Nucleoredoxin promotes adipogenic differentiation through regulation of Wnt/beta-catenin signaling

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Title
Nucleoredoxin promotes adipogenic differentiation through regulation of Wnt/beta-catenin signaling
Author(s)
Yeong Jae Bahn; Kwang-Pyo LeeSeung Min Lee; Jeong Yi Choi; Y S Seo; Ki Sun Kwon
Bibliographic Citation
Journal of Lipid Research, vol. 56, no. 2, pp. 294-303
Publication Year
2015
Abstract
Nucleoredoxin (NRX) is a member of the thioredoxin family of proteins that controls redox homeostasis in cell. Redox homeostasis is a well-known regulator of cell differentiation into various tissue types. We found that NRX expression levels were higher in white adipose tissue of obese ob/ob mice and increased in the early adipogenic stage of 3T3-L1 preadipocyte differentiation. Knockdown of NRX decreased differentiation of 3T3-L1 cells, whereas overexpression increased differentiation. Adipose tissuespecifi c NRX transgenic mice showed increases in adipocyte size as well as number compared with WT mice. We further confi rmed that the Wingless/int-1 class (Wnt) /β -catenin pathway was also involved in NRX-promoted adipogenesis, consistent with a previous report showing NRX regulation of this pathway. Genes involved in lipid metabolism were downregulated, whereas inflammatory genes, including those encoding macrophage markers, were signifi cantly upregulated, likely contributing to the obesity in Adipo-NRX mice. Our results therefore suggest that NRX acts as a novel proadipogenic factor and controls obesity in vivo. - Bahn, Y. J., K-P. Lee, S-M. Lee, J. Y. Choi, Y-S. Seo, and K-S. Kwon. Nucleoredoxin promotes adipogenic differentiation through regulation of Wnt/β -catenin signaling. J. Lipid Res. 2015. 56: 294-303.
Keyword
AdipogenesisInflammationObesityWingless/int-1 class(wnt) signaling
ISSN
0022-2275
Publisher
Amer Soc Biochemistry Molecular Biology Inc
DOI
http://dx.doi.org/10.1194/jlr.M054056
Type
Article
Appears in Collections:
Division of Research on National Challenges > Aging Research Center > 1. Journal Articles
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