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- 저자 : Hwamok Oh (검색결과 3 건)
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Eudesmin impairs adipogenic differentiation via inhibition of S6K1 signaling pathway
Nam, Ki Hong,Yi, Sang Ah,Lee, Jaecheol,Lee, Min Gyu,Park, Jee Hun,Oh, Hwamok,Lee, Jieun,Park, Jong Woo,Han, Jeung-Whan Elsevier 2018 Biochemical and biophysical research communication Vol.505 No.4
<P><B>Abstract</B></P> <P>Eudesmin has been reported to possess diverse therapeutic effects, including anti-tumor, anti-inflammatory, and anti-bacterial activities. However, its molecular action has not been implicated in metabolic disease. In this study, we show that treatment of mesenchymal stem cells (MSCs) with eudesmin disturbs adipogenesis via suppression of S6K1 signaling pathway. Eudesmin treatment inhibited activation and nuclear translocation of S6K1. Consequently, S6K1-mediated phosphorylation of H2B at serine 36 (H2BS36p) was reduced upon eudesmin treatment, further inducing the expression of <I>Wnt6</I>, <I>Wnt10a</I>, and <I>Wnt1</I>0b, which disturbed adipogenic differentiation. Moreover, eudesmin promoted myogenic and osteogenic gene expression in MSCs. Taken together, we found a novel small molecule, eudesmin, to block adipogenesis through down-regulation of S6K1-H2BS36p axis, followed by regulation of cell fate determination genes. This study suggests a promising therapeutic approach with eudesmin to cure obesity and metabolic diseases.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Eudesmin inhibits activation sand nuclear translocation of S6K1. </LI> <LI> Eudesmin promotes <I>Wnt</I> gene expression by reducing S6K1-mediated H2BS36 phosphorylation. </LI> <LI> Eudesmin disturbs adipogenic gene expression and de novo adipocyte generation. </LI> <LI> Eudesmin enhances myogenic and osteogenic gene expression. </LI> </UL> </P>
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Sang Ah Yi,Jieun Lee,Sun Kyu Park,Jeom Yong Kim,Jong Woo Park,Min Gyu Lee,Ki Hong Nam,Jee Hun Park,Hwamok Oh,Saetbyul Kim,Jihoon Han,Bo Kyung Kim,Dong-Gyu Jo,Jeung-Whan Han 고려인삼학회 2020 Journal of Ginseng Research Vol.44 No.1
Background: The biological and pharmacological effects of BST204, a fermented ginseng extract, havebeen reported in various disease conditions. However, its molecular action in metabolic disease remainspoorly understood. In this study, we identified the antiadipogenic activity of BST204 resulting from itsinhibition of the S6 kinase 1 (S6K1) signaling pathway. Methods: The inhibitory effects of BST204 on S6K1 signaling were investigated by immunoblot, nuclearfractionation, immunoprecipitation analyses. The antiadipogenic effect of BST204 was evaluated bymeasuring mRNA levels of adipogenic genes and by chromatin immunoprecipitation and quantitativereal-time polymerase chain reaction analysis. Results: Treatment with BST204 inhibited activation and nuclear translocation of S6K1, furtherdecreasing the interaction between S6K1 and histone H2B in 10T1/2 mesenchymal stem cells. Subsequently,phosphorylation of H2B at serine 36 (H2BS36p) by S6K1 was reduced by BST204, inducing anincrease in the mRNA expression of Wnt6, Wnt10a, and Wnt10b, which disturbed adipogenic differentiationand promoted myogenic and early osteogenic gene expression. Consistently, BST204 treatmentduring adipogenic commitment suppressed the expression of adipogenic marker genes and lipid dropformation. Conclusion: Our results indicate that BST204 blocks adipogenesis of mesenchymal stem cells through theinhibition of S6K1-mediated histone phosphorylation. This study suggests the potential therapeuticstrategy using BST204 to combat obesity and musculoskeletal diseases.
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Yi, Sang Ah,Lee, Jieun,Park, Sun Kyu,Kim, Jeom Yong,Park, Jong Woo,Lee, Min Gyu,Nam, Ki Hong,Park, Jee Hun,Oh, Hwamok,Kim, Saetbyul,Han, Jihoon,Kim, Bo Kyung,Jo, Dong-Gyu,Han, Jeung-Whan The Korean Society of Ginseng 2020 Journal of Ginseng Research Vol.44 No.1
Background: The biological and pharmacological effects of BST204, a fermented ginseng extract, have been reported in various disease conditions. However, its molecular action in metabolic disease remains poorly understood. In this study, we identified the antiadipogenic activity of BST204 resulting from its inhibition of the S6 kinase 1 (S6K1) signaling pathway. Methods: The inhibitory effects of BST204 on S6K1 signaling were investigated by immunoblot, nuclear fractionation, immunoprecipitation analyses. The antiadipogenic effect of BST204 was evaluated by measuring mRNA levels of adipogenic genes and by chromatin immunoprecipitation and quantitative real-time polymerase chain reaction analysis. Results: Treatment with BST204 inhibited activation and nuclear translocation of S6K1, further decreasing the interaction between S6K1 and histone H2B in 10T1/2 mesenchymal stem cells. Subsequently, phosphorylation of H2B at serine 36 (H2BS36p) by S6K1 was reduced by BST204, inducing an increase in the mRNA expression of Wnt6, Wnt10a, and Wnt10b, which disturbed adipogenic differentiation and promoted myogenic and early osteogenic gene expression. Consistently, BST204 treatment during adipogenic commitment suppressed the expression of adipogenic marker genes and lipid drop formation. Conclusion: Our results indicate that BST204 blocks adipogenesis of mesenchymal stem cells through the inhibition of S6K1-mediated histone phosphorylation. This study suggests the potential therapeutic strategy using BST204 to combat obesity and musculoskeletal diseases.
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