운동 중 골격근 내 PGC-1α 농도는 PPARβ/δ를 통한 후전사 기전에 의하여 조절된다: PPARβ/δ silence가 ubiquitin을 통한 PGC-1α 안정성에 미치는 영향
PGC-1α concentration in skeletal muscle by exercise is controlled by PPARβ/δ through post-transcriptional mechanism: the effects of PPARβ/δ silence on PGC-1α ubiquitination and stability
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PURPOSE: The aim of this study was to identified which PPARβ/δ control PGC-1α protein stability in rat skeletal muscle by long-term endurance exercise. METHODS: shPPARβ/δ was over-expressed in rat epitrochlearis (Epi) muscle using electrical pulse-mediated gen transfer (electroporation; EPO) method. Then animal underwent 2 wk long swimming exercise. To evaluate PPARβ/δ, PGC-1α ubiquitination, PGC-1α and mitochondrial enzyme expression in rat skeletal muscle, Epi muscles were dissected 18h post final bout of swimming exercise. RESULTS: PPARβ/δ, PGC-1α, COX I and NADH protein expression in shPPARβ/δ over-expression sedentary (Sed) skeletal muscle were significantly decreased over 55%, but PGC-1α ubiquitination was significantly increased 2.6 fold when compared to scramble (Scr) treated Sed muscle. PPARβ/δ, PGC-1α, COX I and NADH protein expression in 2 wks swimming exercise with Scr gene treated muscle were significantly increased over 2 fold, but PGC-1α ubiquitination was significantly decreased 66% when compared to Scr gene treated Sed muscle. PPARβ/δ, PGC-1α, COX I and NADH protein expression in 2 wks swimming exercise with shPPARβ/δ gene treated muscle were not increased, but PGC-1α ubiquitination was significantly increased 1.96 fold when compared to Scr gene treated Sed muscle. CONCLUSIONS: Our results indicate that PPARβ/δ controls PGC-1α protein stability in rat skeletal muscle following long-term endurance exercise.
Abstract
PURPOSE: The aim of this study was to identified which PPARβ/δ control PGC-1α protein stability in rat skeletal muscle by long-term endurance exercise. METHODS: shPPARβ/δ was over-expressed in rat epitrochlearis (Epi) muscle using electrical pulse-mediated gen transfer (electroporation; EPO) method. Then animal underwent 2 wk long swimming exercise. To evaluate PPARβ/δ, PGC-1α ubiquitination, PGC-1α and mitochondrial enzyme expression in rat skeletal muscle, Epi muscles were dissected 18h post final bout of swimming exercise. RESULTS: PPARβ/δ, PGC-1α, COX I and NADH protein expression in shPPARβ/δ over-expression sedentary (Sed) skeletal muscle were significantly decreased over 55%, but PGC-1α ubiquitination was significantly increased 2.6 fold when compared to scramble (Scr) treated Sed muscle. PPARβ/δ, PGC-1α, COX I and NADH protein expression in 2 wks swimming exercise with Scr gene treated muscle were significantly increased over 2 fold, but PGC-1α ubiquitination was significantly decreased 66% when compared to Scr gene treated Sed muscle. PPARβ/δ, PGC-1α, COX I and NADH protein expression in 2 wks swimming exercise with shPPARβ/δ gene treated muscle were not increased, but PGC-1α ubiquitination was significantly increased 1.96 fold when compared to Scr gene treated Sed muscle. CONCLUSIONS: Our results indicate that PPARβ/δ controls PGC-1α protein stability in rat skeletal muscle following long-term endurance exercise.
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