4.6 Article

Liver X Receptor (LXR) activation negatively regulates visfatin expression in macrophages

期刊

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.12.002

关键词

Nuclear receptors; Adipocytokines; Visfatin; Inflammation; Macrophages

资金

  1. European Community [FP7/2007-2013, 20160]
  2. Nouvelle Societe Francaise d'Atherosclerose
  3. Fondation Coeur et Arteres

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Adipose tissue macrophages (ATM) are the major source of visfatin, a visceral fat adipokine upregulated during obesity. Also known to play a role in B cell differentiation (pre-B cell colony-enhancing factor (PBEF)) and NAD biosynthesis (nicotinamide phosphoribosyl transferase (NAMPT)), visfatin has been suggested to play a role in inflammation. Liver X Receptor (LXR) and Peroxisome Proliferator-Activated Receptor (PPAR)gamma are nuclear receptors expressed in macrophages controlling the inflammatory response. Recently, we reported visfatin as a PPAR gamma target gene in human macrophages. In this study, we examined whether LXR regulates macrophage visfatin expression. Synthetic LXR ligands decreased visfatin gene expression in a LXR-dependent manner in human and murine macrophages. The decrease of visfatin mRNA was paralleled by a decrease of protein secretion. Consequently, a modest and transient decrease of NAD(+) concentration was observed. Interestingly, LXR activation decreased the PPAR gamma-induced visfatin gene and protein secretion in human macrophages. Our results identify visfatin as a gene oppositely regulated by the LXR and PPAR gamma pathways in human macrophages. (C) 2010 Elsevier Inc. All rights reserved.

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