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Coagulation Antibodies

A range of mouse monoclonal antibodies to detect components of the coagulation cascade and clotting pathways including Thrombin III, Christmas Factor and Von Willebrand Factor.

Coagulation is an important part of haemostasis: clot formation stops bleeding from the damaged vessel and the platelet and fibrin plug also begin the repair process.

In addition to our range of haemostasis diagnostic reagents Alpha Laboratories also offer antibodies for research applications.

BioPorto offers a number of monoclonal antibodies to detect key proteins within the clotting cascade, including regulatory proteins such a Protein C and fibrin degradation products such as D-dimers.

Extrinsic Pathway

The Extrinsic pathway is mediated almost exclusively by the Tissue Factor Pathway.  TF is a membrane protein localised in most tissues and released in response to injury.  It can also be generated by arteriosclerotic plaques and monocytes exposed to inflammatory stimuli.  TF and Factor VII form an active complex which in turn activates Factor X and the onward clotting cascade.

Intrinsic Pathway

As the vessel endothelium is ruptured underlying tissue and collagen fibres are exposed, the intrinsic or contact pathway begins with the formation of a primary complex on the collagen surface.  This initiating complex incorporates high molecular weight kininogen (HMWK), prekalikrein and Factor XII and results in activation of prekalikrein to kalikrein which in turn activates Factor XII.  The activation cascade continues as Factor XII activates Factor XI which subsequently activates Factor IX (Christmas Factor).  In the presence of calcium and Platelet Factor 3 (PF3) the active Factor IX leads to activation of Factor VIII which goes on to activate Factor X where both pathways merge.

Common Pathway

Clotting events downstream of Factor X activation resulting in clot formation are the same irrespective of the initiating pathway.  Active Factor X together with Calcium , Factor V, PF3 or Tissue Thromboplastin  enable prothrombin activator to convert Prothrombin (Factor II) into Thrombin.  Thrombin activatesFibrinogen (a soluble protein) into fibrin (an insoluble protein that aggregates).  Thrombin also activates Factor XIII which cross-links the fibrin to form a gel scaffold for clot formations.

Factor Deficiencies and clotting disorders

Clotting abnormalities are usually revealed by the diagnostic Prothrombin Time (PT) and Activated Partial Thromboplastin Time (APTT) tests.  These assess the extrinsic and intrinsic pathways respectively.  Bleeding disorders can result from pro-coagulant Factor deficiencies or platelet pathologies.  Haemophilia A is the result of a pro-coagulation Factor deficiency; affected individuals produce dysfunctional Factor VIII (qualitative deficiency) or fail to produce sufficient amounts of Factor VII (quantitative deficiency).  In the case of Haemophilia B (Christmas disease) it is Factor IX that is deficient.  These are hereditable disorders and the use of Factor Deficient Plasmas (FDPs) in mixing studies can aid diagnosis by identifying which Factor is not functioning correctly

Platelet Aggregation

Platelet adhesion takes place primarily between platelets, adhesive proteins and injured vessel endothelium.  Platelet aggregation is the result of inter-platelet contacts mediated by fibrinogen, von Willebrand Factor (vWF) and other proteins.  Aggregation takes place after stimulation of platelets by collagen, thrombin or other activating mediators.  Platelet pathologies can also cause clotting disorders such as von Willebrand disease (abnormal function or deficiency of vWF), Bernard-Soulier Syndrome (abnormal glycoprotein Ib-IX-V complex) or gray platelet syndrome (deficient alpha granules).  Platelet aggregometry is a specialised technique which can be used to aid the diagnosis of platelet disorders.  Platelet rich plasma is stimulated in-vitro with activating mediators such as epinephrine or ristocetin co-factor and as the platelets aggregate the change in optical density is used to generate a reaction curve.

Protein C and Protein S

The coagulation cascade is tightly controlled with several feedback mechanisms designed to regulate clotting and prevent thrombosis.   One of the major regulators is Protein C, a vitamin K dependent protease that is activated by thrombin to give activated protein C (APC), which proteolytically degrades active Factor V and Factor VIII.  Protein C deficiency may lead to thrombophilia, an increased tendency towards thrombosis. Quantitative and qualitative Protein C deficiency can be detected using chromogenic or functional assays.  Impaired action of Protein C (APC resistance) can also result from the Factor V Leiden mutation.   Protein S is a cofactor for Protein C and similarlyProtein S deficiencies can lead to increased thrombotic risk.

Serpins – Serine Protease Inhibitors

Antithrombin is a member of the serpin family and also serves to regulate coagulation.  This serine protease inhibitor degrades thrombin and active Factors IX, X and XII.  Inborn or acquired deficiency of antithrombin also leads to thrombophilia.  Other serpin members, Protein C Inhibitor (PCI) and Alpha -1  antitrypsin  (AAT),  inhibit activated Protein C.  Circulating APC-PCI andAPC-AAT complexes can serve as a marker of Protein C activation.

Fibrinolysis

Tissue plasminogen activator (tPA) catalyses the proteolytic cleavage of plasminogen to give the active enzyme plasmin.  Plasmin cleaves the fibrin gel clot and digests the resulting fragments.  One of the small fibrin degradation products is the D-Dimer, typically containing two D and one E domain from the original fibrinogen molecule.  D-Dimers are not normally present in the plasma and therefore diagnostic assays for D-Dimer are used as an indication of coagulation system activation indicating the presence of a clot.

Exogenous regulators

Agents that modulate coagulation have been investigated for therapeutic use. Aprotinin is the bovine version of basic pancreatic trypsin inhibitor (BPTI) which inhibits trypsin and other related enzymes.  Administration of aprotinin was intended to reduce bleeding during complex surgical procedures and thereby reduce the need for blood transfusion and organ damage resulting from hypotension.  Aprotinin slows the process of fibrinolysis.

Conversely, hirudin is an anticoagulant.  Hirudin is a naturally occurring peptide found in the salivary glands of medicinal leeches and a potent and specific inhibitor of thrombin.  Unlike other anticoagulants Hirudin exerts its thrombolytic effect without influencing other serum protein activity.

 

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