Abstract
Muscular atrophy is a loss of muscle tissue that can occur due to inactivity or underlying disease processes. Studies have shown that muscle pathology may be linked to levels of sialic acid (SA), an essential glycan found capping extracellular glycan chains of muscle cells. This is particularly evident in GNE myopathy, a disease of muscle wasting in which the causative genetic mutation is linked to decreased SA production. However, the relationship between muscle atrophy and sialylation is poorly understood. Here, we have assessed SA levels in an in vitro model of atrophy in which C2C12 mouse myotubes were treated with dexamethasone. We have utilized lectins, glycan‐binding proteins, to probe linkage‐specific effects of atrophy on sialylation in this in vitro model. This work can help to elucidate the relationship between atrophy and muscle sialylation, and may inform future therapeutic development.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
