Dexamethasone-induced selenoprotein S degradation is required for adipogenesis

Title
Dexamethasone-induced selenoprotein S degradation is required for adipogenesis
Author(s)
김춘영김기홍[김기홍]
Keywords
ENDOPLASMIC-RETICULUM STRESS; UBIQUITIN-PROTEASOME SYSTEM; UNFOLDED PROTEIN RESPONSE; ADIPOCYTE DIFFERENTIATION; DEPENDENT PROTEOLYSIS; SKELETAL-MUSCLE; HEPG2 CELLS; C/EBP-BETA; ER STRESS; GLUCOCORTICOIDS
Issue Date
201308
Publisher
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
Citation
JOURNAL OF LIPID RESEARCH, v.54, no.8, pp.2069 - 2082
Abstract
Although adipogenesis is associated with induction of endoplasmic reticulum (ER) stress, the role of selenoprotein S (SEPS1), an ER resident selenoprotein known to regulate ER stress and ER-associated protein degradation, is unknown. We found an inverse relationship between SEPS1 level in adipose tissue and adiposity in mice. While SEPS1 expression was increased during adipogenesis, a markedly reduced SEPS1 protein level was found in the early phase of adipogenesis due to dexamethasone (DEX)-induced proteosomal degradation of SEPS1. Overexpression of SEPS1 in the early phase of cell differentiation resulted in impairment of adipogenesis with reduced levels of CCAAT/enhancer binding protein alpha and other adipocyte marker genes during the course of adipogenesis. Conversely, knockdown of SEPS1 resulted in the promotion of adipogenesis. Additionally, altered SEPS1 expression was associated with changes in expression of ER stress marker genes in the early phase of adipogenesis, and ubiquitin-proteasome system (UPS)-related ubiquitination and proteasome function. Our study reveals that SEPS1 is a novel anti-adipogenic selenoprotein that modulates ER stress- and UPS-dependent adipogenesis. Our results also identifies a novel function of DEX in the regulation of adipogenesis through induction of SEPS1 degradation. Taken together, DEX-dependent degradation of SEPS1 in the early phase of adipogenesis is necessary for initiating ER stress- and UPS-dependent maturation of adipocytes.
URI
http://hdl.handle.net/YU.REPOSITORY/29207http://dx.doi.org/10.1194/jlr.M034603
ISSN
0022-2275
Appears in Collections:
생활과학대학 > 식품영양학과 > Articles
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