Organelle dynamics for fate determination of injured neurons
| Project/Area Number |
16H05117
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General anatomy (including histology/embryology)
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| Research Institution | Nagoya University |
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Principal Investigator |
Kiyama Hiroshi 名古屋大学, 医学系研究科, 教授 (00192021)
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| Co-Investigator(Renkei-kenkyūsha) |
KIRYU-SEO Sumiko 名古屋大学, 大学院医学系研究科, 准教授 (70311529)
KONISHI Hiroyuki 名古屋大学, 大学院医学系研究科, 講師 (90448746)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2018: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2017: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2016: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | ミトコンドリア / 神経損傷 / 軸索再生 / 軸索障害 / 運動神経 / オルガネラ / 神経再生 / 神経変性 / 軸索損傷 / ATF3 / 解剖学 / 運動ニューロン / 細胞・組織 / 脳神経疾患 |
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| Outline of Final Research Achievements |
We have investigated significances of organelle dynamics which are observed in response to nerve injury. We used the BAC transgenic mice, which express mitochondria labelling GFP and Cre recombinase protein simultaneously and specifically in nerve injured neurons in response to nerve injury. After nerve injury the mitochondria in injured nerve became smaller and moved quicker, although the mitochondrial size in cell soma was not changed. This morphological alteration of mitochondria would be important for delivering mitochondria to regenerating nerve tip. The deletion of Dpr1, which is a responsible molecule for the mitochondrial fission, induced mitochondrial enlargement, and the Drp1 deleted motor neurons died quickly in response to nerve injury.
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| Academic Significance and Societal Importance of the Research Achievements |
運動神経損傷後に生じるオルガネラ動態の変化が、損傷神経細胞の生存や再生に重要な役割を果たしていることが明らかになった。特にミトコンドリアは融合と分裂を繰り返すことで機能を維持しているが、分裂の欠損により神経損傷に対する耐性が失われることが明らかになった。これらの結果は、オルガネラ動態の異常に起因する神経変性疾患の変性メカニズムの解明に繋がることが予想され、これら疾患の治療法開発への貢献が期待される。本研究の成果は、神経変性疾患以外にも外傷後の運動神経再生や神経障害性疼痛の治療法開発にも新たな知見を提供すると考えられる。
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Report
(4 results)
Research Products
(12 results)
