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

Title
The effect of oxidized low density lipoprotein (oxLDL)-induced heme oxygenase-1 on LPS-induced inflammation in RAW 264.7 macrophage cells
Author(s)
조경현민경진[민경진]권택규[권택규]
Keywords
FACTOR-KAPPA-B; MONOCYTE CHEMOATTRACTANT PROTEIN-1; ATHEROSCLEROTIC LESION FORMATION; NITRIC-OXIDE PRODUCTION; NECROSIS-FACTOR-ALPHA; GENE-EXPRESSION; ENDOTHELIAL-CELLS; HEMEOXYGENASE-1 EXPRESSION; PERITONEAL-MACROPHAGES; ACTIVATOR PROTEIN-1
Issue Date
201206
Publisher
ELSEVIER SCIENCE INC
Citation
CELLULAR SIGNALLING, v.24, no.6, pp.1215 - 1221
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-1 beta, tumor necrosis factor-alpha, 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-1 beta, 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-kappa B nuclear translocation by inhibiting inhibitory kappa B (I kappa B) degradation. Taken together, our results suggest that oxLDL could modulate LPS-induced inflammatory responses by inhibiting NF-kappa B signaling independently of HO-1 expression. (c) 2012 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/28038http://dx.doi.org/10.1016/j.cellsig.2012.02.001
ISSN
0898-6568
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생명공학부 > 생명공학부 > Articles
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