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Yong An Kim(김용안),Young Sang Kim(김영상) 한국생명과학회 2011 생명과학회지 Vol.21 No.3
Autophagy는 항상성 유지와 스트레스반응을 효율적으로 조정하기 위해 필수적인 세포 내 질적 조절작용이다. 노화가 진행되는 동안 autopahgy에 의한 degradation 효율성 저하와 그로 인한 세포 내 부산물의 축적이 증가하여 결국, 근육의 약화를 초래한다. 그러므로 본 연구의 목적은 골격근에서 운동에 의한 autopahgy 관련 단백질의 변화를 규명하는데 있다. 이를 위해 24마리의 Young 그룹과 Old 그룹을 나누어 각각 대조군(n=6)과 운동군(n=6)으로 배정하였다. 운동은 8주간 주 5회 실시하였고, 트레드밀 속도 16.4 m/min와 경사도 4%로 설정하여 40분간 지속적인 운동을 실시하였다. autopahgy 관련 단백질에 대한 검증 결과 Young 그룹과 비교하여 Old 그룹에서 LC3-1, Beclin-1, Atg7은 모두 유의하게 감소하였다. 그러나 8주간의 규칙적인 운동에 의하여 autophagy 관련 단백질은 증가하는 것으로 나타났다. 따라서 노화에 의해 약화된 autopahgy 기능은 규칙적인 운동에 의해 개선될 수 있을 것으로 사료된다. 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±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.
Tau23 동물에서 손상된 HSP90-mediated autophagic/lysosomal pathway의 운동의 개선 효과
김용안(Kim Yong-An),손희정(Son Hee-Jeong),박준영(Park Joon-Young),김범수(Kim Bum-Soo),하재여(Ha Jae-Yeo),조임형(Cho lim-Hyeong),임예현(Leem Yea-Hyun) 한국체육과학회 2011 한국체육과학회지 Vol.20 No.2
The objective of this study is to investigate whether chronic endurance exercise attenuates tau hyperphosphorylation and alters incomplete autophagic pathway. To achieve the objective of current study, 16 months of age of Tau23 mice were subjected to treadmill-running with 12m/min or 19m/min of speed for 12 weeks of period. the levels of neuropathophysiological phospho-sites on tau (pSer202, 204, 396, 404) were profoundly reduced in response to exercise. Autolysosomal activity-related LC3-Ⅱ/LC3-Ⅰ expression ratio and Cathepsin D expression were enhanced in Tg mice, but inversely declined in exercised Tg mice. Beeline-1 and p62, which were linked to autophagosome formation, expression levels were significantly reduced in Tg mice. HSP90 and CHIP, which play key role in escorting toward autophagy, expression levels were increased or decreased, respectively in Tg mice, and were reversed in exercised Tg mice. Based on our findings, chronic exercise suggests to ameliorate the incomplete and immature autophagic activity by Tau overexpression and hyperphosphorylation, resulting in reduction of Tau hyperphosphorylation.