Journal
INTERNATIONAL JOURNAL OF HEMATOLOGY
Volume 95, Issue 4, Pages 333-345Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s12185-012-1059-0
Keywords
Protein C; Protein S; Thrombomodulin; Endothelial protein C receptor; Neuroprotection
Categories
Funding
- NHLBI NIH HHS [R01 HL063290, P01 HL031950, R01 HL104165, R01 HL052246] Funding Source: Medline
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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.
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