Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 450, Issue C, Pages 43-53Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2017.04.015
Keywords
E4BP4; Adipogenesis; 3T3-L1; Dexamethasone; GR; COX2
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Funding
- National Natural Science Foundation of China [31472075, 31402085]
- Hubei Provincial Creative Team Project of Agricultural Science and Technology [2007-620]
- Key Technology Research and Development Program of Hubei Province [2014ABB014, 2014ABC012]
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Adipogenesis is mediated by glucocorticoids via transcriptional regulation of glucocorticoid receptor (GR) target genes. However, the mechanism by which GR participates in adipogenesis has hitherto been poorly characterized. In this study, E4 promoter-binding protein 4 (E4BP4) was found to have a critical role in adipogenic differentiation of preadipocytes. Gain-of-function and loss-of-function studies revealed that E4BP4 acts as a positive regulator of adipogenesis in 3T3-L1 cells. E4BP4 was markedly induced by glucocorticoid (dexamethasone) via GR and cAMP response element-binding protein (CREB) during adipogenesis. Knockdown of E4BP4 abolished dexamethasone-induced adipogenesis, and over expression of E4BP4 partially accounted for the actions of dexamethasone in adipogenic differentiation. Promoter deletion analysis confirmed that E4BP4 transcriptionally represses COX2 promoter activity, whereas COX2 overexpression reversed the acceleration of E4BP4 in adipogenesis. Thus, E4BP4 acts as a key pro-adipogenic transcription factor by trans-repressing COX2 in glucocorticoid-associated adipocyte differentiation. (C) 2017 Elsevier B.V. All rights reserved.
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