Chan S, Head S I, Morley J W
School of Medical Sciences, Univ. of New South Wales, Sydney 2052, Australia.
Am J Physiol Cell Physiol. 2007 Sep;293(3):C985-92. doi: 10.1152/ajpcell.00128.2007. Epub 2007 Jun 13.
We demonstrated that the susceptibility of skeletal muscle to injury from lengthening contractions in the dystrophin-deficient mdx mouse is directly linked with the extent of fiber branching within the muscles and that both parameters increase as the mdx animal ages. We subjected isolated extensor digitorum longus muscles to a lengthening contraction protocol of 15% strain and measured the resulting drop in force production (force deficit). We also examined the morphology of individual muscle fibers. In mdx mice 1-2 mo of age, 17% of muscle fibers were branched, and the force deficit of 7% was not significantly different from that of age-matched littermate controls. In mdx mice 6-7 mo of age, 89% of muscle fibers were branched, and the force deficit of 58% was significantly higher than the 25% force deficit of age-matched littermate controls. These data demonstrated an association between the extent of branching and the greater vulnerability to contraction-induced injury in the older fast-twitch dystrophic muscle. Our findings demonstrate that fiber branching may play a role in the pathogenesis of muscular dystrophy in mdx mice, and this could affect the interpretation of previous studies involving lengthening contractions in this animal.
我们证明，在缺乏抗肌萎缩蛋白的mdx小鼠中，骨骼肌对拉长收缩损伤的易感性与肌肉内纤维分支的程度直接相关，并且随着mdx动物年龄的增长，这两个参数都会增加。我们对分离的趾长伸肌施加15%应变的拉长收缩方案，并测量由此产生的力产生下降（力亏缺）。我们还检查了单个肌纤维的形态。在1-2月龄的mdx小鼠中，17%的肌纤维有分支，7%的力亏缺与年龄匹配的同窝对照无显著差异。在6-7月龄的mdx小鼠中，89%的肌纤维有分支，58%的力亏缺显著高于年龄匹配的同窝对照的25%力亏缺。这些数据表明，在老年快肌营养不良肌肉中，分支程度与收缩诱导损伤的更大易感性之间存在关联。我们的研究结果表明，纤维分支可能在mdx小鼠肌肉营养不良的发病机制中起作用，这可能会影响以前涉及该动物拉长收缩的研究的解释。
