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.