Role of satellite cells in muscle growth and maintenance of muscle mass.
ABSTRACT Changes in muscle mass may result from changes in protein turnover, reflecting the balance between protein synthesis and protein degradation, and changes in cell turnover, reflecting the balance between myonuclear accretion and myonuclear loss. Myonuclear accretion, i.e. increase in the number of myonuclei within the muscle fibers, takes place via proliferation and fusion of satellite cells, myogenic stem cells associated to skeletal muscle fibers and involved in muscle regeneration. In developing muscle, satellite cells undergo extensive proliferation and most of them fuse with myofibers, thus contributing to the increase in myonuclei during early postnatal stages. A similar process is induced in adult skeletal muscle by functional overload and exercise. In contrast, satellite cells and myonuclei may undergo apoptosis during muscle atrophy, although it is debated whether myonuclear loss occurs in atrophying muscle. An increase in myofiber size can also occur by changes in protein turnover without satellite cell activation, e.g. in late phases of postnatal development or in some models of muscle hypertrophy. The relative role of protein turnover and cell turnover in muscle adaptation and in the establishment of functional muscle hypertrophy remains to be established. The identification of the signaling pathways mediating satellite cell activation may provide therapeutic targets for combating muscle wasting in a variety of pathological conditions, including cancer cachexia, renal and cardiac failure, neuromuscular diseases, as well as aging sarcopenia.
- SourceAvailable from: Mara Fornaro[Show abstract] [Hide abstract]
ABSTRACT: We have previously shown that activation of Gαi2, an α subunit of the heterotrimeric G protein complex, induces skeletal muscle hypertrophy and myoblast differentiation. To determine whether Gαi2 is required for skeletal muscle growth or regeneration, mice null for Gαi2 were analyzed. Gαi2 knockout mice display decreased lean body mass, reduced muscle size and impaired skeletal muscle regeneration after cardiotoxin-induced injury. shRNA-mediated knockdown of Gαi2 in satellite cells (SCs) leads to defective satellite cell proliferation, fusion and differentiation ex vivo. The impaired differentiation is consistent with the observation that the myogenic regulatory factors MyoD and Myf5 are down-regulated upon knockdown of Gαi2. Interestingly, the expression of miR-1, miR-27b and miR-206, three microRNAs that have been shown to regulate SC proliferation and differentiation, is increased by a constitutively active mutant of Gαi2 (Q205L) and counter-regulated by Gαi2 knockdown. As to mechanism, this study demonstrates that Gαi2(Q205L) regulates satellite cell differentiation into myotubes in a PKC and HDAC-dependent manner.Molecular and Cellular Biology 12/2013; · 5.04 Impact Factor
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ABSTRACT: Detrimental effects of acute and chronic alcohol (ethanol) consumption on human physiology are well documented in the literature. These adversely influence neural, metabolic, cardiovascular, and thermoregulatory functions. However, the side effects of ethanol consumption on hormonal fluctuations and subsequent related skeletal muscle alterations have received less attention and as such are not entirely understood. The focus of this review is to identify the side effects of ethanol consumption on the major hormones related to muscle metabolism and clarify how the hormonal profiles are altered by such consumption.Nutrition and metabolism 01/2014; 11:26.