Abstract
Skeletal muscle atrophy can occur as a result of disuse, disease, or aging. Mechanistic pathways among these conditions vary, but in most cases, levels of intracellular calcium (IC Ca2+) increase. This rise in IC Ca2+ stimulates calpain activity and subsequent protein degradation. Calpains cleave the structural proteins that hold the sarcomere together, thereby releasing the contractile proteins for proteasome degradation; this is thought to be the rate‐limiting step in skeletal muscle proteolysis. Little is known about the regulation of calpain activity, but nitric oxide (NO) has been proposed as a possible mediator. This study used the Ca2+ ionophore calcimycin to increase IC Ca2+ and to induce calpain activity in L6 myotubes. We hypothesized that treatment with an NO donor would attenuate calpain proteolysis and myotube atrophy in a dose‐dependent manner following treatment with calcimycin. Results show an attenuation of calpain‐specific talin proteolysis with 1 μM and 10 μM PAPA‐NO after 60 minutes of calcimycin treatment, and preliminary data show prevention of myotube atrophy with DETA‐NO after 24–48 hours of calcimycin treatment. Therefore, moderate doses of NO can prevent calpain proteolysis and possibly skeletal muscle atrophy following a Ca2+ challenge in L6 myotubes. This study was funded by the American Heart Association.
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