TGF-beta receptors, in a Smad-independent manner, are required for terminal skeletal muscle differentiation.

Skeletal muscle differentiation is strongly inhibited by transforming growth factor type beta (TGF-beta), although muscle formation as well as regeneration normally occurs in an environment rich in this growth factor. In this study, we evaluated the role of intracellular regulatory Smads proteins as well as TGF-beta-receptors (TGF-beta-Rs) during skeletal muscle differentiation. We found a decrease of TGF-beta signaling during differentiation.

Extracellular proteoglycans modify TGF-beta bio-availability attenuating its signaling during skeletal muscle differentiation.

The onset and progression of skeletal muscle regeneration are controlled by a complex set of interactions between muscle precursor cells and their environment. Satellite cells constitute the main source of muscle precursor cells for growth and repair. After skeletal muscle injury, cell-derived signals induce their re-entry into the cell cycle and their migration into the damaged zone, where they proliferate and differentiate into mature myofibers.