肌卫星细胞在骨骼肌生长发育和出生后骨骼肌损伤修复中起着重要的作用,但是有关肌萎缩中肌卫星细胞的可塑性变化、作用及其机制尚不清楚.本研究采用小鼠尾悬吊模拟失重效应诱导失重肌萎缩,动态分析了失重肌萎缩发生过程中不同类型肌纤维的肌卫星细胞数量和增殖、分化潜能可塑性的改变,发现在失重肌萎缩过程中,处于安静状态的肌卫星细胞显著增多、激活增殖的肌卫星细胞显著减少,而具有成肌分化潜能的肌卫星细胞有持续减少趋势.此外,在失重肌萎缩比目鱼肌单根肌纤维移出的体外培养中,证明了失重肌萎缩肌纤维肌卫星细胞可塑性降低的特征性变化.进一步,通过对比分析Smad3基因敲除及其同窝野生型小鼠,在失重肌萎缩中肌卫星细胞可塑性的差异性变化,揭示了Smad3在调控失重肌萎缩肌卫星细胞可塑性变化中的关键作用.
Muscle satellite cells play an important role in the growth and development as well as postnatal injury and repair of skeletal muscles, however, it keeps unclear about muscle satellite cell plasticity, effect and mechanism in atrophied muscle. In the present study, we investigated the changes in the satellite cell number and potency of proliferation and differentiation during weightless muscle atrophy induced by mouse hindlimb suspension, and found that the number of quiet satellite cells significantly increased but that of activated cells significantly decreased, and the potential of cell myogenic differentiation also appeared a reduced tendency.Moreover, we verified the above changes of muscle satellite cell plasticity in the cultures of ex vivo single myofibers isolated from weightless atrophied soleus. Finally, Smad3 knockout mice and its wild-type littermates were subjected to hindlimb suspension induced muscle atrophy, and the variability analysis demonstrated that the key role of Smad3 in regulating the plasticity of muscle satellite cells weightless muscle atrophy.