Neutralization of Autoprothrombin C Activity With Antithrombin

Seegers, Walter H.; Cole, Edmond R.; Harmison, Charles R.; Monkhouse, Frank C.

doi:10.1139/o64-043

Cited by 65 publications

(21 citation statements)

References 10 publications

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“…Both the esterolytic and coagulant activities of X, are slowly inhibited by soya bean trypsin inhibitor (70) and by plasma antithrombin (243). X, is rapidly inactivated by 2,3-dimercaptopropan-1-01 (39,128), and by DFP in the cold at 4 : l molar ratio of inhibitor to protein, inactivation being complete in 1 hr, as judged by the rate of hydrolysis of carbobenzoxy phenylalanine nitrophenol ester (128).…”

Section: Factor X and Activated Factor X (X)mentioning

confidence: 99%

Enzymology and the Blood Clotting Mechanism

Esnouf¹,

Macfarlane²

1968

Advances in Enzymology - And Related Areas of Molecular Biology

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Section: Factor X and Activated Factor X (X)mentioning

confidence: 99%

Enzymology and the Blood Clotting Mechanism

Esnouf¹,

Macfarlane²

1968

Advances in Enzymology - And Related Areas of Molecular Biology

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“…Autoprothrombin I I I is the precursor of autoprothrombin C and is not altered by antithrombin. With autoprothrombin I we found (14) that the activity disappears rapidly when placed in plasma or serum, or in solution with the antithrombin preparation of JIonkhouse and AIilojevic (15).…”

Section: Introductionmentioning

confidence: 93%

Inactivation of Purified Autoprothrombin I With Antithrombin

Wh¹,

Schroeer²,

Kagami³

1964

Can. J. Biochem.

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Autoprothrombin I, was obtained by activating prothrombin preparations with autoprothrombin C. Autoprothrombin I, was obtained by activating prothrombin with the use of calcium ions and purified platelet factor 3. Both of these prothrombin derivatives were found to be inactivated by plasma and serum. Autoprothrombin I, was studied most extensively and was found to be inactivated by purified antithrombin. When antithrombin was first combined to capacity with purified thrombin the power to neutralize autoprothrombin I was almost eliminated. Autoprothrombin I1 was not destroyed by antithrombin and was found in serum as the main procoagulant. Most likely it is not in plasma.Autoprothrombin I,, autoprothrombin I,, autoprothrombi11 C, and thrombin all have reactive groups that combine with antithrombin. The activity in 1 n~g of purified autoprothrombin I, was neutralized by 50 ml plasma. One milligram of autoprothrombin C was neutralized by 5 ml plasma, and 7 ml plasma was sufficient to neutralize 1 mg of thrombin. Antithrombin IV is regarded as a kinetic effect and not as a substance. From a review of the literature it is concluded that there is no adequate evidence for appreciable quantities of factor VII in serum, or that it occurs in plasma independent of prothrombin.

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“…Several investigators have demonstrated the capacity of antithrombin to inhibit activated Factor X [3,50]. Rosenberg et al have examined the serine proteases of the intrinsic coagulation pathway in regard to their capacity to be antagonized by antithrombin and heparin [4,46].…”

Section: Intrinsic Coagulation Pathwaymentioning

confidence: 99%

Plasma Inhibitors of The Hageman Factor Dependent Pathways

Schreiber¹

2008

Semin Thromb Hemost

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Activation of Hageman factor is initiated by negatively charged surfaces which may be provided by several biologic substances [20,28,35,53]. Activation of Hageman factor results in the initiation of three plasma protein systems: the kinin generation system [30,52], the fibrinolytic sequence [21,36], and the intrinsic pathway of coagulation [41]. Bradykinin generation results from the action of activated Hageman factor or its fragments on prekallikrein, generating kallikrein [23] which cleaves the active peptide bradykinin from kininogen, an alpha-glycoprotein. Bradykinin both enhances vascular permeability and produces peripheral vasodilation and, therefore, is important in the inflammatory response. Similarly, Hageman factor or its fragments activate the fibrinolytic sequence by converting the plasminogen proactivator to the plasminogen activator [24,26]. This active molecule then converts plasminogen to plasmin, the active fibrinolytic enzyme in man. The third plasma protein system initiated by the activation of Hageman factor is the intrinsic pathway of coagulation. Activated Hageman factor converts pre-plasma thromboplastin antecedent (pre-PTA) to its active form PTA (the 11th clotting factor) [41], which then activates factor IX in the coagulation sequence. Thus, the contribution of Hageman factor activation to tissue injury is not merely limited to the initiation of coagulation by activation of factor XI, but includes activation of prekallikrein to achieve bradykinin generation and activation of plasminogen proactivator in order to form plasmin. In addition, two enzymes activated in these sequences, kallikrein and plasminogen activator, also function in neutrophil chemotaxis [25,27]. Subsequent interactions may also generate biologically active products from the complement system, as well, primarily via the action of plasmin on C1, the first component of complement [42], and on C3, the third component of complement [33]. Thus, the activation of Hageman factor by immunologic or nonimmunologic events introduces coagulation and fibrinolysis, augments leukocyte chemotaxis and results in enhanced vascular permeability. Therefore, regulation and control of these biologically active products resulting from Hageman factor activation are critical to modulating the effects of tissue injury. In this section we will discuss the circulating plasma factors which appear operative in regulating the biologic activity of these pathways. We will discuss each of the Hageman factor dependent systems in sequence.

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Neutralization of Autoprothrombin C Activity With Antithrombin

Cited by 65 publications

References 10 publications

Enzymology and the Blood Clotting Mechanism

Enzymology and the Blood Clotting Mechanism

Inactivation of Purified Autoprothrombin I With Antithrombin

Plasma Inhibitors of The Hageman Factor Dependent Pathways

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