Lorenzon Paola, Bandi Elena, de Guarrini Francesca, Pietrangelo Tiziana, Schäfer Ralf, Zweyer Margit, Wernig Anton, Ruzzier Fabio
Department of Physiology and Pathology and Centre for Neuroscience B.R.A.I.N., University of Trieste, via A. Fleming 22, I-34127 Trieste, Italy.
Exp Gerontol. 2004 Oct;39(10):1545-54. doi: 10.1016/j.exger.2004.07.008.
The ageing process causes a reduction in the regenerative potential of skeletal muscles eventually leading to diminished muscle strength. In this work we investigated if ageing affects the excitation-contraction coupling mechanism in human myotubes derived from human satellite cells, thereby contributing to the loss in muscle strength in the aged. To test this hypothesis, satellite cells from differently aged donors were differentiated in vitro and the maturation of the excitation-contraction mechanism was followed by the videoimaging technique monitoring the efficiency of such a mechanism in generating intracellular calcium transients. Our experiments showed a delay in the establishment of the excitation-contraction coupling mechanism depending on the age of the donor. Remarkably, the effect was reproducible in human satellite cells from a young donor aged in vitro, suggesting that the delayed functional maturation was strictly dependent on the number of satellite cell divisions and independent from the host environment.
衰老过程会导致骨骼肌再生潜力下降,最终致使肌肉力量减弱。在这项研究中,我们探究了衰老是否会影响源自人类卫星细胞的人肌管中的兴奋-收缩偶联机制,进而导致老年人肌肉力量的丧失。为验证这一假设,我们将来自不同年龄供体的卫星细胞进行体外分化,并通过视频成像技术监测兴奋-收缩机制在产生细胞内钙瞬变方面的效率,以此追踪兴奋-收缩机制的成熟过程。我们的实验表明,兴奋-收缩偶联机制的建立存在延迟,且这种延迟取决于供体的年龄。值得注意的是,在体外老化的年轻供体的人类卫星细胞中也能重现这一效应,这表明功能成熟延迟严格依赖于卫星细胞的分裂次数,而与宿主环境无关。