Inhibition of platelet function by high-density lipoprotein from a patient with apolipoprotein E deficiency

Biochem Biophys Res Commun. 1991 Dec 31;181(3):1331-6. doi: 10.1016/0006-291x(91)92084-w.

Abstract

Apolipoprotein E-(apoE-) rich high-density lipoprotein (HDL) of normal subjects showed marked inhibitory effects on platelet aggregation and ATP release as compared with apoE-poor HDL, suggesting that apoE has inhibitory effects on platelet function (Desai et al. J. Lipid Res. 30:831, 1989; Higashihara et al. FEBS Lett. 282:82, 1991). A patient with apoE deficiency showed evidence of decreased platelet aggregability in platelet-rich plasma, but normal aggregability in washed platelets. Both patient's plasma and HDL fraction inhibited platelet aggregation of normal subjects. Patient's HDL reconstituted with recombinant apoE showed further inhibitory effects on platelet function. These results suggest that apoE is a potent, but not unique, inhibitory factor for HDL.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Diphosphate / pharmacology
  • Adult
  • Apolipoproteins E / deficiency*
  • Apolipoproteins E / pharmacology
  • Collagen / pharmacology
  • Humans
  • In Vitro Techniques
  • Kinetics
  • Lipoproteins, HDL / blood*
  • Lipoproteins, HDL / pharmacology
  • Male
  • Platelet Aggregation Inhibitors / pharmacology
  • Platelet Aggregation* / drug effects
  • Recombinant Proteins / pharmacology
  • Thrombin / pharmacology

Substances

  • Apolipoproteins E
  • Lipoproteins, HDL
  • Platelet Aggregation Inhibitors
  • Recombinant Proteins
  • Adenosine Diphosphate
  • Collagen
  • Thrombin