Mitochondria Mediate Tumor Necrosis Factor-α/NF-κB Signaling in Skeletal Muscle Myotubes
作者： Yi-Ping Li , Coleen M. Atkins , J. David Sweatt , Michael B. Reid
关键词:
摘要: Tumor necrosis factor-alpha (TNF-alpha) is implicated in muscle atrophy and weakness associated with a variety of chronic diseases. Recently, we reported that TNF-alpha directly induces protein degradation differentiated skeletal myotubes, where it rapidly activates nuclear factor kappaB (NF-kappaB). We also have found loss induced by NF-kappaB dependent. In the present study, analyzed signaling pathway which myotubes from C2C12 rat primary myoblasts. activation was blocked rotenone or amytal, inhibitors complex I mitochondrial respiratory chain. On other hand, antimycin A, an inhibitor III, enhanced NK-kappaB. These results suggest key role mitochondria-derived reactive oxygen species (ROS) mediating muscle. addition, stimulated kinase C (PKC) activity. However, signal transduction mediators including ceramide, Ca2+, phospholipase A2 (PLA2), nitric oxide (NO) do not appear to be involved NF-kappaB.
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