Suppression of inducible nitric oxide synthase and cyclooxygenase-2 gene expression by 22(R)-hydroxycholesterol requires de novo protein synthesis in activated macrophages
Use this link to cite this item : https://ir.lib.hiroshima-u.ac.jp/00014745
ID | 14745 |
file | |
creator |
Yuge, Osafumi
Ninomiya, Yuichi
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subject | 22(R)-Hydroxycholesterol
Inflammation
Macrophage
22R-HC
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NDC |
Medical sciences
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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.
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journal title |
The Journal of Steroid Biochemistry and Molecular Biology
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volume | Volume 97
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issue | Issue 4
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start page | 376
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end page | 383
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date of issued | 2005-12
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publisher | Elsevier Ltd
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issn | 0960-0760
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publisher doi | |
pubmed id | |
language |
eng
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nii type |
Journal Article
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HU type |
Journal Articles
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DCMI type | text
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format | application/pdf
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text version | author
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rights | Copyright (c) 2005 Elsevier Ltd
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relation is version of URL | http://dx.doi.org/10.1016/j.jsbmb.2005.06.030
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department |
Graduate School of Biomedical Science
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