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Articles in PresS, published online ahead of print April 24, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00418.2001
Submitted on August 28, 2001
Accepted on April 16, 2002
1 Pulmonology, Maastricht University, Maastricht, The Netherlands
2 Pathology, University of Vermont, Burlington, VT, USA
* To whom correspondence should be addressed. E-mail: yjanssen{at}zoo.uvm.edu.
Muscle wasting is associated with circulating inflammatory cytokines and oxidative stress. We previously demonstrated that tumor necrosis factor alpha (TNF
), inhibits myogenic differentiation via the activation of Nuclear Factor kappa 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 elevated oxidant levels. Importantly, N-acetyl-L-cysteine (NAC) administration prior to treatment with TNF almost completely restored the formation of multinucleated myotubes, but failed to reverse the inhibitory effects of TNF on troponin I (TnI) promoter activation or creatine kinase (CK) activity. NAC decreased the TNF-induced activation of NF-B partially, indicating that the redox or thiol -sensitive component of the inhibition of myogenic differentiation by TNF occurred independently, or downstream of NF-B. In support of this, hydrogen peroxide also resulted in an inhibition of myogenic differentiation, which occurred without concurrent activation of NF-B. Our observations suggest that a redox dependent mechanism is important in the block of myotube formation associated with exposure to cytokines or oxidants, whereas muscle specific protein expression can be regulated in a redox dependent or independent manner.
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