| Project/Area Number |
26670109
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Environmental physiology(including physical medicine and nutritional physiology)
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| Research Institution | University of Tsukuba |
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Principal Investigator |
Shoda Junichi 筑波大学, 医学医療系, 教授 (90241827)
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| Co-Investigator(Kenkyū-buntansha) |
YANAGAWA Toru 筑波大学, 医学医療系, 准教授 (10312852)
SAKAI Syunn 筑波大学, 医学医療系, 講師 (30282362)
WARABI Eiji 筑波大学, 医学医療系, 講師 (70396612)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 骨格筋 / 酸化ストレス / 転写因子 / 細胞死 / 運動機能 / 運動 / 自食作用 / 筋萎縮 |
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| Outline of Final Research Achievements |
Exercise plays an important role in preventing skeletal muscle atrophy and maintaining muscle volume. On the other hand, muscle contraction yields excessive amounts of reactive oxygen species (ROSs) in the tissues. The increased amounts of ROSs disturb the function of muscles. In this study, we revealed that excessive contractions of C2C12 myotuble cells generate excessive amounts of ROS, that transcription factor Nrf2 and its targeting genes contribute to the deletion of the ROSs, that the excessive amounts of ROSs induce apoptosis of the myotuble cells, and that activation of Nrf2 inhibits the cell apoptosis by deleting the ROSs. In other words, it is suggested that Nrf2 plays a role in protecting muscle tissues from the oxidative stress to maintain the function, and that the ROSs generated by muscle contractions are derived from the mitochondria in the muscles. Collectively, Nrf2 is closely involved in the maintenance of energy metabolic function during exercise.
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