Percutaneous electrical stimulation-induced muscle contraction prevents the decrease in ribosome RNA and ribosome protein during pelvic hindlimb suspension
Percutaneous electrical stimulation-induced muscle contraction prevents the decrease in ribosome RNA and ribosome protein during pelvic hindlimb suspension
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DOI：
10.1152/japplphysiol.00204.2022
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发表时间：
2022-10-01
影响因子：
3.3
通讯作者：
Nakazato，Koichi
中科院分区：
文献类型：
--
作者：
Kotani，Takaya;Tamura，Yuki;Nakazato，Koichi
骨骼肌卸载导致肌肉萎缩。核糖体合成由于其翻译能力而被认为是重要的骨骼肌质量调节剂。肌肉去负荷导致核糖体合成和含量减少，伴随肌肉萎缩。经皮肌肉电刺激（pEMS）诱导的肌肉收缩被广泛用于临床，以改善肌肉质量。然而，其在挽救核糖体合成减少中的功效迄今尚未得到解决。我们研究了每日pEMS治疗对小鼠后肢卸载过程中核糖体合成和含量的影响。将雄性C57 BL/6 J小鼠随机分配到久坐（SED）组和通过骨盆悬吊（HU）的后肢去负荷组。肌肉收缩由HU组（HU + pEMS）的子集的右腓肠肌的pEMS处理触发。后肢卸载6天显着降低28 S rRNA，rpL 10，和rpS 3的表达，这是拯救每天pEMS治疗。HU + pEMS组磷酸化p70 S6 K和UBF蛋白表达明显高于HU组。HU组和HU + pEMS组的噬核糖体受体Nufip 1 mRNA表达均增加。蛋白质轻链3（LC 3）-II的表达和LC 3-II/LC 3-I的比例增加HU，但pEMS减弱这种增加。我们的研究结果表明，在HU期间，每日pEMS治疗可防止与核糖体合成相关的一些蛋白质水平的降低。此外，HU诱导的核糖体降解的活化可被减弱。这些数据提供了对肌肉废用期间核糖体含量调节和pEMS治疗减轻肌肉萎缩机制的见解。新&值得注意的是，肌肉不活动会减少萎缩期间核糖体的合成和含量。经皮肌肉电刺激（pEMS）诱导的肌肉收缩是否挽救了肌肉卸载过程中核糖体的合成和含量尚不清楚。使用小鼠后肢卸载模型与骨盆悬挂，我们提供的证据表明，每日pEMS诱导的肌肉收缩在后肢卸载救援的一些核糖体合成相关的蛋白质和核糖体含量的表达减少在腓肠肌。
Skeletal muscle unloading leads to muscle atrophy. Ribosome synthesis has been implicated as an important skeletal muscle mass regulator owing to its translational capacity. Muscle unloading induces a reduction in ribosome synthesis and content, with muscle atrophy. Percutaneous electrical muscle stimulation (pEMS)-induced muscle contraction is widely used in clinics to improve muscle mass. However, its efficacy in rescuing the reduction in ribosomal synthesis has not been addressed thus far. We examined the effects of daily pEMS treatment on ribosome synthesis and content during mouse hindlimb unloading. Male C57BL/6J mice were randomly assigned to sedentary (SED) and hindlimb unloading by pelvic suspension (HU) groups. Muscle contraction was triggered by pEMS treatment of the right gastrocnemius muscle of a subset of the HU group (HU + pEMS). Hindlimb unloading for 6 days significantly lowered 28S rRNA, rpL10, and rpS3 expression, which was rescued by daily pEMS treatment. The protein expression of phospho-p70S6K and UBF was significantly higher in the HU + pEMS than in the HU group. The mRNA expression of ribophagy receptor Nufip1 increased in both the HU and HU + pEMS groups. Protein light chain 3 (LC3)-II expression and the LC3-II/LC3-I ratio were increased by HU, but pEMS attenuated this increase. Our findings indicate that during HU, daily pEMS treatment prevents the reduction in the levels of some proteins associated with ribosome synthesis. In addition, the HU-induced activation of ribosome degradation may be attenuated. These data provide insights into ribosome content regulation and the mechanism of attenuation of muscle atrophy by pEMS treatment during muscle disuse.NEW & NOTEWORTHYMuscle inactivity reduces ribosome synthesis and content during atrophy. Whether percutaneous electrical muscle stimulation (pEMS)-induced muscle contraction rescues the ribosome synthesis and content during muscle unloading is unclear. Using a mouse hindlimb-unloading model with pelvic suspension, we provide evidence that daily pEMS-induced muscle contraction during hindlimb unloading rescues the reduction in the expression of some ribosome synthesis-related proteins and ribosome content in the gastrocnemius muscle.