Ontell M, Feng K C, Klueber K, Dunn R F, Taylor F
Anat Rec. 1984 Feb;208(2):159-74. doi: 10.1002/ar.1092080203.
Patterns of growth and regeneration in 2-, 4-, 8-, and 17-week-old murine dystrophic (129 ReJ dy/dy) extensor digitorum longus muscles have been determined. Necrosis and myofiber loss, hypertrophy, and regeneration result in a reduced population of myofibers whose diameter distribution is more extensive than that found in the extensor digitorum longus muscles of age-matched normal mice. At the onset of dystrophic symptoms (2 weeks postnatal), the ratio of myosatellite cell nuclei to the total sublaminal nuclear population (myonuclei + myosatellite cells) is similar to that found in 2-week-old control muscles. The frequency of finding myosatellite cells decreases with age in both control and dystrophic muscles. Myosatellite cells account for 11%, 6%, 5%, and 3% of the total sublaminal nuclear population in control muscle and 12%, 8%, 6%, and 5% of the total sublaminal nuclear population in dystrophic muscle at 2, 4, 8, and 17 weeks, respectively. No preferential association of myosatellite cells with myofibers of a particular diameter is found in control muscle or in the two youngest dystrophic groups. At 8 and 17 weeks, myosatellite cells are less frequently encountered on small-diameter, regenerating myofibers of dystrophic muscle, and they are preferentially associated with large diameter, hypertrophied myofibers. The labeling index of myosatellite cells decreases with age in both normal and dystrophic muscle. At all ages the myosatellite cell labeling index is higher in dystrophic muscle (23%, 7%, 5%, and 2% at 2, 4, 8, and 17 weeks, respectively) than in normal muscle (5%, less than 1% at 2 and 4 weeks, respectively), with no labeled myosatellite cells being found in 8- and 17-week-old normal muscles. It is suggested that the magnitude of the regenerative response of dystrophic murine muscle decreases with age and that this factor may be responsible for the inability of the regenerative response of dystrophic muscle to keep pace with the rapid muscle deterioration.
已确定2周、4周、8周和17周龄的小鼠营养不良型（129 ReJ dy/dy）趾长伸肌的生长和再生模式。坏死、肌纤维损失、肥大和再生导致肌纤维数量减少，其直径分布比年龄匹配的正常小鼠的趾长伸肌更广泛。在营养不良症状出现时（出生后2周），肌卫星细胞核与总板层下核群体（肌核+肌卫星细胞）的比例与2周龄对照肌肉中的比例相似。在对照肌肉和营养不良肌肉中，发现肌卫星细胞的频率均随年龄增长而降低。在2周、4周、8周和17周时，肌卫星细胞分别占对照肌肉总板层下核群体的11%、6%、5%和3%，占营养不良肌肉总板层下核群体的12%、8%、6%和5%。在对照肌肉或两个最年轻的营养不良组中，未发现肌卫星细胞与特定直径的肌纤维有优先关联。在8周和17周时，在营养不良肌肉的小直径再生肌纤维上较少遇到肌卫星细胞，它们优先与大直径、肥大的肌纤维相关联。正常肌肉和营养不良肌肉中肌卫星细胞的标记指数均随年龄增长而降低。在所有年龄段，营养不良肌肉中的肌卫星细胞标记指数均高于正常肌肉（2周、4周、8周和17周时分别为23%、7%、5%和2%），而正常肌肉（2周和4周时分别为5%、小于1%），在8周和17周龄的正常肌肉中未发现标记的肌卫星细胞。提示营养不良小鼠肌肉的再生反应强度随年龄增长而降低，这一因素可能是营养不良肌肉的再生反应无法跟上肌肉快速退化的原因。
