Glycoprotein (Gp130) Protein Expression During Mouse Skeletal Muscle Disuse Atrophy

Physical inactivity, bed rest, and immobilization result in skeletal muscle disuse atrophy, which can negatively affect physical function and quality of life. The IL-6 cytokine’s signaling through the gp130 receptor has established roles in both muscle growth and atrophy. While muscle gp130/STAT3 signaling has been implicated in mechanical ventilation-induced diaphragm atrophy, less is known about gp130 protein expression during hindlimb muscle unloading atrophy. The purpose of this study is to examine gp130 protein expression during mouse skeletal muscle disuse atrophy. It was hypothesized that muscle gp130 protein expression would increase in skeletal muscle undergoing disuse atrophy. Female 10-week C57BL/6 mice underwent hindlimb suspension (HS; N=6) for 5 days, while loadbearing mice served as cage controls (CC; N=6). Hindlimb suspension decreased relative RF muscle mass compared to cage control. Data analysis showed that gp130 protein expression decreased in the rectus femoris of the hindlimb suspended mice. Hindlimb unloading did not alter in gp130 downstream target proteins STAT3 and ERK 1/2. The results concluded that disuse muscle atrophy causes different gp130 protein expressions for various parts of the body. National Institutes of Health Grant: NCI R01-CA121249 to James A. Carson funded this research