Mechanical loading of tissue engineered skeletal muscle prevents dexamethasone induced myotube atrophy.
Mechanical loading of tissue engineered skeletal muscle prevents dexamethasone induced myotube atrophy.
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组织工程化骨骼肌的机械负荷预防地塞米松诱导的肌管萎缩。
DOI：
10.1007/s10974-020-09589-0
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发表时间：
2021-06
影响因子：
2.7
通讯作者：
Lewis MP
中科院分区：
文献类型：
--
作者：
Aguilar-Agon KW;Capel AJ;Fleming JW;Player DJ;Martin NRW;Lewis MP
由于急性和慢性疾病、固定、肌肉萎缩症和衰老导致的骨骼肌萎缩导致严重的肌肉无力、不活动和死亡率增加。机械负荷被认为是骨骼肌肥大的主要驱动力，然而机械负荷可以抵消肌肉紧张的程度尚未得到彻底的探讨。骨骼肌的体外3D模型提供了一个可控的、高通量的环境，并减轻了体内实验期间存在的许多伦理和方法学限制。这项工作旨在确定机械负荷是否会抵消地塞米松（DEX）诱导的骨骼肌萎缩，在肌肉工程使用C2 C12鼠细胞系。机械负荷成功地抵消了与DEX相关的肌管萎缩和功能退化，无论负荷发生在DEX治疗24小时之前还是之后。此外，机械负荷防止了肌肉萎缩的关键调节因子MuRF-1和MAFbx mRNA表达的增加。总的来说，我们展示了组织工程肌肉在研究骨骼肌健康和疾病中的应用，为未来更好地了解骨骼肌萎缩的治疗方式提供了巨大的潜力。本文的在线版本（10.1007/s10974-020-09589-0）包含补充材料，可供授权用户使用。
Skeletal muscle atrophy as a consequence of acute and chronic illness, immobilisation, muscular dystrophies and aging, leads to severe muscle weakness, inactivity and increased mortality. Mechanical loading is thought to be the primary driver for skeletal muscle hypertrophy, however the extent to which mechanical loading can offset muscle catabolism has not been thoroughly explored. In vitro 3D-models of skeletal muscle provide a controllable, high throughput environment and mitigating many of the ethical and methodological constraints present during in vivo experimentation. This work aimed to determine if mechanical loading would offset dexamethasone (DEX) induced skeletal muscle atrophy, in muscle engineered using the C2C12 murine cell line. Mechanical loading successfully offset myotube atrophy and functional degeneration associated with DEX regardless of whether the loading occurred before or after 24 h of DEX treatment. Furthermore, mechanical load prevented increases in MuRF-1 and MAFbx mRNA expression, critical regulators of muscle atrophy. Overall, we demonstrate the application of tissue engineered muscle to study skeletal muscle health and disease, offering great potential for future use to better understand treatment modalities for skeletal muscle atrophy. The online version of this article (10.1007/s10974-020-09589-0) contains supplementary material, which is available to authorized users.
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