Screening of muscle regenerative molecules for Duchenne muscular dystrophy

小鼠的核磁共振成像显示耳朵穿孔伤口完全愈合。然而，加速伤口愈合的遗传和分子机制在很大程度上仍然未知。我们将缺乏肌营养不良蛋白的mdx小鼠与MRL小鼠交配，以产生和表征MRL引入的mdx小鼠。与mdx小鼠相比，MRL-mdx小鼠显示肌纤维大小和中心核肌纤维数量增加，但膈肌纤维化减少。通过比较mdx和MRL-mdx小鼠膈肌的基因表达谱，我们发现了几个候选基因对mrl来源的肌肉再生有贡献。其中，两个基因最终加速了培养成肌细胞中肌管的形成。我们的研究结果表明，MRL伤口愈合剂的引入通过减少肌肉纤维化来加速肌肉再生，从而成为抗营养不良蛋白缺乏症的一种新的治疗选择。

The MRL mouse shows complete closure of ear punch wounds. However, genetic and molecular mechanisms underlying the accelerated wound healing have remained largely unknown. We have mated dystrophin-deficient mdx mice with MRL mice to generate and characterize MRL-introduced mdx mice. Compared to the mdx mice, the MRL-mdx mice showed increased myofiber size and centrally-nucleated myofiber number, but decreased fibrosis in the diaphragm. By comparing the gene expression profile in diaphragm between mdx and MRL-mdx mice, we found several candidate genes contributing to the MRL-originated muscle regeneration. Among them, two genes eventually accelerating myotube formation in cultured myoblasts. Our results suggest that the introduction of the MRL wound-healer accelerates muscle regeneration by reducing muscle fibrosis, thereby becoming a novel therapeutic option for the dystrophin-deficient muscular dystrophy.