Early changes in muscle fiber size and gene expression in response to spinal cord transection and exercise

Early changes in muscle fiber size and gene expression in response to spinal cord transection and exercise
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DOI:
10.1152/ajpcell.1998.275.4.c1124
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发表时间:
1998-10-01
影响因子:
5.5
通讯作者:
Peterson, CA
Peterson, CA
中科院分区:
生物学2区
文献类型:
--
作者:
Dupont-Versteegden, EE;Houlé, JD;Peterson, CA

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脊髓横断的大鼠肌肉表现出严重的萎缩,并向更快的表型转移。锻炼可以部分预防这些变化。本研究的目的是研究参与调节肌肉对脊柱横断和被动后肢运动反应的早期事件。成年雌性Sprague-Dawley大鼠麻醉后,除对照组外,所有大鼠均出现完整的脊髓横断损伤(T-10)。大鼠在横断后5、10天处死,或从横断后5天开始每天骑摩托车运动,在第一次运动后0.5、1、5天处死。研究了比目鱼肌和指长伸肌(EDL)的结构和生化特征。运动5天后,比目鱼肌所有纤维类型以及EDL 2a型和2x型纤维的萎缩均有所减轻。然而,运动似乎没有影响脊髓横断后5天内纤维类型的改变:表达肌球蛋白重链2x的纤维在比目鱼和EDL中增加,肌球蛋白重链在比目鱼中明显广泛共表达。无论运动状态如何,在横断的大鼠的两条肌肉中都观察到卫星细胞的激活,MyoD和肌原素的积累增加证明了这一点。除了MyoD在比目鱼中保持升高外,表达增加是短暂的。在两种肌肉的肌纤维和卫星细胞核中均检测到MyoD和myogenin,但在比目鱼肌中,MyoD优先在卫星细胞核中表达,而在EDL中,MyoD更容易在肌纤维核中检测到,这表明MyoD和myogenin在不同肌肉中具有不同的功能。运动不影响MyoD和肌原素表达的水平或定位。同样,在脊髓横断后,Id-1在比目鱼和EDL中的表达短暂升高,运动对其无影响。这些结果表明,被动运动可以改善脊髓横断后的肌肉萎缩,卫星细胞激活可能在脊髓横断和运动后的肌肉可塑性中起作用。最后,维持肌肉质量的机制可能不同于控制肌球蛋白重链表达的机制。
Muscles of spinal cord-transected rats exhibit severe atrophy and a shift toward a faster phenotype. Exercise can partially prevent these changes. The goal of this study was to investigate early events involved in regulating the muscle response to spinal transection and passive hindlimb exercise. Adult female Sprague-Dawley rats were anesthetized, and a complete spinal cord transection lesion (T-10) was created in all rats except controls. Rats were killed 5 or 10 days after transection or they were exercised daily on motor-driven bicycles starting at 5 days after transection and were killed 0.5, 1, or 5 days after the first bout of exercise. Structural and biochemical features of soleus and extensor digitorum longus (EDL) muscles were studied. Atrophy was decreased in all fiber types of soleus and in type 2a and type 2x fibers of EDL after 5 days of exercise. However, exercise did not appear to affect fiber type that was altered within 5 days of spinal cord transection: fibers expressing myosin heavy chain 2x increased in soleus and EDL, and extensive coexpression of myosin heavy chain in soleus was apparent. Activation of satellite cells was observed in both muscles of transected rats regardless of exercise status, evidenced by increased accumulation of MyoD and myogenin. Increased expression was transient, except for MyoD, which remained elevated in soleus. MyoD and myogenin were detected both in myofiber and in satellite cell nuclei in both muscles, but in soleus, MyoD was preferentially expressed in satellite cell nuclei, and in EDL, MyoD was more readily detectable in myofiber nuclei, suggesting that MyoD and myogenin have different functions in different muscles. Exercise did not affect the level or localization of MyoD and myogenin expression. Similarly, Id-1 expression was transiently increased in soleus and EDL upon spinal cord transection, and no effect of exercise was observed. These results indicate that passive exercise can ameliorate muscle atrophy after spinal cord transection and that satellite cell activation may play a role in muscle plasticity in response to spinal cord transection and exercise. Finally, the mechanisms underlying maintenance of muscle mass are likely distinct from those controlling myosin heavy chain expression.