<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="6.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Dayong Wu</style></author><author><style face="normal" font="default" size="100%">Liping Liu</style></author><author><style face="normal" font="default" size="100%">Mohsen Meydani</style></author><author><style face="normal" font="default" size="100%">Simin Nikbin Meydani</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Vitamin E increases production of vasodilator prostanoids in human aortic endothelial cells through opposing effects on cyclooxygenase-2 and phospholipase A2</style></title><secondary-title><style face="normal" font="default" size="100%">The Journal of Nutrition</style></secondary-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arachidonic Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyclooxygenase 1</style></keyword><keyword><style  face="normal" font="default" size="100%">Cyclooxygenase 2</style></keyword><keyword><style  face="normal" font="default" size="100%">Dinoprostone</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelium</style></keyword><keyword><style  face="normal" font="default" size="100%">Epoprostenol</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Membrane Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Phospholipases A</style></keyword><keyword><style  face="normal" font="default" size="100%">Phospholipases A2</style></keyword><keyword><style  face="normal" font="default" size="100%">Vascular</style></keyword><keyword><style  face="normal" font="default" size="100%">Vasodilation</style></keyword><keyword><style  face="normal" font="default" size="100%">{alpha-Tocopherol</style></keyword><keyword><style  face="normal" font="default" size="100%">{Prostaglandin-Endoperoxide} Synthases</style></keyword><keyword><style  face="normal" font="default" size="100%">} Aorta</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2005</style></year><pub-dates><date><style  face="normal" font="default" size="100%">08/2005</style></date></pub-dates></dates><urls><web-urls><url><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/16046707</style></url></web-urls></urls><number><style face="normal" font="default" size="100%">8</style></number><volume><style face="normal" font="default" size="100%">135</style></volume><pages><style face="normal" font="default" size="100%">1847–1853</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">Impairment of endothelium-dependent vasodilation is associated with the initiation and development of atherosclerosis. Vasodilator prostanoids constitute a protective mechanism in maintaining normal vasomotor function. In the current study, we determined the effect of in vitro vitamin E supplementation at physiologically relevant concentrations (10-60 {micromol/L)} on the production of the vasodilator prostanoids prostaglandin I(2) {(PGI(2);} prostacyclin) and prostaglandin {E(2)(PGE(2))} by human aortic endothelial cells {(HAECs)} as well as its underlying mechanism. Results showed that vitamin E dose dependently (10-40 {micromol/L)} increased the production of both prostanoids by {HAECs.} This was associated with a dose-dependent (10-40 {micromol/L)} upregulation of cytosolic phospholipase A(2) {(cPLA(2))} expression and arachidonic acid release. In contrast, vitamin E dose dependently (10-60 {micromol/L)} inhibited cyclooxygenase {(COX)} activity but did not affect the expression of either {COX-1} or {COX-2,} indicating that the effect of vitamin E on {COX} activity was post-translational. Thus, vitamin E had opposing effects on the 2 key enzymes in prostanoid biosynthesis; at the concentrations used in this study, this resulted in a net increase in the production of vasodilator prostanoids. The vitamin E-induced increase in {PGI(2)} and {PGE(2)} production may contribute to its suggested beneficial effect in preserving endothelial function.</style></abstract><notes><style face="normal" font="default" size="100%">{PMID:} 16046707</style></notes></record></records></xml>