Document Detail

Physiological effects of oxidized phospholipids and their cellular signaling mechanisms in inflammation.
MedLine Citation:
PMID:  22080084     Owner:  NLM     Status:  MEDLINE    
Oxidized phospholipids, such as the products of the oxidation of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine by nonenzymatic radical attack, are known to be formed in a number of inflammatory diseases. Interest in the bioactivity and signaling functions of these compounds has increased enormously, with many studies using cultured immortalized and primary cells, tissues, and animals to understand their roles in disease pathology. Initially, oxidized phospholipids were viewed largely as culprits, in line with observations that they have proinflammatory effects, enhancing inflammatory cytokine production, cell adhesion and migration, proliferation, apoptosis, and necrosis, especially in vascular endothelial cells, macrophages, and smooth muscle cells. However, evidence has emerged that these compounds also have protective effects in some situations and cell types; a notable example is their ability to interfere with signaling by certain Toll-like receptors (TLRs) induced by microbial products that normally leads to inflammation. They also have protective effects via the stimulation of small GTPases and induce up-regulation of antioxidant enzymes and cytoskeletal rearrangements that improve endothelial barrier function. Oxidized phospholipids interact with several cellular receptors, including scavenger receptors, platelet-activating factor receptors, peroxisome proliferator-activated receptors, and TLRs. The various and sometimes contradictory effects that have been observed for oxidized phospholipids depend on their concentration, their specific structure, and the cell type investigated. Nevertheless, the underlying molecular mechanisms by which oxidized phospholipids exert their effects in various pathologies are similar. Although our understanding of the actions and mechanisms of these mediators has advanced substantially, many questions do remain about their precise interactions with components of cell signaling pathways.
Fiona H Greig; Simon Kennedy; Corinne M Spickett
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2011-10-31
Journal Detail:
Title:  Free radical biology & medicine     Volume:  52     ISSN:  1873-4596     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-06     Completed Date:  2012-05-01     Revised Date:  2014-02-20    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  266-80     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
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MeSH Terms
Atherosclerosis / immunology,  metabolism,  pathology
Cell Membrane / metabolism
Cell Proliferation
Chlorohydrins / metabolism
Endothelium / immunology,  metabolism,  physiopathology
Inflammation / metabolism*
Inflammation Mediators / blood,  metabolism
Lipoproteins, LDL / blood,  metabolism*
Peroxisome Proliferator-Activated Receptors / metabolism
Phospholipids / blood,  metabolism*
Signal Transduction*
Toll-Like Receptors / metabolism
Grant Support
FS/08/071///British Heart Foundation; FS/08/071/26212//British Heart Foundation
Reg. No./Substance:
0/Chlorohydrins; 0/Inflammation Mediators; 0/Lipoproteins, LDL; 0/Peroxisome Proliferator-Activated Receptors; 0/Phospholipids; 0/Toll-Like Receptors; 0/oxidized low density lipoprotein

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