INHIBITORY EFFECT OF LYSOPHOSPHATIDYLCHOLINE AND PHOSPHOLIPASE A(2) -TREATED LOW-DENSITY LIPOPROTEINS ON RECEPTOR-DEPENDENT REGULATION OF [CA2+](I) IN PLATELETS
Aa. Korotaeva et al., INHIBITORY EFFECT OF LYSOPHOSPHATIDYLCHOLINE AND PHOSPHOLIPASE A(2) -TREATED LOW-DENSITY LIPOPROTEINS ON RECEPTOR-DEPENDENT REGULATION OF [CA2+](I) IN PLATELETS, Platelets, 8(1), 1997, pp. 43-51
Treatment of LDL with phospholipase A(2) from bee venom resulted in fo
rmation of lipid-protein particles (pl-LDL) with increased content of
lysophosphatidylcholine (LPC). At the same time, composition of other
lipids and protein structure were unaffected, Both pl-LDL and LPC abol
ished PAF-, ADP- and thrombin-induced Ca2+ elevation in platelets and
platelet aggregation, while LDL had no effect on hormone-stimulated in
crease in the intracellular Ca2+ content ([Ca2+](i)), The effect persi
sted in Ca2+-free medium, indicating that pl-LDL and LPC also abolish
Ca2+ mobilisation from intracellular stores, Neither LPC nor pl-LDL ch
anged platelet Ca2+ levels and inhibited platelet aggregation induced
by phorbolmyristate acetate, a PKC activator, and thapsigargin, a spec
ific inhibitor of the endoplasmic reticulum Ca2+ ATPase, The inhibitor
y effect depended on LPC concentration, incubation time and the struct
ure of LPC: lysophosphatidylethanolamine and phosphatidylcholine produ
ced no inhibitory effect. The half-maximum-effective concentrations we
re the same for LPC and pl-LDL (2-4 mu M), The results obtained indica
te that LPC and pl-LDL inhibit the receptor-dependent increase in Ca2, It can be suggested that the effect of LPC is mediated by redistribu
tion of the plasma membrane integral proteins, which leads to disinteg
ration of the intracellular signalling systems.