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首页> 外文期刊>Molecular and Cellular Biology >Muscle-Derived Extracellular Signal-Regulated Kinases 1 and 2 Are Required for the Maintenance of Adult Myofibers and Their Neuromuscular Junctions
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Muscle-Derived Extracellular Signal-Regulated Kinases 1 and 2 Are Required for the Maintenance of Adult Myofibers and Their Neuromuscular Junctions

机译：肌肉衍生的细胞外信号调节激酶1和2是维持成人肌纤维及其神经肌肉接头的必需条件。

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The Ras–extracellular signal-regulated kinase 1 and 2 (ERK1/2) pathway appears to be important for the development, maintenance, aging, and pathology of mammalian skeletal muscle. Yet no gene targeting of Erk1/2 in muscle fibers in vivo has been reported to date. We combined a germ line Erk1 mutation with Cre-loxP Erk2 inactivation in skeletal muscle to produce, for the first time, mice lacking ERK1/2 selectively in skeletal myofibers. Animals lacking muscle ERK1/2 displayed stunted postnatal growth, muscle weakness, and a shorter life span. Their muscles examined in this study, sternomastoid and tibialis anterior, displayed fragmented neuromuscular synapses and a mixture of modest fiber atrophy and loss but failed to show major changes in fiber type composition or absence of cell surface dystrophin. Whereas the lack of only ERK1 had no effects on the phenotypes studied, the lack of myofiber ERK2 explained synaptic fragmentation in the sternomastoid but not the tibialis anterior and a decrease in the expression of the acetylcholine receptor (AChR) epsilon subunit gene mRNA in both muscles. A reduction in AChR protein was documented in line with the above mRNA results. Evidence of partial denervation was found in the sternomastoid but not the tibialis anterior. Thus, myofiber ERK1/2 are differentially required for the maintenance of myofibers and neuromuscular synapses in adult mice.
机译：Ras-细胞外信号调节激酶1和2（ERK1 / 2）途径似乎对哺乳动物骨骼肌的发育，维持，衰老和病理学很重要。迄今为止，还没有报道 Erk1 / 2 在肌内体内的基因靶向。我们在骨骼肌中将种系 Erk1 突变与Cre-loxP Erk2 失活相结合，首次产生了在骨骼肌纤维中选择性缺乏ERK1 / 2的小鼠。缺少肌肉ERK1 / 2的动物表现出发育迟缓的生长，肌肉无力和寿命较​​短​​。在这项研究中，他们的肌肉（胸骨前肌和胫骨前肌）显示出破碎的神经肌肉突触以及适度的纤维萎缩和丢失的混合物，但未能显示出纤维类型组成的重大变化或细胞表面肌营养不良蛋白的缺失。缺少ERK1对所研究的表型没有影响，而缺乏肌纤维ERK2则说明了在胸骨乳突突触中的断裂，但在胫骨前突中没有，并且在两块肌肉中乙酰胆碱受体（AChR）ε亚基基因mRNA的表达均降低了。 。与上述mRNA结果一致，证明了AChR蛋白的减少。在胸锁乳突肌中发现了部分神经支配的证据，而在胫骨前肌中则没有。因此，成年小鼠维持肌纤维和神经肌肉突触需要肌纤维ERK1 / 2。

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