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KMID : 0613820180280101127
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Journal of Life Science
2018 Volume.28 No. 10 p.1127 ~ p.1131
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Effects of Cortisol on Endoplasmic Reticulum-stress, Apoptosis, and Autophagy in Mouse Muscle C2C12 Cells
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Shin Dong-Hyun
Kim Kyoung-Hwan
Lee Ji-Hyun
Cho Byung-Wook
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Abstract
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Cortisol, a steroid hormone, functions within metabolism, immune response, and stress. Intense or prolonged physical exercise increases cortisol levels to enhance the gluconeogenesis pathway and stabilize blood glucose level. However, cortisol also exerts a negative impact on muscle function and creates a stressful environment in skeletal muscle cells. The present study investigated the function of cortisol as a stress hormone. To examine the effect of the exercise-induced hormone cortisol on skeletal muscles, C2C12 cells were cultured and treated with cortisol at different concentrations. As a result, we found that the morphology of C2C12 changed remarkably with 5 ug/ml cortisol treatment. Western blot analysis was conducted to learn whether ER-stress and autophagy were induced. We found that the expression ratio of LC3I/LC3II decreased and BiP expression increased after cortisol treatment. In addition, immunocytochemistry analysis with IER3 antibody clearly showed that apoptosis is induced after 12-hour cortisol treatment. These results indicate that cortisol treatment could induce apoptosis, ER-stress, and autophagy in muscle cells. This study would provide valuable information in the study of the effects of exercise on skeletal muscle cells and the development of additives to reduce cortisol stress.
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KEYWORD
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Autophagy, apoptosis, C2C12, cortisol, ER-stress
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