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RISS 인기검색어
- 검색키워드
- 저자 : Seo Arnold Y. (검색결과 4 건)
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Mitochondrial iron accumulation with age and functional consequences
Seo, Arnold ,Y. ,Xu, Jinze ,Servais, Stephane ,Hofer, Tim ,Marzetti, Emanuele ,Wohlgemuth, Stephanie ,E. ,Knutson, Mitchell ,D. ,Chung, Hae ,Young ,Leeu Blackwell Publishing Ltd 2008 Aging Cell Vol.7 No.5
<P>Summary</P><P>During the aging process, an accumulation of non-heme iron disrupts cellular homeostasis and contributes to the mitochondrial dysfunction typical of various neuromuscular degenerative diseases. Few studies have investigated the effects of iron accumulation on mitochondrial integrity and function in skeletal muscle and liver tissue. Thus, we isolated liver mitochondria (LM), as well as quadriceps-derived subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM), from male Fischer 344× Brown Norway rats at 8, 18, 29 and 37 months of age. Non-heme iron content in SSM, IFM and LM was significantly higher with age, reaching a maximum at 37 months of age. The mitochondrial permeability transition pore (mPTP) was more susceptible to the opening in aged mitochondria containing high levels of iron (i.e. SSM and LM) compared to IFM. Furthermore, mitochondrial RNA oxidation increased significantly with age in SSM and LM, but not in IFM. Levels of mitochondrial RNA oxidation in SSM and LM correlated positively with levels of mitochondrial iron, whereas a significant negative correlation was observed between the maximum Ca<SUP>2+</SUP> amounts needed to induce mPTP opening and iron contents in SSM, IFM and LM. Overall, our data suggest that age-dependent accumulation of mitochondrial iron may increase mitochondrial dysfunction and oxidative damage, thereby enhancing the susceptibility to apoptosis.</P>
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Sang Woon Chung,Mi Kyung Kim,정재헌,김대현,최재수,Stephen Anton,Arnold Y. Seo,박건영,Takako Yokozawa,이숙희,Byung Pal Yu,정해영 한국식품영양과학회 2009 Journal of medicinal food Vol.12 No.2
Peroxisome proliferator-activated receptors (PPARs), members of the nuclear hormone receptor family, are key regulators of various metabolic pathways related to lipid and glucose metabolism as well as inflammation. We examined the effect of zingerone, a major ingredient of ginger, on PPAR, hepatic nuclear factor-4 (HNF-4), and nuclear factor-κB (NF-κB) expression in 21-month-old male Sprague-Dawley rats. Two experimental groups receiving doses of either 2 or 8 mg/kg/day zingerone for 10 days were compared with young rats (6 months old) and an age-matched control group. For molecular work, the endothelial cell line YPEN-1 was used. Both the 2 and 8 mg/kg/day dose of zingerone significantly increased DNA binding activities of PPARs (2.8-fold). Expression of HNF-4 was also increased in the group receiving the 8 mg/kg/day dose. We further showed that zingerone partially prevented the age-related decline in PPAR expression. In vitro experiments revealed zingerone (10 μM) increased PPAR expression (2.5-fold) to a similar extent as the PPAR agonist fibrate (5 μM) and suppressed pro-inflammatory transcription factor NF-κB activity. Collectively, our findings suggest that zingerone exerts its potent anti-inflammatory action by increasing HNF-4 and PPAR activities, while suppressing NF-κB activity.
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Chung, Sang-Woon,Kim, Mi-Kyung,Chung, Jae-Heun,Kim, Dae-Hyun,Choi, Jae-Sue,Anton, Stephen,Seo, Arnold Y.,Park, Kun-Young,Yokozawa, Takako,Rhee, Sook-Hee,Yu, Byung-Pal,Chung, Hae-Young The Korean Society of Food Science and Nutrition 2009 Journal of medicinal food Vol.12 No.2
Peroxisome proliferator-activated receptors (PPARs), members of the nuclear hormone receptor family, are key regulators of various metabolic pathways related to lipid and glucose metabolism as well as inflammation. We examined the effect of zingerone, a major ingredient of ginger, on PPAR, hepatic nuclear factor-4 (HNF-4), and nuclear factor-${\kappa}B$ (NF-${\kappa}B$) expression in 21-month-old male Sprague-Dawley rats. Two experimental groups receiving doses of either 2 or 8 mg/kg/day zingerone for 10 days were compared with young rats (6 months old) and an age-matched control group. For molecular work, the endothelial cell line YPEN-1 was used. Both the 2 and 8 mg/kg/day dose of zingerone significantly increased DNA binding activities of PPARs (2.8-fold). Expression of HNF-4 was also increased in the group receiving the 8 mg/kg/day dose. We further showed that zingerone partially prevented the age-related decline in PPAR expression. In vitro experiments revealed zingerone ($10\;{\mu}M$) increased PPAR expression (2.5-fold) to a similar extent as the PPAR agonist fibrate ($5\;{\mu}M$) and suppressed pro-inflammatory transcription factor NF-${\kappa}B$ activity. Collectively, our findings suggest that zingerone exerts its potent anti-inflammatory action by increasing HNF-4 and PPAR activities, while suppressing NF-${\kappa}B$ activity.
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Lee Bonggi,An Hye Jin,Kim Dae Hyun,Lee Min-Kyeong,Jeong Hyeon Hak,Chung Ki Wung,고영훈,Seo Arnold Y.,Kim Il Yong,Seong Je Kyung,Yu Byung Pal,LEE, JAE-WON,Im Eunok,Lee In-Kyu,Lee Myung-Shik,Yamada Ken-ich 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
The vitamin-C-synthesizing enzyme senescent marker protein 30 (SMP30) is a cold resistance gene in Drosophila, and vitamin C concentration increases in brown adipose tissue post-cold exposure. However, the roles of SMP30 in thermogenesis are unknown. Here, we tested the molecular mechanism of thermogenesis using wild-type (WT) and vitamin C-deficient SMP30-knockout (KO) mice. SMP30-KO mice gained more weight than WT mice without a change in food intake in response to short-term high-fat diet feeding. Indirect calorimetry and cold-challenge experiments indicated that energy expenditure is lower in SMP30-KO mice, which is associated with decreased thermogenesis in adipose tissues. Therefore, SMP30-KO mice do not lose weight during cold exposure, whereas WT mice lose weight markedly. Mechanistically, the levels of serum FGF21 were notably lower in SMP30-KO mice, and vitamin C supplementation in SMP30-KO mice recovered FGF21 expression and thermogenesis, with a marked reduction in body weight during cold exposure. Further experiments revealed that vitamin C activates PPARα to upregulate FGF21. Our findings demonstrate that SMP30-mediated synthesis of vitamin C activates the PPARα/FGF21 axis, contributing to the maintenance of thermogenesis in mice.
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