| Project/Area Number |
25460250
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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 |
General anatomy (including histology/embryology)
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| Research Institution | Jichi Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
YAJIMA Hiroshi 自治医科大学, 医学部, 講師 (10433583)
TAKAHASHI Masanori 自治医科大学, 医学部, 講師 (20361074)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 筋ジストロフィー / 筋再生 / 筋衛星細胞 / Six遺伝子 / mdxマウス / 筋力低下 / 寿命 / 運動負荷 / Six4 / Six5 / mdx / 筋繊維 / クレアチンキナーゼ / 筋発生 |
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| Outline of Final Research Achievements |
Skeletal muscle is the essential organ that supports our posture and locomotion. Muscle disease such as muscular dystrophy threatens our existence and quality of life. In this study, we revealed that the Six family genes encoding for transcription factors which are responsible for the development of skeletal muscle, are involved in the regeneration of skeletal muscle. When we lowered the gene dosages of Six4 and Six5 in mdx mice, which is a model mouse of Duchenne Muscular Dystrophy, the index of systemic symptoms of the mice were improved, myofibers became thick, and the mice was resistant to the muscle weakness induced by treadmill exercise. The mean-age at death was prolonged around 30%. These results indicate that Six4 and Six5 are possible candidates for therapeutic targets of muscle dystrophy.
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