Spontaneous regeneration of older dystrophic muscle does not reflect its regenerative capacity.
Spontaneous regeneration of older dystrophic muscle does not reflect its regenerative capacity.
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老年营养不良肌肉的自发再生并不能反映其再生能力。
DOI：
10.1002/aja.1001810102
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Taylor,F
中科院分区：
文献类型：
--
作者：
Bourke,DL;Ontell,M;Taylor,F
年轻的营养不良(Dy)小鼠肌肉能够(自发)再生(即，在没有外部创伤的情况下再生)；然而，当小鼠出生8周时，这种再生停止。营养不良肌肉再生的停止可能是由于疾病早期肌卫星细胞的有丝分裂能力耗尽所致。为了验证这种假说，我们对14-16周龄的129只Rej/++和129只Rej/Dydy小鼠进行了完整的指长伸肌原位移植。移植的营养不良肌在移植后100天内能产生并维持356±22条肌纤维，与年龄匹配的营养不良肌相似。陈旧性营养不良肌肉在极端创伤后的再生能力表明，(自发)再生的停止是由于肌卫星细胞有丝分裂能力衰竭以外的因素(S)所致。此外，在移植的正常肌肉和营养不良肌肉(移植后100天)之间，肌卫星细胞频率没有显著差异。移植肌肉中的肌卫星细胞频率与年龄匹配、未受创伤的肌肉中的频率相似。虽然年轻的营养不良肌肉移植改变了通常与小鼠营养不良相关的组织病理学变化的表型表达，但老年营养不良肌肉移植的移植物表现出广泛的结缔组织渗透，肌纤维明显少于年龄匹配的正常肌肉移植物。早在移植后14天，就有可能区分陈旧、正常和营养不良的肌肉移植物。这表明，移植时营养不良肌肉中存在的结缔组织基质可能会在移植过程中存活下来。
Young dystrophic (dy) murine muscle is capable of ( spontaneous) regeneration (i.e., regeneration in the absence of external trauma); however, by the time the mice are 8 weeks old, this regeneration ceases. It has been suggested that the cessation of regeneration in dystrophic muscle may be due to exhaustion of the mitotic capability of myosatellite cells during the early stages of the disease. To test this hyptothesis, orthotopic transplantation of bupivacaine treated, whole extensor digitorum longus muscles has been performed on 14 to 16‐week‐old 129 ReJ/++ and 129 ReJ/dydy mice. The grafted dystrophic muscle is able to produce and maintain for 100 days post‐transplantation 356 ± 22 myofibers, a number similar to that found in age‐matched dystrophic muscle. The ability of old dystrophic muscle to regenerate subsequent to extreme trauma indicates that the cessation of ( spontaneous) regeneration is due to factor(s) other than the exhaustion of mitotic capability of myosatellite cells. Moreover, there is no significant difference in myosatellite cell frequencies between grafted normal and dystrophic muscles (100 days post‐transplantation). Myosatellite cell frequencies in grafted muscles are similar to those in age‐matched, untraumatized muscles. While grafting of young dystrophic muscle modifies the phenotypic expression of histopathological changes usually associated with murine dystrophy, grafts of older dystrophic muscle show extensive connective‐tissue infiltration and significantly fewer myofibers than do grafts of age‐matched normal muscle. As early as 14 days post‐transplantation, it is possible to distinguish between grafts of old, normal and dystrophic muscles. It is suggested that the connective tissue stroma, present in the dystrophic muscle at the time of transplantation, may survive the grafting procedure.