The effect of heat stress on signal transduction during the recovery from skeletal muscle atrophy induced by hindlimb-unweighted

后肢失重引起的骨骼肌萎缩恢复过程中热应激对信号转导的影响

基本信息

  • 批准号:
    15500446
  • 负责人:
  • 金额:
    $ 2.43万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    2003
  • 资助国家:
    日本
  • 起止时间:
    2003 至 2004
  • 项目状态:
    已结题

项目摘要

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.
最近有报道称,AKT/MTOR/P70^<S6K>/S6和钙调蛋白信号通路是骨骼肌肥大的关键调节剂。我们已经表明,热应力加速了后肢不加权引起的骨骼肌萎缩的恢复。但是,促进热应激对萎缩肌肉的作用的机制尚不清楚。在这项研究中,我们研究了Akt和钙调神经蛋白信号通路在热量及其最佳暴露时间中恢复萎缩的骨骼肌中的作用。 Wistar菌株雄性大鼠(8周龄)分为四组:对照(CON),后肢不加权(HLU),15(热量15)的热应激(热量15)和30(热量30(热量30)后,后肢未加权后。 HLU,HEAT 15和HEAT 30组持续10天。从未加权中释放后立即将热组浸入麻醉下的热水(42℃)中。在0、3和10天后,解剖比目鱼肌肉。 HLU和热量15的肌肉体重与体重比在每组中明显高于0天。在10天恢复期间,热量30的肌原纤维含量明显低于CON。肌肉复发0天后,在热15中磷酸-MTOR的表达显着高于其他组。 3天恢复期后的磷酸-S6核糖体水平明显更高:热15,HLU,HEAT 30和CON。这些结果表明,热应力通过AKT/MTOR/P70^<S6K>/S6信号通路促进萎缩骨骼肌的恢复,并存在其促进的最佳暴露时间。

项目成果

期刊论文数量(6)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Changes in protein kinase B (PKB/Akt) and calcineurin signaling during recovery in atrophied soleus muscle_induced by unloading.
卸载引起的萎缩比目鱼肌恢复过程中蛋白激酶 B (PKB/Akt) 和钙调磷酸酶信号的变化。
Changes in protein kinase B (PKB/Akt) and calcineurin signaling during recovery in atrophied soleus muscle induced by unloading.
卸载引起的萎缩比目鱼肌恢复过程中蛋白激酶 B (PKB/Akt) 和钙调磷酸酶信号的变化。
Changes in protein kinase B(PKB/Akt) and calcineurin signaling during recovery in atrophied soleus muscle induced by unloading
卸载引起的萎缩比目鱼肌恢复过程中蛋白激酶 B (PKB/Akt) 和钙调神经磷酸酶信号的变化
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SUGIURA Takao其他文献

SUGIURA Takao的其他文献

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{{ truncateString('SUGIURA Takao', 18)}}的其他基金

Effects of long-term antioxidant food intake and of mechanical stress to skeletal muscle on sarcopenia
长期抗氧化食物摄入和骨骼肌机械应力对肌肉减少症的影响
  • 批准号:
    16K01726
  • 财政年份:
    2016
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Signaling examination on strategies for suppression of muscular atrophy and facilitation of restoration from muscular atrophy
抑制肌萎缩和促进肌萎缩恢复策略的信号检查
  • 批准号:
    20500578
  • 财政年份:
    2008
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Age-related differences in signal transduction during recovery in atrophied plantaris muscle induced by immobilization
固定引起的萎缩跖肌恢复过程中信号转导的年龄相关差异
  • 批准号:
    17500428
  • 财政年份:
    2005
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Diversity of myosin heavy chain isoform expression in rat single muscle fibers
大鼠单肌纤维中肌球蛋白重链亚型表达的多样性
  • 批准号:
    07680122
  • 财政年份:
    1995
  • 资助金额:
    $ 2.43万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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