계명대학교 의학도서관 Repository

The effect of oxidized low density lipoprotein (oxLDL)-induced heme oxygenase-1 on LPS-induced inflammation in RAW 264.7 macrophage cells

Metadata Downloads
Author(s)
권택규
Alternative Author(s)
Kwon, Taeg Kyu
Publication Year
2012
Abstract
Macrophages take up oxidized low density lipoprotein (oxLDL) after being exposed to it in the blood vessels. oxLDL transforms macrophages into foam cells, which are a hallmark of atherosclerosis. The effects that oxLDL have on the inflammatory responses of foam cells are not clear. Here, we investigated how oxLDL modulates lipopolysaccharide (LPS)-induced inflammatory mediators in RAW 264.7 murine macrophages. Our results showed that oxLDL dramatically induced HO-1 expression, but did not increase pro-inflammatory mediators such as interleukin-1β, tumor necrosis factor-α, iNOS, and monocyte chemoattractant protein (MCP)-1. In RAW 264.7 macrophages, oxLDL markedly inhibited LPS-induced inflammatory mediators such as inducible nitric oxide synthase (iNOS), IL-1β, IL-6, granulocyte macrophage colony-stimulating factor and stromal cell-derived factor-1. Interestingly, however, the down-regulation of HO-1 by siRNA did not recover the inhibition of LPS-induced expression and/or the secretion of inflammatory mediators. oxLDL blocked LPS-induced NF-κB nuclear translocation by inhibiting inhibitory κB (IκB) degradation. Taken together, our results suggest that oxLDL could modulate LPS-induced inflammatory responses by inhibiting NF-κB signaling independently of HO-1 expression.
Department
Dept. of Immunology (면역학)
Publisher
School of Medicine
Citation
Cellular Signalling, Vol.24(6) : 1215-1221, 2012
Type
Article
ISSN
0898-6568
DOI
10.1016/j.cellsig.2012.02.001
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35388
Authorize & License
  • AuthorizeOpen
  • EmbargoForever
Files in This Item:

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.