title: Effect of lysophosphatidylcholine on the structure and function of low density lipoproteins.
abstract: The treatment of LDL with bee-venom phospholipase A2 resulted in the formation of lipid-protein particles (phl-LDL) with an increased content of lysophosphatidylcholine (LPC). At the same time, the composition of other lipids and the protein structure remained unaffected. phl-LDL, as well as LPC, abolished the hormone-induced [Ca2+] increase in platelets and platelet aggregation induced by PAF, AMP and thrombin, whereas LDL produced no effect on the hormone-stimulated increase in the intracellular [Ca2+]. The effect persisted in a Ca(2+)-free medium, indicating that phl-LDL and LPC did not abolish the mobilization of intracellular stores with the above-mentioned inducers. Neither LPC no phl-LDL affected the [Ca2+]i level in platelets and suppressed the platelet aggregation evoked by tapsigargine, a specific inhibitor of endoplasmic reticulum Ca(2+)-ATPase, or by phorbol myristate acetate. The inhibitory effect depended on the LPC concentration and the time of platelet incubation with phl-LDL or LPC. The half-maximum efficient LPC concentrations were identical for LPC and phl-LDL (2-4 microM). The inhibitory effect was dependent on the LPC structure: lysophosphatidylethanolamine and phosphatidylcholine displayed no inhibitory effect. The results suggest that when added to washed platelets, free LPC and phl-LDL inhibit only the receptor-dependent increase of [Ca2+]i.
authors.affiliation: Institute of Experimental Cardiology, Russian Academy of Medical Sciences, Moscow.
authors.forename: A A
authors.initials: AA
authors.lastname: Korotaeva
authors.forename: I B
authors.initials: IB
authors.lastname: Cheglakov
authors.forename: A D
authors.initials: AD
authors.lastname: Morozkin
authors.forename: I V
authors.initials: IV
authors.lastname: Suslova
authors.forename: N V
authors.initials: NV
authors.lastname: Prokazova
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D002118:Calcium / Q000097:blood; D006440:Hemofiltration; D006801:Humans; D008077:Lipoproteins, LDL / Q000737:chemistry / Q000378:metabolism / Q000502:physiology*; D008244:Lysophosphatidylcholines / Q000378:metabolism / Q000494:pharmacology*; D010741:Phospholipases A / Q000378:metabolism / Q000494:pharmacology; D054467:Phospholipases A2; D010972:Platelet Activating Factor / Q000494:pharmacology; D015539:Platelet Activation / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D013329:Structure-Activity Relationship; D013917:Thrombin / Q000494:pharmacology
chemical_list: D008077:Lipoproteins, LDL; D008244:Lysophosphatidylcholines; D010972:Platelet Activating Factor; D010975:Platelet Aggregation Inhibitors; D000244:Adenosine Diphosphate; D010741:Phospholipases A; D054467:Phospholipases A2; D013917:Thrombin; D002118:Calcium