Nobuyuki Murakami, Ian S. McLennan, Ikuya Nonaka, Kyoko Koishi, Christina Baker and Graeme Hammond-Tooke.

The transforming growth factor betas (TGF-bs) are multifunctional growth factors that act on both fibroblasts and myosatellite cells. In rodent models of muscle diseases, high levels of TGF-b2 are expressed by myogenic cells. In this paper, we have examined whether the expression of TGF-b2 is also elevated in diseased human muscles. The disorders examined were Duchenne muscular dystrophy, myotonic dystrophy, myotubular myopathy, spinal muscular atrophy and amyotrophic lateral sclerosis. The levels of TGF-b2 immunoreactivity were elevated in atrophic, necrotic and regenerating fibers and in fibers with central nuclei or cytoplasmic masses, irrespective of whether fibrosis was present. We therefore suggest that TGF-b2 is important for muscle repair and that the presence of a TGF-b within a muscle only leads to fibrosis if certain other factors are present.