Prostaglandins and lipid modification.
Postaglandins(PG) and low-density lipoproteins (LDL) both are playing a key role in atherogenesis. Their interaction at the local vascular level is of central relevance in plaque formation and progression. Details of these complex actions however, still need to be elucidated. Lipoproteins are influencing the PG-production of arterial wall cells and platelets, while PGs in turn have been shown to regulate lipoprotein receptor binding and entry into the arterial wall. Modification of LDL severely influences arterial wall trapping and foam cell formation. During LDL-modification, isoprostanes, a new family of compounds generated by free radical catalysed action, independent of cyclooxygenase, are formed. 8-epi PGF(2alpha) the most well known member exerts a great variety of proatherogenic actions, among them vasoconstriction and platelet activation; it also serves as a mitogen and stimulator of endothelin release. The influence of various eicosanoids on lipoprotein modification, however, has not been assessed yet.
Department of Nuclear Medicine, University of Vienna, Vienna, Austria. Helmut.Sinzinger@akh-wien.ac.at
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D001161:Arteriosclerosis / Q000378:metabolism*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism; D011464:Epoprostenol / Q000737:chemistry / Q000378:metabolism*; D006801:Humans; D015227:Lipid Peroxidation / Q000502:physiology*; D008077:Lipoproteins, LDL / Q000378:metabolism*; D011458:Prostaglandins E / Q000737:chemistry / Q000378:metabolism*; D011460:Prostaglandins F / Q000737:chemistry / Q000378:metabolism*
D008077:Lipoproteins, LDL; D011458:Prostaglandins E; D011460:Prostaglandins F; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D011464:Epoprostenol