Cellular effects of functional unloading and passive strain of soleus muscle in dystrophin-deficient mice

There is a suggestion that dystrophin, a subsarcolemmal protein communicating fiber cytoskeleton to extracellular matrix, participates in signal transduction reflecting the mechanical state of skeletal muscle (mechanotransduction). Recent works indicate the possible signaling role of this protein in the prevention of the activation of proteolytic processes accompanying development of muscle fiber atrophy and in realization of anabolic effects of muscle passive stretching. To assess the role of dystrophin in these processes, the experiment was carried out on two-month old C57 black and mdx (dystrophin-deficient) mice subjected to hind-limb suspension with stretching and without it. Passive stretching results in the partial prevention of atrophy in two muscle fiber types of both C57 black and mdx mice; at the same time, in mdx mice, the slow-to-fast transformation of the soleus muscle fiber type was not observed. Proliferative activity in soleus muscle decreased as a result of hind-limb suspension, but markedly increased during muscle passive stretching. We have found no correlation between the altered dystrophin synthesis and proliferative activity of satellite cells during hind-limb suspension and hind-limb suspension with stretching. Hence, the disturbed dystrophin synthesis retards the atrophy of slow muscle fibers and practically does not affect the stretching preventive action.