Recombinant RANKL causes modulation of inflammatory signaling pathways in C2C12 myotubes

Previous reports indicate that RANKL-RANK signaling participates in regulating muscle mass and strength in denervated animals, while RANKL inhibition by OPG-Fc peptide improves the muscle phenotype in dystrophic mdx mice. RANKL has also been shown to activate STAT3 to regulate osteoclastogenesis, although it is not known whether such interaction also plays a role in skeletal muscle. The objective of this aim is to clarify whether RANKL directly affects skeletal muscle. In order to determine the effects of RANKL on muscle fiber, after 5 days of differentiation C2C12 myotubes were exposed to 100 ng/ml recombinant mouse TRACE/RANK L/TNFSF11 protein for 72 hours.