J. Lipid Res. Neurobiology of Lipids (ISSN1683-5506)
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A more recent version of this article appeared on May 1, 2004

Papers In Press, published online ahead of print March 1, 2004
J. Lipid Res., doi:10.1194/jlr.M300497-JLR200
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Submitted on December 3, 2003
Revised on February 17, 2004
Accepted on February 18, 2004

Linoleic acid-induced endothelial activation: role of calcium and peroxynitrite signaling

Viswanathan Saraswathi, Guoyao Wu, Michal Toborek, and Bernhard Hennig

University of Kentucky, Lexington, KY 40546-0215

Corresponding Author: bhennig{at}uky.edu

Hypertriglyceridemia, an important risk factor of atherosclerosis is associated with increased circulating free fatty acids. Research to date indicates that linoleic acid (LA), the major fatty acid in the American diet may be atherogenic by activating vascular endothelial cells. However, the exact signaling mechanisms involved in LA-mediated pro-inflammatory events in endothelial cells still remain unclear. We previously reported an increased superoxide formation following LA exposure in endothelial cells. The objective of the present investigation is to determine the role calcium and peroxynitrite in mediating the pro-inflammatory effect of LA in vascular endothelial cells. LA exposure increased intracellular calcium, NO and tetrahydrodiopterin (BH4) levels as well as the expression of E-selectin. Inhibiting calcium signaling using BAPTA and heparin decreased the expression of E-selectin. Also, LA-mediated NF-kappa B activation and E-selectin gene expression were suppressed by MnTMPyP (a superoxide scavenger), L-NMMA (an eNOS inhibitor) and FeTPPS (a peroxynitrite scavenger). LA exposure resulted in increased nitrotyrosine levels as observed by Western blotting and immunofluorescence. Our data suggest that the pro-inflammatory effects of LA can be mediated through calcium and peroxynitrite signaling.


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