| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
The purpose of this study was to investigate the effects of extracellular stimuli, such as mechanical loading and heat stress, on the plasticity of skeletal muscle. Absence of heat shock transcription factor 1 (HSF1) gene partially attenuated the overloading-associated skeletal muscle hypertrophy in mice. Heat stress-associated increase in muscle mass and muscle satellite cells was also suppressed by HSF1-deficiency. Furthermore, HSF1-deficiency depressed heat stress-associated activation of Akt/p70 S6 kinase pathway. In addition, upregulation of heat shock proteins (HSPs) in skeletal muscle was attenuated by the absence of HSF1. These observations suggested that HSF1-mediated stress response, including the upregulation of HSPs, may play a key role in skeletal muscle hypertrophy induced by mechanical overloading and heat stress.
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