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首页> 外文期刊>American Journal of Physiology >mTOR function in skeletal muscle hypertrophy: increased ribosomal RNA via cell cycle regulators.
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mTOR function in skeletal muscle hypertrophy: increased ribosomal RNA via cell cycle regulators.

机译：骨骼肌肥大中的mTOR功能：通过细胞周期调节剂增加核糖体RNA。

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The purpose of this study was to identify the potential downstream functions associated with mammalian target of rapamycin (mTOR) signaling during myotube hypertrophy. Terminally differentiated myotubes were serum stimulated for 3, 6, 12, 24, and 48 h. This treatment resulted in significant myotube hypertrophy (protein/DNA) and increased RNA content (RNA/DNA) with no changes in DNA content or indices of cell proliferation. During myotube hypertrophy, the increase in RNA content was accompanied by an increase in tumor suppressor protein retinoblastoma (Rb) phosphorylation and a corresponding increase in the availability of the ribosomal DNA transcription factor upstream binding factor (UBF). Serum stimulation also induced an increase in cyclin D1 protein expression in the differentiated myotubes with a concomitant increase in cyclin D1-dependent cyclin-dependent kinase (CDK)-4 activity toward Rb. The increases in myotube hypertrophy and RNA content were blocked by rapamycin treatment, which also prevented the increase in cyclin D1 protein expression, CDK-4 activity, Rb phosphorylation, and the increase in UBF availability. Our findings demonstrate that activation of mTOR is necessary for myotube hypertrophy and suggest that the role of mTOR is in part to modulate cyclin D1-dependent CDK-4 activity in the regulation of Rb and ribosomal RNA synthesis. On the basis of these results, we propose that common molecular mechanisms contribute to the regulation of myotube hypertrophy and growth during the G1 phase of the cell cycle.
机译：这项研究的目的是确定肌管肥大期间与雷帕霉素（mTOR）信号转导的哺乳动物靶标相关的潜在下游功能。将终末分化的肌管血清刺激3、6、12、24和48小时。这种治疗导致明显的肌管肥大（蛋白质/ DNA）和增加的RNA含量（RNA / DNA），而DNA含量或细胞增殖指数没有变化。在肌管肥大过程中，RNA含量的增加伴随着肿瘤抑制蛋白视网膜母细胞瘤（Rb）磷酸化的增加以及核糖体DNA转录因子上游结合因子（UBF）的可用性的相应增加。血清刺激还诱导分化的肌管中细胞周期蛋白D1蛋白表达增加，同时细胞周期蛋白D1依赖性细胞周期蛋白依赖性激酶（CDK）-4对Rb的活性也随之增加。雷帕霉素治疗可阻止肌管肥大和RNA含量的增加，这也阻止了细胞周期蛋白D1蛋白表达，CDK-4活性，Rb磷酸化和UBF利用率的增加。我们的发现表明，mTOR的激活对于肌肥大是必要的，并且表明mTOR的作用部分是在调节Rb和核糖体RNA合成中调节细胞周期蛋白D1依赖性CDK-4活性。基于这些结果，我们提出常见的分子机制有助于在细胞周期的G1期调节肌管肥大和生长。

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