Heparin cofactor II modulates the response to vascular injury

Research output: Contribution to journalReview article

45 Scopus citations

Abstract

Heparin cofactor II (HCII) has several biochemical properties that distinguish it from other serpins: (1) it specifically inhibits thrombin; (2) the mechanism of inhibition involves binding of an acidic domain in HCII to thrombin exosite I; and (3) the rate of inhibition increases dramatically in the presence of dermatan sulfate molecules having specific structures. Human studies suggest that high plasma HCII levels are protective against in-stent restenosis and atherosclerosis. Studies with HCII knockout mice directly support the hypothesis that HCII interacts with dermatan sulfate in the arterial wall after endothelial injury and thereby exerts an antithrombotic effect. In addition, HCII deficiency appears to promote neointima formation and atherogenesis in mice. These results suggest that HCII plays a unique and important role in vascular homeostasis.

Original languageEnglish
Pages (from-to)454-460
Number of pages7
JournalArteriosclerosis, thrombosis, and vascular biology
Volume27
Issue number3
DOIs
StatePublished - Mar 1 2007

Keywords

  • Atherogenesis
  • Heparin cofactor II
  • Restenosis
  • Thrombin
  • Thrombosis

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