Role of Omi/Beclin-1 signaling pathway in the eccentric exercise-induced skeletal muscle autophagy

doi:10.3969/j.issn.2095-4344.0559

Abstract

Abstract:

BACKGROUND: Eccentric exercise can cause the ultrastructural changes in the skeletal muscle due to autophagy, thereby affecting the normal the contraction of skeletal muscle.
OBJECTIVE: To explore the effect of eccentric exercise on the skeletal muscle cell autophagy and investigate the underlying mechanisms by observing the skeletal muscle cell autophagy and the changes of Omi/Beclim-1 signaling pathway after eccentric exercise.
METHODS: Thirty-two healthy male rats were divided into control (n=8) and experimental (n=24) groups. The rats in the experimental group underwent eccentric exercise on a treadmill (16° decline, 16 m/minute for 90 minutes), and then 8 rats were killed at 0, 24, and 48 hours, respectively. The expression levels of LC3-II, Omi, HAX-1 and Beclin-1 were determined by western blot assay.
RESULTS AND CONCLUSION: The expression levels of LC3-II, Omi, and Beclin-1 protein were significantly increased after eccentric exercise, the expression levels of LC3-II and Omi protein peaked at 0 hour, and the expression level of Beclin-1 peaked at 24 hours. The expression level of HAX-1 protein was significantly decreased after eccentric exercise, reached the lowest level at 24 hours, and then returned to normal level. The expression levels at 48 hours after exercise were significantly different from those in the control group. These results suggest that eccentric exercise can result in an increase in skeletal muscle cell autophagy via upregulating Omi/Beclin-1 signaling pathway probably.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Sports Medicine, Muscle, Skeletal, Autophagy, Tissue Engineering

CLC Number:

R318

Lei Bingkai1, 2, Sun Junzhi1, Zhao Xiaoqin3, Ding Haili1, Liu Yong2, Wang Ruiyuan2, Li Junping2. Role of Omi/Beclin-1 signaling pathway in the eccentric exercise-induced skeletal muscle autophagy[J]. Chinese Journal of Tissue Engineering Research, 2018, 22(36): 5791-5796.

Figures/Tables 6

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