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首页> 外文期刊>The FASEB Journal >A dynamic ribosomal biogenesis response is not required for IGF-1–mediated hypertrophy of human primary myotubes
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A dynamic ribosomal biogenesis response is not required for IGF-1–mediated hypertrophy of human primary myotubes

机译：IGF-1介导的人原发性肌管的肥大不需要动态核糖体生物发生反应

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Increased ribosomal DNA transcription has been proposed to limit muscle protein synthesis, making ribosome biogenesis central to skeletal muscle hypertrophy. We examined the relationship between ribosomal RNA (rRNA) production and IGF-1–mediated myotube hypertrophy in vitro . Primary skeletal myotubes were treated with IGF-1 (50 ng/ml) with or without 0.5 μM CX-5461 (CX), an inhibitor of RNA polymerase I. Myotube diameter, total protein, and RNA and DNA levels were measured along with markers of RNA polymerase I regulatory factors and regulators of protein synthesis. CX treatment reduced 45S pre-rRNA expression (?64 ± 5% vs. IGF-1; P < 0.001) and total RNA content (?16 ± 2% vs. IGF-1; P < 0.001) in IGF-1-treated myotubes. IGF-1-mediated increases in myotube diameter (1.27 ± 0.09-fold, P < 0.05 vs. control) and total protein (+20 ± 2%; P < 0.001 vs. control) were not prevented by CX treatment. Suppression of rRNA synthesis during IGF-1 treatment did not prevent early increases in AKT (+203 ± 39% vs. CX; P < 0.001) and p70 S6K1 (269 ± 41% vs. CX; P < 0.001) phosphorylation. Despite robust inhibition of the dynamic ribosomal biogenesis response to IGF-1, myotube diameter and protein accretion were sustained. Thus, while ribosome biogenesis represents a potential site for the regulation of skeletal muscle protein synthesis and muscle mass, it does not appear to be a prerequisite for IGF-1-induced myotube hypertrophy in vitro. —Crossland, H., Timmons, J. A., Atherton, P. J. A dynamic ribosomal biogenesis response is not required for IGF-1–mediated hypertrophy of human primary myotubes.
机译：提出了增加的核糖体DNA转录以限制肌蛋白合成，使核糖体生物生成中的骨骼肌肥大。我们检查了核糖体RNA（RRNA）生产与IGF-1介导的肌室肥大的关系。用IGF-1（50ng / ml）处理初级骨骼肌，用或没有0.5μmCX-5461（CX），RNA聚合酶I的抑制剂，用标记物测量肌室直径，总蛋白质和RNA和DNA水平RNA聚合酶I调节因子和蛋白质合成调节因子。 CX治疗减少了45s前rRNA表达（α5％Vs.P <0.001）和IGF-1处理的总RNA含量（α16±2％与IGF-1; P <0.001） myotubes。 IGF-1介导的肌管直径增加（1.27±0.09倍，P <0.05 Vs，对照）和总蛋白质（+20±2％; P <0.001 Vs.10.P <0.001 Vs.10.1.01 vs.1.0.1 0.101 vs.1.1.001 Vs.1.001 Vs.10.1.001 Vs.1.001 Vs.10.1.001 vs.10.1.001 vs.COP）。抑制IGF-1处理期间的RRNA合成并未阻止AKT的早期增加（+ 203±39％vs.CX; P <0.001）和P70 S6K1（269±41％与CX; P <0.001）磷酸化。尽管对IGF-1的动态核糖体生物发生反应的稳健抑制，但肌肌管直径和蛋白质增生。因此，虽然核糖体生物发生代表骨骼肌蛋白质合成和肌肉质量的调节的潜在部位，但它似乎并不是IGF-1诱导的肌室肥大在体外的先决条件。 -Crossland，H.，Timmons，J.A.，Atherton，P.J.IGF-1介导的人原发性肌管的肥大不需要动态核糖体生物发生反应。

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