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首页> 美国卫生研究院文献>The Journals of Gerontology Series A: Biological Sciences and Medical Sciences >Age-related Differences in Dystrophin: Impact on Force Transfer Proteins Membrane Integrity and Neuromuscular Junction Stability
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Age-related Differences in Dystrophin: Impact on Force Transfer Proteins Membrane Integrity and Neuromuscular Junction Stability

机译：肌营养不良蛋白的年龄相关差异：对力传递蛋白膜完整性和神经肌肉连接稳定性的影响。

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The loss of muscle strength with age has been studied from the perspective of a decline in muscle mass and neuromuscular junction (NMJ) stability. A third potential factor is force transmission. The purpose of this study was to determine the changes in the force transfer apparatus within aging muscle and the impact on membrane integrity and NMJ stability. We measured an age-related loss of dystrophin protein that was greatest in the flexor muscles. The loss of dystrophin protein occurred despite a twofold increase in dystrophin mRNA. Importantly, this disparity could be explained by the four- to fivefold upregulation of the dystromir miR-31. To compensate for the loss of dystrophin protein, aged muscle contained increased α-sarcoglycan, syntrophin, sarcospan, laminin, β1-integrin, desmuslin, and the Z-line proteins α-actinin and desmin. In spite of the adaptive increase in other force transfer proteins, over the 48 hours following lengthening contractions, the old muscles showed more signs of impaired membrane integrity (fourfold increase in immunoglobulin G-positive fibers and 70% greater dysferlin mRNA) and NMJ instability (14- to 96-fold increases in Runx1, AchRδ, and myogenin mRNA). Overall, these data suggest that age-dependent alterations in dystrophin leave the muscle membrane and NMJ more susceptible to contraction-induced damage even before changes in muscle mass are obvious.
机译：从肌肉质量和神经肌肉接头（NMJ）稳定性下降的角度研究了肌肉强度随着年龄的增长而下降的情况。第三个潜在因素是力传递。这项研究的目的是确定老化肌肉内力传递装置的变化以及对膜完整性和NMJ稳定性的影响。我们测量了在屈肌中最大的与年龄相关的肌营养不良蛋白的丢失。尽管肌营养不良蛋白mRNA增加了两倍，但肌营养不良蛋白的损失还是发生了。重要的是，这种差异可以通过dystromir miR-31的四到五倍上调来解释。为了弥补肌营养不良蛋白的损失，老年肌肉中含有增加的α-糖蛋白，突触核蛋白，肌膜粘连蛋白，层粘连蛋白，β1-整联蛋白，desmuslin以及Z线蛋白α-actinin和desmin。尽管其他力传递蛋白有适应性增加，但在延长收缩后的48小时内，旧肌肉仍显示出更多的膜完整性受损迹象（免疫球蛋白G阳性纤维增加了4倍，dysferlin mRNA增加了70％）和NMJ不稳定性（ Runx1，AchRδ和肌生成素mRNA增加14至96倍。总体而言，这些数据表明肌营养不良蛋白的年龄依赖性改变使肌肉膜和NMJ甚至在明显改变肌肉质量之前就更容易受到收缩引起的损害。

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