Differentiation and Dexamethasone Atrophy on C2C12 myotubes

Skeletal muscle atrophy and weakness are major contributors to morbidity, prolonged recovery, and long-term disability across a wide range of diseases. Atrophy is caused by breakdown of sarcomeric proteins resulting in loss of muscle mass and strength. Molecular mechanism underlying the onset of muscle atrophy and its progression have been analysed in patients, mice, and cell culture but the complementarity of these model systems remains to be explored. Here, we applied deep-coverage transcriptomic and proteomic profiling to characterize dynamic changes during dexamethasone-induced atrophy in the widely used murine skeletal muscle cell line C2C12. Comparison with published datasets confirmed that muscle differentiation is well recapitulated in C2C12 myotubes. Under dexamethasone-induced treatment, this model was particularly suited to capture early atrophy events, prior to disassembly and degradation of sarcomeric proteins. We also identified alterations in mitochondrial gene expression and differential alternative splicing events during early-stage myotube atrophy. This dataset complements existing in vivo data and provides novel insights into the regulatory processes during skeletal muscle wasting. mRNA-seq of undifferentiated C2C12 cells (day 0), differentiated cells (day 7), vehicle treated controls (day 8, day 10) and 100 µM Dexamethasone treated cells (day 8, day 10)