Prostaglandins modulate arterial cholesteryl ester metabolism.
Cholesterol and cholesteryl esters (CE) are the two major classes of lipids which accumulate in arteries during human arteriosclerosis. Mechanisms responsible for this arterial lipid accretion remain to be fully elucidated. In recent years, we have suggested that prostaglandins may have an important role in the modulation of intracellular arterial CE metabolism through their interaction with cyclic nucleotides. This hypothesis was based on observations that arteriosclerotic arteries produce less prostaglandins, particularly prostacyclin, and have altered CE synthetic and hydrolytic activities as compared to uninvolved arteries. This review is a summary of our present knowledge concerning the role of eicosanoids and cyclic nucleotides in the modulation of enzyme activities responsible for arterial CE synthesis and hydrolysis.
D015121:6-Ketoprostaglandin F1 alpha / Q000494:pharmacology; D000527:Alprostadil / Q000031:analogs & derivatives; D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D001161:Arteriosclerosis / Q000097:blood; D002784:Cholesterol / Q000378:metabolism; D002788:Cholesterol Esters / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D015232:Dinoprostone; D011464:Epoprostenol / Q000494:pharmacology; D006801:Humans; D006868:Hydrolysis; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology
D001095:Arachidonic Acids; D002788:Cholesterol Esters; D011453:Prostaglandins; D011458:Prostaglandins E; D016718:Arachidonic Acid; D015121:6-Ketoprostaglandin F1 alpha; C022950:6-ketoprostaglandin E1; D002784:Cholesterol; D011464:Epoprostenol; D000242:Cyclic AMP; D000527:Alprostadil; D015232:Dinoprostone