These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Reversal by high-density lipoprotein of the effect of oxidized low-density lipoprotein on nitric oxide synthase protein expression in human platelets.
    Author: Mehta JL, Chen LY.
    Journal: J Lab Clin Med; 1996 Mar; 127(3):287-95. PubMed ID: 9273362.
    Abstract:
    Oxidized low-density lipoproteins (ox-LDLs) induce vasoconstriction and platelet activation, and high-density lipoproteins (HDLs) reverse these effects of ox-LDL. To determine the involvement of the L-arginine-nitric oxide (NO) pathway in the effects of lipoproteins on platelets, washed human platelets were incubated with native-LDL, ox-LDL, or HDL plus ox-LDL, but not native LDL, potentiated thrombin-induced platelet aggregation and carbon 14-labeled serotonin release, and these effects of ox-LDL were blocked by pretreatment of platelets with HDL. Incubation of ox-LDL with platelets resulted in reduction in the uptake of tritiated L-arginine by intact platelets and in NO synthase activity in platelet lysate. These effects of ox-LDL on platelet NO synthase activity were also reversed by pretreatment of platelets with HDL. Western blot analysis demonstrated about a 50% reduction in the expression of NO synthase protein in platelets treated with ox-LDL. Whereas HDL alone had no effect on NO synthase protein expression, it blocked the decrease in NO synthase expression caused by ox-LDL. Thus ox-LDL stimulates platelet function primarily by diminishing NO synthase expression, and this effect of ox-LDL can be blocked by pretreatment of platelets with HDL.
    [Abstract] [Full Text] [Related] [New Search]