Abstract
Skeletal muscle atrophy is characterized by a decrease in muscle fiber size as a result of a decreased protein synthesis, which leads to degradation of contractile muscle fibers. It can occur after denervation and immobilization, and glucocorticoids (GCs) may also increase protein breakdown contributing to the loss of muscle mass and myofibrillar proteins. GCs are already used in vitro to induce atrophic conditions, but until now no studies with primary human skeletal muscle existed. Therefore, this study deals with the effects of the GC dexamethasone (dex) on primary human myoblasts and myotubes. After incubation with 1, 10, and 100 µM dex for 48 and 72 h, gene and protein expression analyses were performed by qPCR and Western blot. Foxo, MuRF-1, and MAFbx were significantly upregulated by dex, and there was increased gene expression of myogenic markers. However, prolonged incubation periods demonstrated no Myosin protein degradation, but an increase of MuRF-1 expression. In conclusion, applying dex did not only differently affect primary human myoblasts and myotubes, as differences were also observed when compared to murine cells. Based on our findings, studies using cell lines or animal cells should be interpreted with caution as signaling transduction and functional behavior might differ in diverse species.
Highlights
Lower back pain is becoming more and more common in society and is often associated with skeletal muscle atrophy
Our study demonstrated an upregulation of Foxo by dex, an even higher impact could be observed in the murine C2C12 myoblast cell line
Myoblasts and myotubes treated with dex showed an enhanced mRNA expression in the myogenic proliferation and differentiation markers, but myoblasts were restricted in their differentiation potential
Summary
Lower back pain is becoming more and more common in society and is often associated with skeletal muscle atrophy. Patients with non-specific back pain frequently end up physically restricted with functional disorders and injuries in the back [1,2,3]. Another reason for lower back pain is muscle atrophy caused by denervation, immobilization, malnutrition, the natural aging processes, illnesses, physical inactivity, or genetic factors [4]. A decrease in protein synthesis or an increase in proteolysis may cause an imbalance [7] that can be initiated by molecular triggers leading to the disruption of signal transduction cascades. A reduction of protein synthesis leads to a rapid degradation of contractile muscle fibers [8]
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