Isoform-specific Na,K-ATPase alterations precede disuse-induced atrophy of rat soleus muscle.

Isoform-specific Na,K-ATPase alterations precede disuse-induced atrophy of rat soleus muscle.
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异构体特异性 Na,K-ATP 酶改变先于废用引起的大鼠比目鱼肌萎缩。

DOI:
10.1155/2015/720172
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发表时间:
2015
影响因子:
--
通讯作者:
Krivoi,IgorI
Krivoi,IgorI
中科院分区:
生物学3区
文献类型:
--
作者:
Kravtsova,ViolettaV;Matchkov,VladimirV;Bouzinova,ElenaV;Vasiliev,AlexanderN;Razgovorova,IrinaA;Heiny,JudithA;Krivoi,IgorI

文献摘要

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本研究探讨了短期后肢悬吊 (HS) 对大鼠比目鱼肌中 Na,K-ATP 酶的亚型特异性影响。将大鼠暴露于 HS 24-72 小时,我们分析了其对比目鱼肌质量和收缩参数的影响;肌纤维的兴奋性和静息膜电位(RMP); α1 和 α2 Na,K-ATP 酶的电活性、蛋白质和 mRNA 含量; α2 Na,K-ATP酶的功能活性和质膜定位。我们的结果表明,24-72 小时的 HS 特异性降低了 Na,K-ATPaseα2 同工酶的生电活性和比目鱼肌纤维的 RMP。这种减少发生在肌肉萎缩或收缩参数发生任何变化之前。 HS处理24小时后α2 mRNA和蛋白质含量增加,72小时恢复到初始水平;然而,即使增加含量也无法恢复废弃比目鱼肌中的α2酶活性。 α2 Na,K-ATP酶的膜定位没有变化。 α1 Na,K-ATP酶的电活性、蛋白质和mRNA含量没有变化。我们的研究结果表明,α2 Na,K-ATP 酶转运活性绝对需要骨骼肌的使用,并提供了 Na,K-ATP 酶改变先于 HS 诱导的肌肉萎缩的第一个证据。
This study examines the isoform‐specific effects of short‐term hindlimb suspension (HS) on the Na,K‐ATPase in rat soleus muscle. Rats were exposed to 24–72 h of HS and we analyzed the consequences on soleus muscle mass and contractile parameters; excitability and the resting membrane potential (RMP) of muscle fibers; the electrogenic activity, protein, and mRNA content of theα1 andα2 Na,K‐ATPase; the functional activity and plasma membrane localization of theα2 Na,K‐ATPase. Our results indicate that 24–72 h of HS specifically decreases the electrogenic activity of the Na,K‐ATPaseα2 isozyme and the RMP of soleus muscle fibers. This decrease occurs prior to muscle atrophy or any change in contractile parameters. Theα2 mRNA and protein content increased after 24 h of HS and returned to initial levels at 72 h; however, even the increased content was not able to restoreα2 enzyme activity in the disused soleus muscle. There was no change in the membrane localization ofα2 Na,K‐ATPase. Theα1 Na,K‐ATPase electrogenic activity, protein and mRNA content did not change. Our findings suggest that skeletal muscle use is absolutely required forα2 Na,K‐ATPase transport activity and provide the first evidence that Na,K‐ATPase alterations precede HS‐induced muscle atrophy.