| Project/Area Number |
15K01716
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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 |
Applied health science
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| Research Institution | The University of Tokushima |
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Principal Investigator |
IKEDA Yasumasa 徳島大学, 大学院医歯薬学研究部(医学系), 准教授 (60432754)
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| Co-Investigator(Kenkyū-buntansha) |
八木 秀介 徳島大学, 大学院医歯薬学研究部, 特任准教授 (00507650)
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| Co-Investigator(Renkei-kenkyūsha) |
HORINOUCHI Yuya 徳島大学, 大学院医歯薬学研究部(医学系), 助教 (30716593)
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| Research Collaborator |
HAMANO Hirofumi 徳島大学, 大学院医歯薬学研究部(医学系), 大学院生
IMAO Mizuki 徳島大学, 大学院医歯薬学研究部(薬学系), 学部生
SATO Akiho 徳島大学, 大学院医歯薬学研究部(薬学系), 学部生
WATANABE Hiroaki 徳島大学, 大学院医歯薬学研究部(薬学系), 学部生
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 鉄 / サルコペニア / 酸化ストレス / 骨格筋 / 骨格筋萎縮 / ユビキチンリガーゼ |
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| Outline of Final Research Achievements |
Skeletal muscle atrophy is a critical health problem. However, the effect of iron on skeletal muscle atrophy has remained unclear. Mice with excess iron-injected group showed the reduced skeletal muscle mass. The skeletal muscle with iron treatment showed elevated mRNA expression of the muscle atrophy-related E3 ubiquitin ligases, atrogin-1 and muscle ring finger-1(MuRF1). Moreover, iron-treated mice showed reduced phosphorylation of Akt and forkhead box O3 (FOXO3a) in skeletal muscles. In in vitro experiments using C2C12 myotube cells, FOXO3a siRNA inhibited iron-induced upregulation of atrogin-1 and MuRF1 and reversed the reduction in myotube diameters. Iron-load caused oxidative stress, and an oxidative stress inhibitor abrogated iron-induced muscle atrophy by recovering the reduced phosphorylation of Akt-FOXO3a pathway. Iron-induced skeletal muscle atrophy is suggested to involve the inactivation of Akt-FOXO3a-E3 ubiquitin ligase signaling by oxidative stress.
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