Determination of Plasma Protein S - The Protein Cofactor of Activated Protein C

Bertina, Rogier M.; Wijngaarden, A van; Reinalda-Poot, J; Poort, S R; Bom, Vjj

doi:10.1055/s-0038-1661291

Cited by 154 publications

(100 citation statements)

References 1 publication

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“…Using a chromogenic functional assay, the concentration of protein C in rabbit plasma was estimated to be -80% (mean of 10 observations) of that of protein C in human plasma (3)(4)(5) ug/ml). The concentration of protein S in rabbit plasma was estimated from the ability of human C4BP to dose-dependently inhibit the APC cofactor function in rabbit plasma.…”

Section: Resultsmentioning

confidence: 99%

“…This process is potentiated by the vitamin K-dependent protein S. In human plasma, protein S forms a complex with C4b-binding protein (C4BP), which is a regulator of the classical complement pathway (reviewed in 1, 2). Only free protein S acts as a cofactor to APC, whereas the complexed form, which accounts for -60% of total protein S in human plasma, has no anticoagulant cofactor activity (3)(4)(5). Rabbit plasma only contains free protein S, which, however, is readily complexed with human C4BP (6,7).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Protein S as an in vivo cofactor to activated protein C in prevention of microarterial thrombosis in rabbits.

Arnljots¹,

Dahlbäck²

1995

J. Clin. Invest.

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The antithrombotic effects of bovine activated protein C (APC) and protein S were investigated in a rabbit model of microarterial thrombosis. Because of the species specificity of the APC-protein S interaction, bovine APC expresses potent anticoagulant activity in rabbit plasma only when bovine protein S is also present. This provided a way to assess the contribution of bovine protein S to the antithrombotic effect of bovine APC. Rabbits were infused with boluses of activated protein C (0.1, 0.2, 0.4, or 0.8 mg/kg), protein S (0.5 mg/kg), or activated protein C (0.1 or 0.01 mg/kg) plus protein S (0.5 mg/kg). APC alone produced a dose-dependent antithrombotic effect, but only the group receiving the highest dose differed signiflcantly from controls. While a low dose of activated protein C (0.1 mg/kg) alone had no antithrombotic effect, together with protein S (0.5 mg/kg) it produced a potent response. The presented results demonstrate the in vivo significance of protein S as a cofactor to activated protein C. The data show that a potent antithrombotic effect, without hemorrhagic side effects or significant systemic anticoagulation, may be achieved by low doses of activated protein C when combined with protein S. (J.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protein S as an in vivo cofactor to activated protein C in prevention of microarterial thrombosis in rabbits.

Arnljots¹,

Dahlbäck²

1995

J. Clin. Invest.

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“…The criteria of Bertina et al were utilized to establish a laboratory diagnosis of a protein C (20) or protein S deficiency state (21).…”

Section: Methodsmentioning

confidence: 99%

“…The plasma concentrations of protein C, prothrombin, antithrombin, F1+2, and PCP were determined by double antibody RIA as described in earlier reports from our laboratory (13,14,19). Ahtigenic levels of total protein S wete measured with an immunoradiometric assay technique (21). The plasma levels of FPA were established by RIA utilizing a kit provided by Mallinckrodt, Inc.…”

Section: Methodsmentioning

confidence: 99%

Suppression of hemostatic system activation by oral anticoagulants in the blood of patients with thrombotic diatheses.

Conway¹,

Bauer²,

Barzegar³

et al. 1987

J. Clin. Invest.

118

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RIAs for hemostatic system activation were employed to study patients who were anticoagulated with warfarin. The mean prothrombin fragment F1+2 concentration in stably anticoagulated individuals without an inherited thrombotic diathesis (mean prothrombin time [PI] ratio WPT of patient/PT of normal plasma pool] = 1.74) was 0.231 nM as compared with a mean plasma F1+2 level of 1.68 nM for a nonanticoagulated control group (P < 0.0001). The initiation of oral anticoagulants in two subjects who did not exhibit protein C deficiency led to a paradoxical increase in Fl+2 levels during the first day of therapy. We have also shown that a relatively low intensity regimen of warfarin (PT ratio < 1.2) may reduce elevated concentrations of F1+2 into the normal range in patients with a history of recurrent thromboembolism. The mean F1+2 level in antithrombin-deficient individuals on warfarin was significantly elevated (mean = 0.714 nM) as compared with that in anticoagulated subjects with protein C deficiency (mean = 0.205 nM) or in those without an inherited thrombotic disorder (P < 0.01) at equivalent levels of intensity of oral anticoagulation. We therefore conclude that the effect of warfarin on hemostatic system activation is modulated by the endogenous heparan sulfate-antithrombin mechanism.

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“…HC II antigen levels were determined using the Laurell method [7]. Protein C and protein S activities were determined according to the method of Francies and Patch [8] and Bertina et al [9], respectively.…”

Section: Assaysmentioning

confidence: 99%

Recurrent leg ulcers and arterial thrombosis in a 33‐year‐old homozygous variant of antithrombin

Shimizu

Toriyama²,

Ogawa

et al. 2001

American J Hematol

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Determination of Plasma Protein S - The Protein Cofactor of Activated Protein C

Cited by 154 publications

References 1 publication

Protein S as an in vivo cofactor to activated protein C in prevention of microarterial thrombosis in rabbits.

Protein S as an in vivo cofactor to activated protein C in prevention of microarterial thrombosis in rabbits.

Suppression of hemostatic system activation by oral anticoagulants in the blood of patients with thrombotic diatheses.

Recurrent leg ulcers and arterial thrombosis in a 33‐year‐old homozygous variant of antithrombin

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