Recovery of contractile and metabolic phenotypes in regenerating slow muscle after notexin-induced or crush injury
Recovery of contractile and metabolic phenotypes in regenerating slow muscle after notexin-induced or crush injury
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DOI：
10.1023/a:1027387501614
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发表时间：
2003-01-01
影响因子：
2.7
通讯作者：
Bigard, AX
中科院分区：
文献类型：
--
作者：
Fink, E;Fortin, D;Bigard, AX
肌肉损伤后代谢途径的恢复研究很少。观察了两种损伤后慢肌中肌球蛋白重链（MHC）亚型的转变和柠檬酸合酶（CS）活性的恢复，以及乳酸脱氢酶（LDH）和肌酸激酶（CK）亚型的分布。用Notexin注射法和挤压法诱导雄性Wistar大鼠左侧比目鱼肌变性，观察损伤后2 ~ 56天的再生过程。notexin后的肌球蛋白转变发生早于挤压伤后。快速IIx型，更特别是IIa型MHC亚型在notexin接种后第28天消失，而它们在压碎的肌肉中很久之后仍然被检测到。从42天开始，Notexin处理的肌肉中观察到CS活性和H-LDH亚基的比活性的完全恢复，而在压碎的肌肉中测量的值仍然显著低于未损伤的肌肉（P < 0.05）。线粒体CK同工酶（mi-CK）活性受损伤类型影响显著（P < 0.001），挤压伤后mi-CK活性未能恢复正常（P < 0.05）。这项研究的结果表明，相对快速的MHC转换再生过程中的氧化能力的缓慢恢复形成对比。挤压伤后氧化能力的恢复仍然不完全，这是一种已知会导致基底层破坏和血管和神经供应严重中断的损伤模型。
The recovery of metabolic pathways after muscle damage has been poorly studied. We investigated the myosin heavy chain (MHC) isoform transitions and the recovery of citrate synthase (CS) activity, isoform distribution of lactate dehydrogenase (LDH) and creatine kinase (CK) in slow muscles after two types of injury. Muscle degeneration was induced in left soleus muscles of male Wistar rats by either notexin injection or crushing and the regenerative process was examined from 2 to 56 days after injury. Myosin transition occurred earlier after notexin than after crush injury. Fast-type IIx and more particularly type IIa MHC isoform disappeared by day 28 after notexin inoculation, while they were still detected long after in crushed muscles. A full recovery of both the CS activity and the specific activity of the H-LDH subunit was observed from day 42 in notexin-treated muscles, while values measured in crushed muscles remained significantly lower than in non-injured muscles (P < 0.05). The activity of the mitochondrial isoform of CK (mi-CK) was markedly affected by the type of injury (P < 0.001), and failed to reach normal levels after crush injury (P < 0.05). The results of this study show that the relatively rapid MHC transitions during regeneration contrasts with the slow recovery in the oxidative capacity. The recovery of the oxidative capacity remained incomplete after crush injury, a model of injury known to lead to disruption of the basal lamina and severe interruption of the vascular and nerve supply.