Elucidation of the adaptive mechanism to the mechanical and low energy stresses in skeletal muscle
Project/Area Number |
25350813
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Sports science
|
Research Institution | The University of Shiga Prefecture (2015) Osaka University (2013-2014) |
Principal Investigator |
NAKAI NAOYA 滋賀県立大学, 人間文化学部, 教授 (90324508)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | メカニカルストレス / 骨格筋 / タンパク質合成 / 骨格筋培養細胞 / アミノ酸トランスポーター / ロイシン / 低エネルギーストレス |
Outline of Final Research Achievements |
Cellular protein synthesis is believed to be antagonistically regulated by mTOR and AMPK signaling pathways. In the present study, we examined the relationship between mTOR/p70S6K and AMPK in response to mechanical stretch. Phosphorylation of p70S6K and AMPK were concomitantly increased by mechanical stretch. Stimulation of the mTOR pathway by adding leucine and insulin increased the phosphorylation of p70S6K without inactivation of AMPK. In contrast, pharmacological inhibition of AMPK by the addition of compound C enhanced the phosphorylation of p70S6K in response to mechanical stretch. Activation of AMPK by the addition AICAR reduced the phosphorylation of p70S6K in response to mechanical stretch. In conclusion, crosstalk between mTOR and AMPK signaling was not tightly regulated in response to physiological stimuli, such as mechanical stress and/or nutrients. However, pharmacological activation or inactivation of AMPKα affected the mTOR/p70S6K signaling pathway.
|
Report
(4 results)
Research Products
(8 results)