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NF-κB-Induced Loss of MyoD Messenger RNA: Possible Role in Muscle Decay and Cachexia

Science  29 Sep 2000:
Vol. 289, Issue 5488, pp. 2363-2366
DOI: 10.1126/science.289.5488.2363

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Abstract

MyoD regulates skeletal muscle differentiation (SMD) and is essential for repair of damaged tissue. The transcription factor nuclear factor kappa B (NF-κB) is activated by the cytokine tumor necrosis factor (TNF), a mediator of skeletal muscle wasting in cachexia. Here, the role of NF-κB in cytokine-induced muscle degeneration was explored. In differentiating C2C12 myocytes, TNF-induced activation of NF-κB inhibited SMD by suppressing MyoD mRNA at the posttranscriptional level. In contrast, in differentiated myotubes, TNF plus interferon-γ (IFN-γ) signaling was required for NF-κB–dependent down-regulation of MyoD and dysfunction of skeletal myofibers. MyoD mRNA was also down-regulated by TNF and IFN-γ expression in mouse muscle in vivo. These data elucidate a possible mechanism that may underlie the skeletal muscle decay in cachexia.

  • * Present address: Laboratory of Molecular Signaling, Department of Biologic and Material Science, University of Michigan, Ann Arbor, MI 48109, USA.

  • To whom correspondence should be addressed. E-mail: jhall{at}med.unc.edu

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