Protein C anticoagulant and cytoprotective pathways.
Review published in International journal of hematology (2012)
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.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Summary
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...
Why This Matters for Hirudotherapy
This review summarized the protein C anticoagulant and cytoprotective pathways, covering APC's inactivation of factors Va and VIIIa, the enhancing role of protein S and lipids, genetic deficiency associations with thrombosis and purpura fulminans, and APC's neuroprotective effects in murine injury models. The relevance to ASH is minimal — while anticoagulant mechanisms are discussed, the abstract involves no leeches, hirudin, or leech secretome. Caveat: no leech involvement; this is general coagulation biology background with indirect relevance only.
Citation
Protein C anticoagulant and cytoprotective pathways.
Griffin et al. · International journal of hematology, 2012
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