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Science 289 (5488): 2363-2366

Copyright © 2000 by the American Association for the Advancement of Science

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

Denis C. Guttridge,1 Marty W. Mayo,1 Lee V. Madrid,12 Cun-Yu Wang,1* Albert S. Baldwin Jr.123dagger

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

1 Lineberger Comprehensive Cancer Center,
2 Curriculum in Genetics and Molecular Biology,
3 Department of Biology, University of North Carolina, Chapel Hill, Mason Farm Road, Campus Box 7295, Chapel Hill, NC, 27599-7295, USA.
*   Present address: Laboratory of Molecular Signaling, Department of Biologic and Material Science, University of Michigan, Ann Arbor, MI 48109, USA.

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

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