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      NF-kappaB-induced loss of MyoD messenger RNA: possible role in muscle decay and cachexia.

      Science (New York, N.Y.)

      Animals, CHO Cells, Cachexia, etiology, metabolism, pathology, Cell Differentiation, Cell Line, Cricetinae, DNA-Binding Proteins, genetics, Down-Regulation, I-kappa B Proteins, Interferon-gamma, pharmacology, Interleukins, Mice, Mice, Inbred Strains, Mice, Nude, Muscle, Skeletal, cytology, MyoD Protein, NF-kappa B, RNA, Messenger, Transcription Factor RelA, Transcription, Genetic, Transfection, Tumor Necrosis Factor-alpha

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          MyoD regulates skeletal muscle differentiation (SMD) and is essential for repair of damaged tissue. The transcription factor nuclear factor kappa B (NF-kappaB) is activated by the cytokine tumor necrosis factor (TNF), a mediator of skeletal muscle wasting in cachexia. Here, the role of NF-kappaB in cytokine-induced muscle degeneration was explored. In differentiating C2C12 myocytes, TNF-induced activation of NF-kappaB 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-kappaB-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.

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