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首页> 外文期刊>Signal transduction: Receptors, mediators and genes: Official journal of the Signal Transduction Society >Myostatin and NF-κB Regulate Skeletal Myogenesis Through Distinct Signaling Pathways
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Myostatin and NF-κB Regulate Skeletal Myogenesis Through Distinct Signaling Pathways

机译：Myostatin和NF-κB通过不同的信号通路调节骨骼肌的发生。

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Myostatin (Mstn) is a potent negative regulator of skeletal development shown to inhibit myoblast proliferation by impinging on cell cycle and suppressing the synthesis of MyoD. Moreover, Mstn causes muscle wasting and its expression is linked with several conditions of muscle loss, mainly dystrophy and cachexia. NF-κB is a transcription factor that is constitutively active in proliferating myoblasts and also plays a role in cell growth control and skeletal muscle differentiation. NF-κB inhibits myogenesis by promoting myoblast growth and inducing loss of MyoD, and NF-κB activity is required in states of muscle wasting. However, the extracellular factors that regulate NF-κB activity to modulate myogenesis are currently not known. Given the similarities in Mstn and NF-κB activities in muscle cells, we investigated the possibility that Mstn-induced regulation of myogenesis may signal via NF-κB. Using a variety of assays to monitor for NF-κB activity, we found that Mstn signaling does not activate NF-κB in differentiating C2C12 myoblasts, nor is the constitutive activity of NF-B required for Mstn-mediated inhibition of myogenesis. Likewise, in pre-differentiated myotubes, Mstn signaling induces only a modest activation of NF-B DNA binding activity. We also investigated whether NF-B inhibition of myogenesis may occur through the regulation of Mstn. However, activation of NF-κB by TNF or IL-1 failed to induce Mstn expression. These results thus highlight the distinctive differences by which Mstn and NF-κB signal to regulate myogenesis, a finding which broadens our understanding of how these pathways function in both development and disease.
机译：Myostatin（Mstn）是有效的骨骼发育负调节剂，可通过影响细胞周期并抑制MyoD的合成来抑制成肌细胞的增殖。此外，Mstn导致肌肉消瘦，其表达与肌肉丢失的几种状况有关，主要是营养不良和恶病质。 NF-κB是转录因子，在增殖的成肌细胞中具有组成性活性，并且在细胞生长控制和骨骼肌分化中也起作用。 NF-κB通过促进成肌细胞生长和诱导MyoD丧失来抑制肌发生，而在肌肉消瘦状态下，NF-κB活性是必需的。然而，目前尚不清楚调节NF-κB活性以调节肌发生的细胞外因子。考虑到肌肉细胞中Mstn和NF-κB活性的相似性，我们研究了Mstn诱导的肌发生性调节可能通过NF-κB发出信号的可能性。通过使用多种检测方法监测NF-κB活性，我们发现Mstn信号在分化C2C12成肌细胞中不会激活NF-κB，对于Mstn介导的成肌抑制也不需要NF-B的本构活性。同样，在预分化的肌管中，Mstn信号传导仅诱导NF-B DNA结合活性的适度激活。我们还研究了是否可以通过调节Mstn来抑制NF-B对肌发生的抑制。然而，TNF或IL-1对NF-κB的激活未能诱导Mstn表达。因此，这些结果突出了Mstn和NF-κB信号调节肌发生的独特差异，这一发现拓宽了我们对这些途径如何在发育和疾病中起作用的理解。

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