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inhibits myogenesis through
redox-dependent and -independent pathways
1 Department of Pulmonology, Maastricht University, 6202 AZ Maastricht, The Netherlands; and 2 Department of Pathology, University of Vermont, Burlington, Vermont 05405
Muscle wasting accompanies diseases that
are associated with chronic elevated levels of circulating inflammatory
cytokines and oxidative stress. We previously demonstrated that tumor
necrosis factor-
(TNF-) inhibits myogenic differentiation via the
activation of nuclear factor-
B (NF-B). The goal of the present
study was to determine whether this process depends on the induction of oxidative stress. We demonstrate here that TNF- causes a decrease in
reduced glutathione (GSH) during myogenic differentiation of C2C12 cells, which coincides with an elevated
generation of reactive oxygen species. Supplementation of cellular GSH
with N-acetyl-l-cysteine (NAC)
did not reverse the inhibitory effects of TNF- on troponin I
promoter activation and only partially restored creatine kinase activity in TNF--treated cells. In contrast, the administration of
NAC before treatment with TNF- almost completely restored the
formation of multinucleated myotubes. NAC decreased TNF--induced activation of NF-B only marginally, indicating that the
redox-sensitive component of the inhibition of myogenic differentiation
by TNF- occurred independently, or downstream of NF-B. Our
observations suggest that the inhibitory effects of TNF- on
myogenesis can be uncoupled in a redox-sensitive component affecting
myotube formation and a redox independent component affecting myogenic protein expression.
inflammation; glutathione; nuclear factor-B; myotube; myogenic
differentiation
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