LDLs increase the exposure of fibrinogen binding sites on platelets and secretion of dense granules.

摘要: Because previous studies show that lipoproteins affect platelet aggregation, we studied the effect of low-density lipoprotein (LDL) and high-density (HDL) on binding fibrinogen, which mediates platelet-platelet contact. Neither LDL nor HDL induced 125I-fibrinogen at concentrations up to 2 g protein/L. In contrast, platelets stimulated with 10 mumol/L ADP bound 63 734 +/- 2453 molecules fibrinogen per platelet. A 5-minute preincubation (0.5 g/L protein) a dose-dependent increase 91 307 2164 1.5 g/L, is in range found after optimal stimulation alpha-thrombin. The increased presence resulted faster aggregation 16% single disappearance optical 5 protein/L LDL. Inhibition prostaglandin G2/H2-thromboxane A2 formation indomethacin (30 mumol/L) did not change by modification lysine residues LDL, known prevent specific platelets, completely abolished Under same conditions or aggregation. also enhanced alpha-thrombin-induced [14C]serotonin secretion, but this property was affected These data indicate enhances stimulating mechanisms control exposure sites glycoprotein IIB/IIIA complex via mechanism differs from secretion.