| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2004: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2003: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Research Abstract |
It has been recently reported that Akt/mTOR/p70^<S6K>/S6 and calcineurin signaling pathways are a crucial regulator of skeletal muscle hypertrophy. We have showed that the heat stress accelerates the recovery from skeletal muscle atrophy induced by hindlimb unweighting. However, the mechanism responsible for the promoting effects of heat stress on atrophied muscles remains unclear. In this study, we investigated the role of the Akt and calcineurin signaling pathway in the recovery of the atrophied skeletal muscle with heat and its optimum exposure time. Wistar strain male rats (8-week-old) were divided into four groups : control (Con), hindlimb unweighting (HLU), heat stress for 15 (Heat 15) and 30 (Heat 30) min after hindlimb unweighting. HLU, Heat 15 and Heat 30 groups were subjected to hindlimb unweighting for 10 days. Immediately after release from unweighting, heat groups were immersed into hot water (42℃) under anesthesia. After 0, 3 and 10 days, soleus muscles were dissected. Muscle weight-to-body weight ratios of HLU and Heat 15 were significantly higher than 0 day in each group. The myofibrillar content of Heat 30 was significantly lower than Con at 10 day recovery period. The expression of phospho-mTOR in Heat 15 was significantly higher than the other groups after 0 days of muscle reloding. Phospho-S6 ribosomal levels after 3 day recovery period were significantly greater in the order : Heat 15, HLU, Heat 30 and Con. These results suggest that the heat stress promotes the recovery of atrophied skeletal muscle in part via Akt/mTOR/p70^<S6K>/S6 signaling pathway and the optimum exposure time for its promotion exist.
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