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Your search keyword '"Chang, Seo-Hyuk"' showing total 2 results
Start Over Author "Chang, Seo-Hyuk" Publisher korean society for biochemistry and molecular biology
2 results on '"Chang, Seo-Hyuk"'

1. Activation of Nrf2 by sulfuretin stimulates chondrocyte differentiation and increases bone lengths in zebrafish.

Author

Chang SH, Giong HK, Kim DY, Kim S, Oh S, Yun UJ, Lee JS, and Park KW

Subjects
Animals, Zebrafish, Cell Differentiation, Mammals, Chondrocytes, NF-E2-Related Factor 2
Abstract

Elongation of most bones occur at the growth plate through endochondral ossification in postnatal mammals. The maturation of chondrocyte is a crucial factor in longitudinal bone growth, which is regulated by a complex network of paracrine and endocrine signaling pathways. Here, we show that a phytochemical sulfuretin can stimulate hypertrophic chondrocyte differentiation in vitro and in vivo. We found that sulfuretin stabilized nuclear factor (erythroid-derived 2)-like 2 (Nrf2), stimulated its transcriptional activity, and induced expression of its target genes. Sulfuretin treatment resulted in an increase in body length of zebrafish larvae and induced the expression of chondrocyte markers. Consistently, a clinically available Nrf2 activator, dimethyl fumarate (DMF), induced the expression of hypertrophic chondrocyte markers and increased the body length of zebrafish. Importantly, we found that chondrocyte gene expression in cell culture and skeletal growth in zebrafish stimulated by sulfuretin were significantly abrogated by Nrf2 depletion, suggesting that such stimulatory effects of sulfuretin were dependent on Nrf2, at least in part. Taken together, these data show that sulfuretin has a potential use as supporting ingredients for enhancing bone growth. [BMB Reports 2023; 56(9): 496-501].

Published
2023

2. Nrf2 induces Ucp1 expression in adipocytes in response to β3-AR stimulation and enhances oxygen consumption in high-fat diet-fed obese mice.

Author

Chang SH, Jang J, Oh S, Yoon JH, Jo DG, Yun UJ, and Park KW

Subjects
Adipocytes physiology, Adipose Tissue, Brown metabolism, Animals, Cell Line, Diet, High-Fat, Dioxoles pharmacology, Energy Metabolism physiology, Gene Expression genetics, Gene Expression Regulation genetics, Heme Oxygenase-1 genetics, Heme Oxygenase-1 metabolism, Isoproterenol pharmacology, Male, Mice, Mice, Inbred C57BL, Mice, Obese, Mitochondrial Proteins metabolism, NF-E2-Related Factor 2 genetics, Obesity metabolism, Oxygen Consumption physiology, Receptors, Adrenergic, beta-3 metabolism, Thermogenesis, Uncoupling Protein 1 genetics, Adipocytes metabolism, NF-E2-Related Factor 2 metabolism, Uncoupling Protein 1 metabolism
Abstract

Cold-induced norepinephrine activates β3-adrenergic receptors (β3-AR) to stimulate the kinase cascade and cAMP-response element-binding protein, leading to the induction of thermogenic gene expression including uncoupling protein 1 (Ucp1). Here, we showed that stimulation of the β3-AR by its agonists isoproterenol and CL316,243 in adipocytes increased the expression of Ucp1 and Heme Oxygenase 1 (Hmox1), the principal Nrf2 target gene, suggesting the functional interaction of Nrf2 with β3-AR signaling. The activation of Nrf2 by tert-butylhydroquinone and reactive oxygen species (ROS) production by glucose oxidase induced both Ucp1 and Hmox1 expression. The increased expression of Ucp1 and Hmox1 was significantly reduced in the presence of a Nrf2 chemical inhibitor or in Nrf2-deleted (knockout) adipocytes. Furthermore, Nrf2 directly activated the Ucp1 promoter, and this required DNA regions located at -3.7 and -2.0 kb of the transcription start site. The CL316,243- induced Ucp1 expression in adipocytes and oxygen consumption in obese mice were partly compromised in the absence of Nrf2 expression. These data provide additional insight into the role of Nrf2 in β3-AR-mediated Ucp1 expression and energy expenditure, further highlighting the utility of Nrf2-mediated thermogenic stimulation as a therapeutic approach to diet-induced obesity. [BMB Reports 2021; 54(8): 419-424].

Published
2021

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