Narukami H, Yoshioka K, Zhao J, Miike T
Department of Child Development, Kumamoto University Medical School, Japan.
Acta Neuropathol. 1991;81(5):510-6. doi: 10.1007/BF00310131.
Degenerating and regenerating muscle fibers, in serotonin-induced myopathy (SM) of rats, were investigated histochemically, immunohistochemically and electron microscopically with polyclonal antibodies against dystrophin, type IV collagen and laminin. The myopathy produced was characterized by grouping of degenerating and regenerating muscle fibers, and degeneration of capillary endothelial cells. Dystrophin disappeared in an early stage of muscle degeneration and reappeared in an early stage of regeneration. On the other hand, type IV collagen and laminin were well preserved throughout the degeneration and regeneration processes, even on the shrunk and wrinkled basement membrane of empty muscle fibers after phagocytosis. Muscle fiber regeneration was completed within each tube of the preserved basement membrane through the fusion of myoblasts derived from satellite cells of single necrotic fibers, myotubes already being visible on the 1st or 2nd day of regeneration on light microscopy. These small regenerating myotubes did not fuse with each other at all. The findings in the present experimental SM study are compatible with those in Duchenne muscular dystrophy, especially at the preclinical stage.
利用抗肌营养不良蛋白、IV型胶原和层粘连蛋白的多克隆抗体,通过组织化学、免疫组织化学和电子显微镜技术,对大鼠血清素诱导性肌病(SM)中退变和再生的肌纤维进行了研究。所产生的肌病的特征是退变和再生的肌纤维成组,以及毛细血管内皮细胞退变。肌营养不良蛋白在肌肉退变早期消失,并在再生早期重新出现。另一方面,IV型胶原和层粘连蛋白在整个退变和再生过程中都保存良好,即使在吞噬后空肌纤维皱缩的基底膜上也是如此。肌纤维再生通过单根坏死纤维卫星细胞衍生的成肌细胞融合在保留的基底膜的每一根管内完成,在再生的第1天或第2天,光镜下即可见到肌管。这些小的再生肌管根本不会相互融合。本实验性SM研究的结果与杜兴氏肌营养不良症的结果相符,尤其是在临床前期。