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Protein c anticoagulant and cytoprotective pathways

Academic Article
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Overview

authors

  • Griffin, John
  • Zlokovic, B. V.
  • Mosnier, Laurent

publication date

  • April 2012

journal

  • International Journal of Hematology  Journal

abstract

  • Plasma protein C is a serine protease zymogen that is transformed into the active, trypsin-like protease, activated protein C (APC), which can exert multiple activities. For its anticoagulant action, APC causes inactivation of the procoagulant cofactors, factors Va and VIIIa, by limited proteolysis, and APC's anticoagulant activity is promoted by protein S, various lipids, high-density lipoprotein, and factor V. Hereditary heterozygous deficiency of protein C or protein S is linked to moderately increased risk for venous thrombosis, while a severe or total deficiency of either protein is linked to neonatal purpura fulminans. In recent years, the beneficial direct effects of APC on cells which are mediated by several specific receptors have become the focus of much attention. APC-induced signaling can promote multiple cytoprotective actions which can minimize injuries in various preclinical animal injury models. Remarkably, pharmacologic therapy using APC demonstrates substantial neuroprotective effects in various murine injury models, including ischemic stroke. This review summarizes the molecules that are central to the protein C pathways, the relationship of pathway deficiencies to venous thrombosis risk, and mechanisms for the beneficial effects of APC.

subject areas

  • Animals
  • Anticoagulants
  • Cytoprotection
  • Enzyme Activation
  • Humans
  • Models, Molecular
  • Mutation
  • Protein C
  • Protein S
  • Receptors, Cell Surface
  • Signal Transduction
  • Thrombomodulin
  • Venous Thrombosis
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Research

keywords

  • Endothelial protein C receptor
  • Neuroprotection
  • Protein C
  • Protein S
  • Thrombomodulin
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Identity

PubMed Central ID

  • PMC3413316

International Standard Serial Number (ISSN)

  • 0925-5710

Digital Object Identifier (DOI)

  • 10.1007/s12185-012-1059-0

PubMed ID

  • 22477541
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Additional Document Info

start page

  • 333

end page

  • 345

volume

  • 95

issue

  • 4

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