Suppression of inducible nitric oxide synthase and cyclooxygenase-2 gene expression by 22(R)-hydroxycholesterol requires de novo protein synthesis in activated macrophages

The Journal of Steroid Biochemistry and Molecular Biology Volume 97 Issue 4 Page 376-383 published_at 2005-12
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Title ( eng )
Suppression of inducible nitric oxide synthase and cyclooxygenase-2 gene expression by 22(R)-hydroxycholesterol requires de novo protein synthesis in activated macrophages
Creator
Yuge Osafumi
Ninomiya Yuichi
Source Title
The Journal of Steroid Biochemistry and Molecular Biology
Volume 97
Issue 4
Start Page 376
End Page 383
Abstract
Liver X receptors (LXRs) play an important role in lipid metabolism. Recently, a role for these proteins was identified in suppressing the inflammatory response. However, it is not known whether the natural ligands of LXRs, e.g. 22(R)-hydroxycholesterol (22R-HC), can suppress the inflammatory response after the onset of inflammation. We demonstrate here that treatment of Lipopolysaccharide (LPS)-activated RAW264.7 macrophages with 22R-HC markedly suppressed nitric oxide (NO) production and inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) mRNA expression. Additionally, 22R-HC did not affect the DNA binding activity of NF-κB, AP-1 and C/EBP(s), important transcriptional factors for iNOS and COX-2 genes expression. Furthermore iNOS and COX-2 mRNA suppression by 22R-HC was diminished by cellular treatment with cycloheximide. These results suggest that 22R-HC suppresses the expression of iNOS and COX-2 genes through de novo protein synthesis of an unidentified protein in LPS-activated macrophages. © 2005 Elsevier Ltd. All rights reserved.
Keywords
22(R)-Hydroxycholesterol
Inflammation
Macrophage
22R-HC
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type journal article
Publisher
Elsevier Ltd
Date of Issued 2005-12
Rights
Copyright (c) 2005 Elsevier Ltd
Publish Type Author’s Original
Access Rights open access
Source Identifier
[ISSN] 0960-0760
[DOI] 10.1016/j.jsbmb.2005.06.030
[PMID] 16146692
[DOI] http://dx.doi.org/10.1016/j.jsbmb.2005.06.030 isVersionOf