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目的探讨CNTF对失重性肌萎缩及其纤维表型转换的干预作用。方法用尾吊方法制备失重性肌萎缩模型,通过采用RT-PCR和Western blot分析方法检测MHC-I/IIb和p130或Myf5表达的变化,以揭示CNTF对失重性肌萎缩及其纤维表型转换的影响。结果与对照组相比,体内注射CNTF显著逆转失重诱导的慢肌比目鱼肌重量的丢失。此外,尾吊过程中的动态分析结果也提示,CNTF处理可明显削弱失重诱导的慢肌比目鱼肌重量的丢失及其慢肌向快肌纤维表型的转换。课题组进一步发现CNTF的这种干预效应伴随着肌卫星细胞特异标志p130和Myf5蛋白的上调,这就提示了CNTF处理的慢肌比目鱼肌中肌卫星细胞库增加。结论本研究首次揭示了CNTF可通过增加慢肌的肌卫星细胞库干预失重性肌萎缩及其纤维表型的转换。
Objective To investigate the effect of CNTF on weightless muscle atrophy and its phenotypic change. Methods The model of weightless muscle atrophy was prepared by tail-hanging method. The changes of MHC-I / IIb and p130 or Myf5 expression were detected by RT-PCR and Western blot analysis to reveal the effect of CNTF on weightless muscle atrophy and its phenotypic change Impact. Results Compared with the control group, CNTF injection in vivo significantly reversed weight loss in slow muscle-soleus muscle. In addition, the results of dynamic analysis during the tail-hanging also suggested that CNTF treatment could significantly reduce the weight loss-induced slow muscle soleus muscle weight loss and its slow muscle to fast muscle fiber phenotype conversion. The research team further found that this interventional effect of CNTF is accompanied by an upregulation of muscle-satellite-cell-specific markers p130 and Myf5 proteins, suggesting an increase in muscle satellite cell banks in CNTF-treated slow muscle soleus muscles. Conclusions This study reveals, for the first time, that CNTF interferes with the conversion of weightless muscle atrophy and its fibrotic phenotype by augmentation of the slow satellite muscle satellite cell bank.