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Department of Medicine, Baylor College of Medicine, Houston, Texas, 77030 USA
Correspondence: Aladin M. Boriek, Department of Medicine, Pulmonary Division, Suite 520B, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030. E-mail: boriek{at}bcm.tmc.edu
The ex vivo effects of passive mechanical stretch on the activation of nuclear factor-kappaB (NF-
B) pathways in skeletal muscles from normal and mdx mouse, a model of Duchenne muscular dystrophy (DMD), were investigated. The NF-B/DNA binding activity of the diaphragm muscle was increased by the application of axial mechanical stretch in a time-dependent manner. The increased activation of NF-B was associated with a concomitant increase in I-kappaB (IB) kinase activity and the degradation of IB
protein. Pretreatment of the muscles with nifedipine (a Ca2+ channel blocker) and gadolinium(III) chloride (a stretch-activated channel blocker) did not alter the level of activation of NF-B, ruling out involvement of Ca2+ influx through these channels. Furthermore, N-acetyl cysteine, a free radical inhibitor, blocked the mechanical stretch-induced NF-B activation, suggesting the involvement of free radicals. Compared with normal diaphragm, the basal level of NF-B activity was higher in muscles from mdx mice, and it was further enhanced in mechanically stretched muscles. Furthermore, activation of NF-B and increased expression of inflammatory cytokines IL-1ß and tumor necrosis factor in the mdx mouse precede the onset of muscular dystrophy. Our results show that mechanical stretch activates the classical NF-B pathway and this pathway could be predominately active in DMD.
Key Words: mechanical loading • TNF- • IL-1ß • free radicals
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