Botulinum neurotoxin type A causes shifts in myosin heavy chain composition in muscle

Botulinum neurotoxin type A causes shifts in myosin heavy chain composition in muscle
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DOI:
10.1016/j.toxicon.2005.03.022
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发表时间:
2005-08-01
期刊:
影响因子:
2.8
通讯作者:
Dott, C
Dott, C
中科院分区:
医学4区
文献类型:
--
作者:
Dodd, SL;Selsby, J;Dott, C

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A 型肉毒杆菌神经毒素已广泛用于治疗多种神经肌肉疾病。然而,这种毒素对骨骼肌组织学和生化特性的潜在影响在很大程度上仍未被探索。本研究的目的是表征经肉毒杆菌神经毒素治疗的成年大鼠骨骼肌的肌球蛋白重链 (MHC) 分布。将不同剂量的毒素注射到一侧后肢的小腿三头肌群中。定期评估力量生产,以了解所发生的功能缺陷。 10周后,处死动物,取出肌肉,并测定MHC组成。所有组中注射腿的体重、肌肉重量和力量均显着减少,而对侧腿的肌肉重量和力量的损失则各不相同。在注射的跖肌和腓肠肌中,I 型 MHC 增加了约 100%,而 IIa/x 型则减少了约 50%。在对侧腓肠肌中,I 型和 IIa/x MHC 增加约 100%,而 IIb 型减少约 45%。这些数据表明,肉毒杆菌神经毒素会导致注射肌肉和对侧肌肉的 MHC 组成发生变化,这与去神经支配时所见的变化相反,而与衰老时所见的变化相似。 (c) 2005 Elsevier Ltd. 保留所有权利。
Botulinum neurotoxin type A has gained widespread use for treatment of a host of neuromuscular conditions. However, the potential effect of this toxin has on the histological and biochemical properties of skeletal muscle remains largely unexplored. The purpose of this study was to characterize the myosin heavy chain (MHC) distribution of adult rat skeletal muscle treated with botulinum neurotoxin type. Varying doses of the toxin were injected into the triceps surae muscle group of one hind limb. Force production was assessed periodically to access the functional deficit incurred. After 10 weeks, animals were sacrificed, muscles removed, and MHC composition determined. Body weight, muscle weight and force of the injected leg were significantly reduced in all groups, while loss of muscle weight and force in the contralateral leg was variable. In the injected plantaris and gastrocnernius muscles, type I MHC increased similar to 100%, while type IIa/x decreased similar to 50%. In the contralateral gastrocnemius, types I and IIa/x MHC increased similar to 100%, while type IIb decreased similar to 45%. These data suggest that botulinum neurotoxin causes shifts in MHC composition in injected and contralateral muscles that are contrary to those seen with denervation and similar to those seen with aging. (c) 2005 Elsevier Ltd. All rights reserved.