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B
1
* Department of Pulmonology, Maastricht University, Maastricht, The Netherlands, and
Department of Pathology, University of Vermont, Burlington, Vermont 05405, USA
1Correspondence: Department of Pathology, University of Vermont, Medical Alumni Building A143, Burlington VT 05405, USA. E-mail: yjanssen{at}zoo.uvm.edu
Muscle wasting is often associated with chronic inflammation. Because
tumor necrosis factor 
(TNF-) has been implicated as a major
mediator of cachexia, its effects on C2C12 myocytes were examined.
TNF- activated nuclear factor-
B (NF-B) and interfered with the
expression of muscle proteins in differentiating myoblasts.
Introduction of a mutant form of inhibitory protein B (IB)
restored myogenic differentiation in myoblasts treated with TNF- or
interleukin 1ß. Conversely, activation of NF-B by overexpression
of IB kinase was sufficient to block myogenesis, illustrating the
causal link between NF-B activation and inhibition of myogenic
differentiation. The inhibitory effects of TNF- on myogenic
differentiation were reversible, indicating that the effects of the
cytokine were not due to nonspecific toxicity. Treatment of
differentiated myotubes with TNF- did not result in a striking loss
of muscle-specific proteins, which shows that myogenesis was
selectively affected in the myoblast stage by TNF-. An important
finding was that NF-B was activated to the same extent in
differentiating and differentiated cells, illustrating that once
myocytes have differentiated they become refractory to the effects of
NF-B activation. These results demonstrate that inflammatory
cytokines may contribute to muscle wasting through the inhibition of
myogenic differentiation via a NF-B-dependent pathway.—Langen,
R. C. J., Schols, A. M. W. J., Kelders,
M. C. J. M., Wouters, E. F. M.,
Janssen-Heininger, Y. M. W. Inflammatory cytokines inhibit
myogenic differentiation through activation of nuclear factor-B.
Key Words: cachexia • muscle wasting • TNF- • NF-B • myogenic differentiation
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A.W. Boots, G.R.M.M. Haenen, and A. Bast Oxidant metabolism in chronic obstructive pulmonary disease Eur. Respir. J., November 2, 2003; 22(46_suppl): 14s - 27s. [Abstract] [Full Text] [PDF]
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R.T. Jagoe and M.P.K.J. Engelen Muscle wasting and changes in muscle protein metabolism in chronic obstructive pulmonary disease Eur. Respir. J., November 2, 2003; 22(46_suppl): 52s - 63s. [Abstract] [Full Text] [PDF]
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Y.-P. Li TNF-{alpha} is a mitogen in skeletal muscle Am J Physiol Cell Physiol, August 1, 2003; 285(2): C370 - C376. [Abstract] [Full Text] [PDF]
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 S. R. Broussard, R. H. MCCusker, J. E. Novakofski, K. Strle, W. Hong Shen, R. W. Johnson, G. G. Freund, R. Dantzer, and K. W. Kelley Cytokine-Hormone Interactions: Tumor Necrosis Factor {alpha} Impairs Biologic Activity and Downstream Activation Signals of the Insulin-Like Growth Factor I Receptor in Myoblasts Endocrinology, July 1, 2003; 144(7): 2988 - 2996. [Abstract] [Full Text] [PDF]
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K. J. Ladner, M. A. Caligiuri, and D. C. Guttridge Tumor Necrosis Factor-regulated Biphasic Activation of NF-kappa B Is Required for Cytokine-induced Loss of Skeletal Muscle Gene Products J. Biol. Chem., January 17, 2003; 278(4): 2294 - 2303. [Abstract] [Full Text] [PDF]
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