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首页> 外文期刊>American Journal of Physiology >Neuregulin-dependent protein synthesis in C2C12 myotubes and rat diaphragm muscle.
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Neuregulin-dependent protein synthesis in C2C12 myotubes and rat diaphragm muscle.

机译：C2C12肌管和大鼠diaphragm肌中神经调节蛋白依赖性蛋白的合成。

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The nerve-derived trophic factor neuregulin (NRG) is a prime candidate molecule for modulating muscle fiber growth. NRG regulates signal transduction in skeletal muscle through activation of ErbB receptors present at the neuromuscular junction. In this study, we hypothesize that NRG increases protein synthesis in maturing muscle via a phosphatidylinositol 3-kinase (PI3K)-dependent mechanism. NRG signal transduction and its ability to stimulate protein synthesis (measured by incorporation of [(3)H]phenylalanine into the protein pool) were investigated in differentiated C(2)C(12) myotubes and rat diaphragm muscle (DIAm). In C(2)C(12) myotubes, NRG dose dependently increased phosphorylation of ErbB3 and recruitment of the p85 subunit of PI3K. NRG also increased phosphorylation of Akt, a downstream effector of PI3K. NRG treatment increased total protein synthesis by 35% compared with untreated control myotubes. This NRG-induced increase in Akt phosphorylation and protein synthesis was completely blocked bywortmannin, an inhibitor of PI3K but was unaffected by PD-98059, an inhibitor of MEK. In DIAm obtained from 3-day-old rat pups, Akt phosphorylation increased approximately 30-fold with NRG treatment (vs. untreated DIAm). NRG treatment also significantly increased protein synthesis in the DIAm by 29% after 3 h of incubation with [(3)H]phenylalanine (vs. untreated DIAm). Pretreatment with wortmannin abolished the NRG-induced increase in protein synthesis, suggesting a critical role for PI3K in this response. The results of the present study support the hypothesis that nerve-derived NRG contributes to the regulation of skeletal muscle mass by increasing protein synthesis via activation of PI3K.
机译：神经源性营养因子神经调节蛋白（NRG）是调节肌肉纤维生长的主要候选分子。 NRG通过激活神经肌肉接头处的ErbB受体来调节骨骼肌中的信号转导。在这项研究中，我们假设NRG通过磷脂酰肌醇3激酶（PI3K）依赖性机制增加成熟肌肉的蛋白质合成。在分化的C（2）C（12）肌管和大鼠（肌（DIAm）中，研究了NRG信号转导及其刺激蛋白质合成的能力（通过将[（3）H]苯丙氨酸掺入蛋白质池中进行测量）。在C（2）C（12）肌管中，NRG剂量依赖性地增加了ErbB3的磷酸化和PI3K的p85亚基的募集。 NRG还增加了PI3K的下游效应子Akt的磷酸化。与未处理的对照肌管相比，NRG处理可使总蛋白质合成增加35％。 NRG诱导的​​Akt磷酸化和蛋白质合成的这种增加被PI3K抑制剂渥曼青霉素完全阻断，但不受MEK抑制剂PD-98059影响。在从3天大的幼崽中获得的DIAm中，用NRG处理后Akt磷酸化增加了约30倍（与未处理的DIAm相比）。与[（3）H]苯丙氨酸孵育3小时后，NRG处理还显着提高了DIAm中的蛋白质合成29％（相对于未处理的DIAm）。用渥曼青霉素预处理消除了NRG诱导的​​蛋白质合成增加，表明PI3K在此反应中起关键作用。本研究的结果支持以下假设：神经源性NRG通过激活PI3K来增加蛋白质合成，从而有助于骨骼肌质量的调节。

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