリア / アミロイドβ / 磁気共鳴 / ダイナミン様蛋白 / 一酸化窒素 / 酸化ストレス |
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| Research Abstract |
The purpose of our study was to clarify whether S-nitrosylation induced excessive mitochondrial fission and fragmentation in the brain. We stereotactically administered glyceryl trinitrate in the mouse brain of both triple transgenic (3xTg) and wild type (Wt) mice, and measured SNO-Drp1 by biotin switch assay and compared mitochondrial morphology by deconvolution fluorescence microscopy using mito-DsRed2 staining. SNO-Drp1 formation was increased in a dose-dependent manner induced by glyceryl trinitrate, and this phenomenon was more prominent in 3xTg than in Wt mice. Mito-DsRed2 staining showed excessive mitochondrial fission and fragmentation in the brain of 3xTg but not prominently in the brain of Wt mice. These results suggest that β-amyloid may cause excessive mitochondrial fragmentation and mitochondrial dysfunction by induction of excessive SNO-Drp1 production.
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