Delaporte C, Defer G, Diaz C, Gherardi R, Dautréaux B, Degos J D
INSERM U. 153, Paris, France.
J Neurol Sci. 1991 Oct;105(2):183-91. doi: 10.1016/0022-510x(91)90143-u.
Proliferation and differentiation of myoblasts from hypertrophic muscles were studied "in vitro" in two cases of syringomyelia with muscle hypertrophy (MH). Their myoblast growth was compared with that of muscle cells sampled on the contralateral side in the same patients and in control subjects. The effect of a circulating factor was tested using patient sera in place of fetal calf and horse sera. The results showed that MH cells were morphologically abnormal (giant and granular). MH myoblasts proliferated more rapidly than contralateral and normal myoblasts, their fusion was accelerated and the resulting myotubes synthesized higher levels of protein. MH sera increased these effects. Serum factors are therefore likely to be involved in "in vivo" muscle hypertrophy. These findings suggest that the pathogenesis of muscle hypertrophy in syringomyelia involves acquired abnormalities due to molecules released in response to neural lesions.
在两例伴有肌肉肥大（MH）的脊髓空洞症患者中，对来自肥大肌肉的成肌细胞的增殖和分化进行了“体外”研究。将其成肌细胞生长情况与同一患者对侧以及对照受试者的肌肉细胞进行比较。使用患者血清替代胎牛血清和马血清来测试循环因子的作用。结果显示，MH细胞在形态上异常（巨大且呈颗粒状）。MH成肌细胞的增殖比同侧及正常成肌细胞更快，其融合加速，并且所形成的肌管合成的蛋白质水平更高。MH血清增强了这些效应。因此，血清因子可能参与了“体内”肌肉肥大过程。这些发现提示，脊髓空洞症中肌肉肥大的发病机制涉及因神经损伤而释放的分子所导致的后天性异常。
