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Journal articles
Liver X Receptor (LXR) activation negatively regulates visfatin expression in macrophages.
Abstract : 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)γ are nuclear receptors expressed in macrophages controlling the inflammatory response. Recently, we reported visfatin as a PPARγ 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 PPARγ-induced visfatin gene and protein secretion in human macrophages. Our results identify visfatin as a gene oppositely regulated by the LXR and PPARγ pathways in human macrophages.
Cited literature [19 references]
https://www.hal.inserm.fr/inserm-00554308
Contributor : Marie-Hélène Derudas <>
Submitted on : Monday, January 10, 2011 - 3:50:04 PM
Last modification on : Friday, July 17, 2020 - 10:54:02 AM
Long-term archiving on: : Monday, April 11, 2011 - 4:22:43 PM
Contributor : Marie-Hélène Derudas <>
Submitted on : Monday, January 10, 2011 - 3:50:04 PM
Last modification on : Friday, July 17, 2020 - 10:54:02 AM
Long-term archiving on: : Monday, April 11, 2011 - 4:22:43 PM
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