Date of Award
Pond, Amber L.
Skeletal muscle atrophy results from an imbalance of protein degradation and protein synthesis which produces a net loss of protein. This loss occurs mainly through the ubiquitin proteasome pathway (UPP). The ether-a-go-go related gene (ERG1A) is a voltage-gated K+ channel that is upregulated in atrophying skeletal muscle. Expression of ERG1A in skeletal muscle increases UPP activity and induces atrophy. Because ERG1A appears variably expressed in muscles composed of mixed fiber types and is a K+ channel which has the potential to modulate contraction speed by enhancing repolarization, we hypothesized that ERG1A would be more abundant in slow-twitch fibers than in fast-twitch fibers in skeletal muscle. To test this hypothesis, we cryo-sectioned Soleus (SOL), Extensor Digitorum Longus (EDL), and Gastrocnemius muscles of rats. These muscles were chosen because the SOL and EDL have an abundance of slow and fast-twitch fibers, respectively, while the Gastrocnemius contains a heterogeneous composition. The sections were co-immunostained for the ERG1A protein and either the fast or slow-twitch MyHC. ERG1A fluorescence was measured in the sarcolemma of each fiber type and compared. The data reveal that the ERG1A protein is more abundant in muscle fibers of the SOL than the EDL. Further, the data show that there is a 3.2-fold increase in ERG1A expression in slow fibers than fast fibers in the Gastrocnemius. Diet and exercise remain the best treatment for muscle atrophy, however not all patients are able to participate in these, thus futher research into skeletal muscle atrophy is needed to develop future treatments.