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首页> 外文期刊>American Journal of Physiology >Differential regulation of myofilament protein isoforms underlying the contractility changes in skeletal muscle unloading.
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Differential regulation of myofilament protein isoforms underlying the contractility changes in skeletal muscle unloading.

机译：骨骼肌卸载中收缩力变化背后的肌丝蛋白同工型的差异调节。

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Weight-bearing skeletal muscles change phenotype in response to unloading. Using the hindlimb suspension rat model, we investigated the regulation of myofilament protein isoforms in correlation to contractility. Four weeks of continuous hindlimb unloading produced progressive atrophy and contractility changes in soleus but not extensor digitorum longus muscle. The unloaded soleus muscle also had decreased fatigue resistance. Along with the decrease of myosin heavy chain isoform I and IIa and increase of IIb and IIx, coordinated regulation of thin filament regulatory protein isoforms were observed: gamma- and beta-tropomyosin decreased and alpha-tropomyosin increased, resulting in an alpha/beta ratio similar to that in normal fast twitch skeletal muscle; troponin I and troponin T (TnT) both showed decrease in the slow isoform and increases in the fast isoform. The TnT isoform switching began after 7 days of unloading and TnI isoform showed detectable changes at 14 days while other protein isoform changes were not significant until 28 days of treatment. Correlating to the early changes in contractility, especially the resistance to fatigue, the early response of TnT isoform regulation may play a unique role in the adaptation of skeletal muscle to unloading. When the fast TnT gene expression was upregulated in the unloaded soleus muscle, alternative RNA splicing switched to produce more high molecular weight acidic isoforms, reflecting a potential compensation for the decrease of slow TnT that is critical to skeletal muscle function. The results demonstrate that differential regulation of TnT isoforms is a sensitive mechanism in muscle adaptation to functional demands.
机译：负重骨骼肌响应卸载而改变表型。使用后肢悬吊大鼠模型，我们调查了与收缩力相关的肌丝蛋白亚型的调节。连续四周卸载后肢会导致比目鱼肌进行性萎缩和收缩力改变，但不会导致趾长伸肌。空的比目鱼肌也降低了疲劳抵抗力。随着肌球蛋白重链同工型I和IIa的减少以及IIb和IIx的增加，观察到细丝调节蛋白同工型的协调调节：γ-和β-原肌球蛋白减少，而α-原肌球蛋白增加，导致alpha / beta比率与正常的快速抽搐骨骼肌相似;肌钙蛋白I和肌钙蛋白T（TnT）均显示出慢同工型减少而快同工型增加。 TnT亚型转换在卸载7天后开始，TnI亚型在14天时显示可检测到的变化，而其他蛋白亚型的变化直到治疗28天才显着。与收缩力的早期变化（尤其是对疲劳的抵抗力）相关，TnT亚型调节的早期响应可能在骨骼肌适应卸载中起独特作用。当空载的比目鱼肌中快速TnT基因表达上调时，替代的RNA剪接转换为产生更多的高分子量酸性同工型，反映出对骨骼肌功能至关重要的慢TnT降低的潜在补偿。结果表明，TnT亚型的差异调节是肌肉适应功能需求的敏感机制。

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