The basic analysis of connective tissue fibrosis after muscle strain injury
| Project/Area Number |
21700663
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Sports science
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| Research Institution | Meiji Gakuin University |
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Principal Investigator |
OCHI Eisuke Meiji Gakuin University, 教養教育センター, 専任講師 (90468778)
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| Co-Investigator(Renkei-kenkyūsha) |
NAKAZATO Koichi 日本体育大学, 大学院・体育科学研究科, 教授 (00307993)
ISHII Naokata 東京大学, 大学院・総合文化研究科, 教授 (20151326)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 筋損傷 / エキセントリック収縮 / 結合組織 / 瘢痕化 / 肉離れ / 動物モデル / コラーゲン / in vivo |
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| Research Abstract |
The purpose of this study was to investigate the repetitive effects of contraction-induced injury on muscular mass, function, structure, and protein expressions. We employed our originally developed device with lengthening contractions (LCs) mode used in rat gastrocnemius muscle. The results showed that both medial and lateral gastrocnemius muscle were significantly smaller than those in control. The muscle content of myostatin was significantly higher in LCs than in control. In addition, FOXO1 and FOXO3 showed significantly enhanced expression in LCs than in control. These results suggest that repeated bouts of LCs in our model induced decreases in muscular mass and strength. We also observed the activation of protein degradation signaling pathways and myostatin while inactivation of protein synthesis. We conclude that the LCs-induced atrophy and torque deficit are associated with activation of the protein degradation process not apotosis process.
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Report
(3 results)
Research Products
(44 results)
