2018 Fiscal Year Final Research Report
Cessation of electrically-induced contractile activity induces atrophy in hypertrophied myotubes.
| Project/Area Number |
16K12938
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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 |
Rehabilitation science/Welfare engineering
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| Research Institution | Oita University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
笹井 宣昌 鈴鹿医療科学大学, 保健衛生学部, 准教授 (20454762)
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| Research Collaborator |
KAWASHIMA takafumi
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Keywords | 理学療法 / 筋萎縮 / 培養細胞 / 機械刺激 |
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| Outline of Final Research Achievements |
To address precise mechanisms of disused-muscle atrophy, we challenged to replicate inactive-induced muscle atrophy in vitro. Myotubes were cultured under repeated muscle contraction evoked by ES for 2 days. After the contraction period, ES was stopped and myotubes were cultured under inactive state for another 2 days. When the ES was removed, the myotube diameter was 16.4±0.6 μm. In unload group, the myotube diameter was significantly decreased (13.0±0.7 μm). Several hours of unloaded state increased LC3-II protein levels (i.e., autophagic activity). Phosphorylation of Akt was decreased 1 hour after the cessation of ES. After 24 hours, the phosphorylation went back to the basal level. This cultured myotube model which shows atrophic responses induced by inactivity would help to reveal mechanism of inactive-induced muscle atrophy.
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| Free Research Field |
理学療法
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| Academic Significance and Societal Importance of the Research Achievements |
脱負荷による筋萎縮モデルが、ヒトや動物の廃用性筋萎縮時に起こる既知の蛋白質分解機構や合成機構の応答を備え持ち、臨床現象を反映した廃用性筋萎縮の培養細胞モデルになりうるかどうかを判明させた。本研究成果は、廃用性筋萎縮のメカニズムの解明に役立つとともに、正常筋とは比べ物にならないほど速い、筋肥大のメカニズムを明らかにさせる糸口となると考える。また、これらが判明したら、効果的な筋萎縮抑制方法や萎縮からの回復促進方法開発へと萌芽する。
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