NDLI: Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation.

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Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Limin Gill, Rajan Pedersen, Theresa L. Higgins, Laura J. Newman, John W. Rutledge, John C.
Description	Country affiliation: United States Author Affiliation: Wang L ( Division of Endocrinology, Clinical Nutrition, and Vascular Medicine, University of California, Davis, Davis, CA, USA. lwang@ucdavis.edu)
Abstract	Triglyceride-rich lipoprotein (TGRL) lipolysis products provide a pro-inflammatory stimulus that can alter endothelial barrier function. To probe the mechanism of this lipolysis-induced event, we evaluated the pro-inflammatory potential of lipid classes derived from human postprandial TGRL by lipoprotein lipase (LpL). Incubation of TGRL with LpL for 30 min increased the saturated and unsaturated FFA content of the incubation solutions significantly. Furthermore, concentrations of the hydroxylated linoleates 9-hydroxy ocatadecadienoic acid (9-HODE) and 13-HODE were elevated by LpL lipolysis, more than other measured oxylipids. The FFA fractions elicited pro-inflammatory responses inducing TNFalpha and intracellular adhesion molecule expression and reactive oxygen species (ROS) production in human aortic endothelial cells (HAECs). The FFA-mediated increase in ROS was blocked by both the cytochrome P450 2C9 inhibitor sulfaphenazole and NADPH oxidase inhibitors. Compared with linoleate, 13-HODE was found to be a more potent inducer of ROS production in HAECs, an activity that was insensitive to both NADPH oxidase and cytochrome P450 inhibitors. Therefore, although the oxidative metabolism of FFA in endothelial cells can produce inflammatory responses, TGRL lipolysis can also release preformed mediators of oxidative stress (e.g., HODEs) that may influence endothelial cell function in vivo by stimulating intracellular ROS production.
File Format	HTM / HTML
ISSN	00222275
e-ISSN	15397262
DOI	10.1194/jlr.M700505-JLR200
Journal	The Journal of Lipid Research
Issue Number	2
Volume Number	50
Language	English
Publisher	American Society for Biochemistry and Molecular Biology
Publisher Date	2009-02-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Biochemistry Endothelial Cells Metabolism Fatty Acids, Nonesterified Inflammation Mediators Lipolysis Physiology Lipoproteins Triglycerides Cells, Cultured Lipoprotein Lipase Blood Oxidation-reduction Postprandial Period Reactive Oxygen Species Tumor Necrosis Factor-alpha Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Research Support, U.s. Gov't, Non-p.h.s.
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Endocrinology

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