Efficacy of passive repetitive stretching of skeletal muscle on myofiber hypertrophy and genetic suppression on MAFbx, MuRF1, and myostatin.

IF 1.7 3区 生物学 Q4 CELL BIOLOGY
Yumin Wang, Satoshi Ikeda, Katsunori Ikoma
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引用次数: 4

Abstract

Skeletal muscles undergo adaptations in response to mechanical stimuli such as stretching. However, there is limited evidence regarding the hypertrophic effects of passive repetitive stretching in vivo. We examined the effect of passive repetitive stretching on skeletal muscle myofiber morphology, satellite cell content, and messenger RNA expression of myogenic regulatory factors and signaling molecules involved in muscle protein synthesis and degradation. The gastrocnemius muscles of mice were stretched 15 times/min by manual ankle dorsiflexion for 15 min, 5 days a week for 2 weeks. We found that passive repetitive stretching significantly increased myofiber cross-sectional area. In stretched gastrocnemius muscles, the messenger RNA expression of p70S6K and myogenin was upregulated, whereas MuRF1, MAFbx, myostatin, and 4E-BP1 were downregulated. The phosphorylation level of p70S6K was significantly increased in stretched muscles. The number of Pax7+ cells was unaffected. Passive repetitive stretching induces muscle hypertrophy by regulating signaling pathways involved in muscle protein turnover. These findings are applicable to clinical muscle strengthening and for the maintenance of skeletal muscle mass and function in patients who are unconscious or paralyzed.

被动重复拉伸骨骼肌对肌纤维肥大的影响以及对MAFbx、MuRF1和肌肉生长抑制素的基因抑制。
骨骼肌对拉伸等机械刺激进行适应。然而,关于体内被动重复拉伸的肥厚效应的证据有限。我们研究了被动重复拉伸对骨骼肌肌纤维形态、卫星细胞含量、肌生成调节因子和参与肌肉蛋白合成和降解的信号分子的信使RNA表达的影响。采用手动踝关节背伸法拉伸小鼠腓肠肌15次/min,持续15 min,每周5天,连续2周。我们发现被动重复拉伸显著增加肌纤维横截面积。在拉伸腓肠肌中,p70S6K和myogenin的信使RNA表达上调,而MuRF1、MAFbx、myostatin和4E-BP1的表达下调。拉伸肌肉中p70S6K的磷酸化水平显著升高。Pax7+细胞数量不受影响。被动重复拉伸通过调节参与肌肉蛋白转换的信号通路诱导肌肉肥大。这些发现适用于临床肌肉强化以及昏迷或瘫痪患者骨骼肌质量和功能的维持。
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来源期刊
CiteScore
6.20
自引率
0.00%
发文量
21
审稿时长
>12 weeks
期刊介绍: The Journal of Muscle Research and Cell Motility has as its main aim the publication of original research which bears on either the excitation and contraction of muscle, the analysis of any one of the processes involved therein, the processes underlying contractility and motility of animal and plant cells, the toxicology and pharmacology related to contractility, or the formation, dynamics and turnover of contractile structures in muscle and non-muscle cells. Studies describing the impact of pathogenic mutations in genes encoding components of contractile structures in humans or animals are welcome, provided they offer mechanistic insight into the disease process or the underlying gene function. The policy of the Journal is to encourage any form of novel practical study whatever its specialist interest, as long as it falls within this broad field. Theoretical essays are welcome provided that they are concise and suggest practical ways in which they may be tested. Manuscripts reporting new mutations in known disease genes without validation and mechanistic insight will not be considered. It is the policy of the journal that cells lines, hybridomas and DNA clones should be made available by the developers to any qualified investigator. Submission of a manuscript for publication constitutes an agreement of the authors to abide by this principle.
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