Selenium modulates 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (PAF) biosynthesis in bovine aortic endothelial cells.
Selenium (Se) deficiency has been reported to increase platelet-activating factor (PAF) production in human endothelial cells; however, the mechanism is unclear. This study demonstrated that tumor necrosis factor-alpha (TNF-alpha) stimulated Se-deficient bovine aortic endothelial cells (BAEC) produced significantly more PAF than Se-supplemented cells. Moreover, the increase in the level of PAF was associated with enhanced activity of two anabolic enzymes in the remodeling pathway: phospholipase A2 and Lyso-PAF:acetyl-coenzyme A acetyltransferase (Lyso-PAF-AcT). In contrast, the activity of the PAF catabolic enzyme, PAF-acetylhydrolase, was not affected by Se status. Interestingly, prostacyclin, a potent vasodilator and inhibitor of platelet aggregation, inhibited the activity of Lyso-PAF-AcT and reduced the PAF production in TNF-alpha-stimulated BAEC. Therefore, we conclude that Se deficiency alters PAF production in TNF-alpha-stimulated BAEC by altering the activity of anabolic enzymes involved in the remodeling pathway partially through the inhibition of prostacyclin production.
Cao
Y Z
YZ
Department of Veterinary Science, The Pennsylvania State University, University Park 16802, USA.
Cohen
Z S
ZS
Weaver
J A
JA
Sordillo
L M
LM
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001011:Aorta / Q000166:cytology; D002417:Cattle; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000166:cytology; D011464:Epoprostenol / Q000494:pharmacology; D010972:Platelet Activating Factor / Q000096:biosynthesis*; D010974:Platelet Aggregation; D017382:Reactive Oxygen Species; D012643:Selenium / Q000378:metabolism / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D000975:Antioxidants; D010972:Platelet Activating Factor; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D011464:Epoprostenol; D012643:Selenium