Protein C System Chemiluminescense Immunoassay Kit

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Coagulation Solution


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Protein C System

Systematic Assay of Protein C

Protein C

Systematic Assay of Protein S

Protein S

The protein C system mainly includes protein C (PC), protein S (PS), thrombomodulin (thrombomodulin, TM, also known as thrombomodulin and protein C inhibitor). PC forms activated protein C (APC) under the action of thrombin, which can mainly inactivate coagulation cofactors FVa and Fla; hinder the binding of factor Xa to platelets; promote fibrinolysis; PS mainly plays its role by accelerating the inactivation of Fla by APC Function;   TM is fixed on the cell membrane and is essentially a thrombin receptor.   In the presence of Ca2+, it accelerates the activation of PC .

Activated protein C (APC) acts as an “on demand” anticoagulant, reducing thrombin formation.    Reduced plasma levels of APC or protein C (PC) are associated with an increased risk of venous thromboembolism.    APC also displays cytoprotective functions and its therapeutic use has been evaluated in severe sepsis and is under evaluation in several diseases with an important inflammatory component.

Activated protein C (APC) is a serine protease derived from its inactive precursor, protein C (PC), which acts as a potent natural anticoagulant by inactivating factors Va and VIIIa .   Normal APC generation depends on the precise assemblage of thrombin, thrombomodulin, PC and the endothelial cell PC receptor (EPCR) on the surface of endothelial cells.     Therefore, any change in the efficiency of this assemblage may cause a reduction or an increase in APC generation that modifies the risk of thrombosis .

There are evidences for APC generation in vivo. Thus, it has been reported the presence of circulating amounts of a PC activation peptide and of complexes of APC with its physiological inhibitors . The physiological relevance of PC in the regulation of blood coagulation arises from the description of an increase in the risk of venous thromboembolism (VTE) associated with both hereditary PC deficiency and low circulating APC levels.

Although suspected conceptually in the 60 s, Protein C and Protein S activities in hemostasis were investigated and reported from the mid-80 s, followed by the discovery of Thrombomodulin, an endothelial cell membrane associated protein, playing the most important heamostatic role. These 3 proteins act in regulating thrombogenesis and protecting against thrombo-embolic events. When blood is activated, any trace of circulating thrombin is captured by Thrombomodulin in the microcirculation, making thrombin become an anticoagulant through its capacity to activate Protein C to Activated Protein C, which operates as a sentinel in blood coagulation, in the form of a complex with free Protein S, to block any new blood activation site, and more especially circulating activated Factors V and VIII.            Protein S not only acts as the Activated Protein C cofactor, but also as the cofactor of Tissue Factor Pathway Inhibitor. In addition, it has some functions in the complement pathway through its binding to C4b-BP. Another capability of activated protein C is to lower fibrinolytic activity, as the Activated Protein C Inhibitor is also known as Plasminogen Activator Inhibitor 3. The Protein C-Protein S system becomes less efficient in the presence of mutated Factor V (Factor V-Leiden or other variants), which is resistant to its inactivating effect. Other pathologies linked to this system concern the development of allo- or autoantibodies to Protein S or to thrombin, which can generate severe thrombotic complications in affected patients. Activated Protein C (especially in patients with sepsis) or Thrombomodulin are proposed as antithrombotic medications. Most importantly, congenital or acquired Protein C or Protein S deficiencies are associated with severe recurrent thrombotic events.

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