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Journal of Undergraduate Research

Keywords

myostatin signaling pathway, cultured muscle cells, novel small molecule

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). Myostatin is a protein that negatively regulates muscle mass and is primarily expressed within skeletal muscle (Lee & McPherron, 2001). It exerts its effect by binding to a receptor and initiating a signaling cascade that involves phosphorylation of two kinase proteins called SMAD-2 and SMAD-3 (Sartori et al., 2009). Genetic studies have shown that inhibition of myostatin signaling may be an effective way to attenuate muscle wasting (Heineke et al., 2010). However, a pharmacologic agent capable of inhibiting myostatin has not yet been identified. In this study, we performed in vitro analyses to test the effectiveness of a novel small molecule (SGI) in inhibiting myostatin signaling in a cultured muscle cell model. Specifically, we determined how SGI dose and treatment time affected phosphorylation of SMAD-2 and SMAD.

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