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Reevaluation of the role of HDL in the anticoagulant activated protein C system in humans.

In English

Författare

Summary, in English

HDL has anti-atherogenic properties, and plasma levels of HDL cholesterol correlate inversely with risk of coronary artery disease. HDL reportedly functions as a cofactor to the anticoagulant activated protein C (APC) in the degradation of factor Va (FVa). The aim of the present study was to elucidate the mechanism by which HDL functions as cofactor to APC. Consistent with a previous report, HDL isolated from human plasma by ultracentrifugation was found to stimulate APC-mediated degradation of FVa. However, further purification of HDL by gel filtration revealed that the stimulating activity was not a property of HDL. Instead, the stimulating activity eluted completely separately from HDL in the high-molecular-weight void volume fractions. The active portion of these fractions stimulated FVa degradation by APC and supported the assembly of factor Xa and FVa into a functional prothrombinase complex. Both the procoagulant and anticoagulant activities were blocked by addition of annexin V, suggesting that the active portion was negatively charged phospholipid membranes. These results demonstrate that HDL does not stimulate the APC/protein S effect and that the activity previously reported to be a property of HDL is instead caused by contaminating negatively charged phospholipid membranes.

Publiceringsår

2010

Språk

Engelska

Sidor

1396-1399

Publikation/Tidskrift/Serie

Journal of Clinical Investigation

Volym

120

Issue

5

Dokumenttyp

Artikel i tidskrift

Förlag

The American Society for Clinical Investigation

Ämne

  • Medicinal Chemistry

Nyckelord

  • Thromboplastin: metabolism
  • Protein C: metabolism
  • Phospholipids: metabolism
  • Liposomes: metabolism
  • HDL: metabolism
  • Lipoproteins
  • Factor Xa: metabolism
  • Factor Va: metabolism
  • Annexin A5: metabolism
  • Anticoagulants: metabolism

Status

Published

Forskningsgrupp

  • Clinical Chemistry, Malmö

ISBN/ISSN/Övrigt

  • ISSN: 0021-9738