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Journal of Undergraduate Research

Keywords

morphology of human myoblasts, cultured muscle cells, novel small molecule SGI

College

Life Sciences

Department

Exercise Sciences

Abstract

Muscle wasting is a symptom of cancer, AIDS, renal failure, heart failure, aging, prolonged bed rest, and has been seen in rodent models for burn, and kidney disease (Han, 2013). Muscle wasting negatively impacts quality of life by decreasing functional independence and increasing morbidity and mortality (Anker, 1997). Muscle wasting is an especially serious issue given that the body weight of an average human is 40-50 percent skeletal muscle (Han, 2013). Myostatin is a protein that negatively regulates muscle mass and is primarily expressed within skeletal muscle (Lee & McPherron, 2001). Genetic studies have shown that inhibition of myostatin signaling may be an effective way to attenuate muscle wasting (Heineke et al., 2010). Data I collected in 2014 indicates that SGI is capable of inhibiting myostatin in cultured muscle cells. In this project, we performed in vitro analyses to test the effectiveness of SGI to promote growth and differentiation of human myoblasts in a cultured muscle cell model. My first aim was to determine how SGI influenced myoblast differentiation. We hypothesized that SGI would accelerate myoblast differentiation into myotubes. My second aim was to determine how SGI influenced myotubes. We hypothesized that SGI would increase the average size of a myotube. To accomplish these aims we analyzed our cells using myosin heavy chain which appears in differentiated myoblasts only, myoD, a nuclear protein that induces differentiation of myoblasts, and myogenin which regulates expression of differentiation genes in myoblasts. Cytological detection of these proteins allowed me to measure how SGI affected growth and differentiation of the cultured myotubes.

Included in

Kinesiology Commons

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