期刊
SCIENCE
卷 289, 期 5488, 页码 2363-2366出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.289.5488.2363
关键词
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资金
- NCI NIH HHS [K01 CA78595, CA72771] Funding Source: Medline
- NIAID NIH HHS [AI35098] Funding Source: Medline
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 post-transcriptional 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.
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