• Journal of Life Science
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• v.21 no.3
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• pp.400-405
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• 2011

Autophagy, a highly conserved mechanism of internal quality control, is essential for the maintenance of cellular homeostasis and for the orchestration of an efficient cellular response to stress. During aging, the efficiency of autophagic degradation declines and intracellular waste products accumulate. Therefore, the aim of this study is to investigate the effects of exercise on autophagic response in skeletal muscle. Twenty-four Young (4 month) and Old (12 month) ICR-type white male mice were divided into a control group (CON: n=6) and exercise training group (Tr: n=6) after an adaptation period of 1 week. Exercise consisted of treadmill running at 16.4 m/min with a 4% incline, 40 min/day and 5 days/week for 8 weeks. Cervical dislocation was performed at 48 hours after the last round of exercise, after which the gastrocnemius skeletal muscle were immediately collected. The results of verifying autophagy formation showed that the Sarcopenia index was decreased in the Old mice compared to the Young. However, it increased with exercise training in the Old. Lipidation LC3-II, Becline-1, and Atg7 were decreased in the Old mice compared to the Young. However, Lipidation LC3-II was significantly increased in the trained Old mice (Young:1 Vs Old:$1.32{\pm}0.042$, p<0.05). Based on these data, we suggest that autophagy regulatory events are the attenuated in Old mice, but that they are enhanced with exercise training.

• The Journal of the Korea Contents Association
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• v.9 no.4
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• pp.355-363
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• 2009

Increased oxidative stress by abnormal mitochondrial function can damage cell signal transduction and gene expression, and induce insulin resistance or diabetes. Autophagy, however, improve insulin resistance by clearance of malfunctioning mitochondria. Exercise also recovers the muscle dysfunction and degeneration by activating mitochondrial biogenesis. As it seems that exercise and autophagy might act as an orchestrated network to induce mitochondrial biogenesis, we investigated whether autophagy is involved in AMPK signal pathway stimulated by exercise or AICAR to increase mitochondrial biogenesis. And it showed that PGC-1 and mtTFA, but not autophagy marker LC3 mRNA expression were significantly increased by 6 hr of acute exercise. On the other hand, PGC-1 and mtTFA mRNA expression were upregulated by AICAR treatment to C2C12 myotube. However these genes were not inhibited by LC3 siRNA transfection. These results provide the evidence that autopahgy affects on mitochondrial biogenesis through different signal pathway from AMPK signal transduction.

• The Korean Journal of Physiology and Pharmacology
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• v.15 no.2
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• pp.107-114
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• 2011

Neurofibrillary tangle (NFT) is a characteristic hallmark of Alzheimer's disease. GSK3β has been reported to play a major role in the NFT formation of tau. Dysfunction of autophagy might facilitate the aggregate formation of tau. The present study examined the role of GSK3${\beta}$-mediated phosphorylation of tau species on their autophagic degradation. We transfected wild type tau (T4), caspase-3-cleaved tau at Asp421 (T4C3), or pseudophosphorylated tau at Ser396/Ser404 (T4-2EC) in the presence of active or enzyme-inactive GSK3${\beta}$. Trehalose and 3-methyladenine (3-MA) were used to enhance or inhibit autophagic activity, respectively. All tau species showed increased accumulation with 3-MA treatment whereas reduced with trehalose, indicating that tau undergoes autophagic degradation. However, T4C3 and T4-2EC showed abundant formation of oligomers than T4. Active GSK3${\beta}$ in the presence of 3-MA resulted in significantly increased formation of insoluble tau aggregates. These results indicate that GSK3${\beta}$-mediated phosphorylation and compromised autophagic activity significantly contribute to tau aggregation.