Two ELISA's for measurement of protein S, and their use in the laboratory diagnosis of protein S deficiency

Deutz-Terlouw, P P; Ballering, Leo; Wijngaarden, A van; Bertina, Rogier M.

doi:10.1016/0009-8981(90)90318-m

Cited by 44 publications

(24 citation statements)

References 13 publications

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“…The laboratory methods used and the interpretation of results for all kits were as specified in the manufacturer's instructions. Levels of proteins C, S, and antithrombin III were measured by ELISA as described elsewhere [17][18][19], in each case with use of the appropriate rabbit antihuman antibody (Dako).…”

Section: Laboratory Methodsmentioning

confidence: 99%

Coagulation Abnormalities in Dengue Hemorrhagic Fever: Serial Investigations in 167 Vietnamese Children with Dengue Shock Syndrome

Wills¹,

Oragui²,

Stephens³

et al. 2002

CLIN INFECT DIS

223

185

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The pathophysiological basis of hemorrhage in dengue infections remains poorly understood, despite the increasing global importance of these infections. A large prospective study of 167 Vietnamese children with dengue shock syndrome documented only minor prolongations of prothrombin and partial thromboplastin times but moderate to severe depression of plasma fibrinogen concentrations. A detailed study of 48 children revealed low plasma concentrations of the anticoagulant proteins C, S, and antithrombin III, which decreased with increasing severity of shock, probably because of capillary leakage. Concurrent increases in the levels of thrombomodulin, tissue factor, and plasminogen activator inhibitor type 1 (PAI-1) indicated increased production of these proteins. Thrombomodulin levels suggestive of endothelial activation correlated with increasing shock severity, whereas PAI-1 levels correlated with bleeding severity. Dengue virus can directly activate plasminogen in vitro. Rather than causing true disseminated intravascular coagulation, dengue infection may activate fibrinolysis primarily, degrading fibrinogen directly and prompting secondary activation of procoagulant homeostatic mechanisms.

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Section: Laboratory Methodsmentioning

confidence: 99%

Coagulation Abnormalities in Dengue Hemorrhagic Fever: Serial Investigations in 167 Vietnamese Children with Dengue Shock Syndrome

Wills¹,

Oragui²,

Stephens³

et al. 2002

CLIN INFECT DIS

223

185

View full text Add to dashboard Cite

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“…PS Measurements-Total PS antigen levels in culture media were determined by ELISA as described previously (37), with the following modifications. ELISA plates were coated with goat anti-human PS IgG (Kordia, Leiden, The Netherlands) overnight at 4°C.…”

Section: Methodsmentioning

confidence: 99%

The Constitutive Expression of Anticoagulant Protein S Is Regulated through Multiple Binding Sites for Sp1 and Sp3 Transcription Factors in the Protein S Gene Promoter

Wolf

Cupers

Bertina

et al. 2006

Journal of Biological Chemistry

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Protein S (PS) is a vitamin K-dependent plasma protein that inhibits blood coagulation by serving as a nonenzymatic cofactor for activated protein C in the protein C anticoagulant pathway. Low PS levels are a risk factor for the development of deep venous thrombosis. The regulation of PS levels through transcriptional regulation of the PS gene was investigated in this report. A minimal PS gene promoter 370 bp upstream from the translational initiation codon was sufficient for maximal promoter activity in transient transfections regardless of the cell type. A pivotal role for Sp1 in the constitutive expression of the PS gene was demonstrated through electrophoretic mobility shift assay experiments, transient expression of mutant PS promoter-reporter gene constructs, and chromatin immunoprecipitations in HepG2 cells. At least four Sp-binding sites were identified. The two sites most proximal to the translational start codon were found to be indispensable for PS promoter activity, whereas mutation of the two most distal Sp-binding sites had a negligible influence on basal promoter activity. In addition, all other major promoter-binding proteins that were found by electrophoretic mobility shift assay could be positively identified in supershift assays. We identified binding sites for the hepatocyte-specific forkhead transcription factor FOXA2, nuclear factor Y, and the cAMP-response element-binding protein/activating transcription factor family of transcription factors. Their relevance was investigated using site-directed mutagenesis.The coagulation cascade is a complex system in which the consecutive activation of multiple coagulation factors leads to the production of thrombin and ultimately to the formation of fibrin polymers, the primary component of blood clots (for a recent review see Ref. 1). Protein S (PS)2 is a vitamin K-dependent plasma protein that functions as a nonenzymatic cofactor for activated protein C in the down-regulation of the coagulation cascade via proteolytic inactivation of coagulant factors Va and VIIIa (2-5). PS has also been shown to display activated protein C-independent anticoagulant activity in purified systems as well as in plasma (6 -8). Recent studies indicate that PS may have a second function unrelated to coagulation in the clearance of apoptotic cells (9, 10).Over the past two decades low PS plasma levels have become a well established risk factor for the development of deep venous thrombosis (11-13). However, not all mechanisms underlying low plasma PS levels have been fully characterized. Hereditary PS deficiency has been shown to be an autosomal dominant trait, and many causative genetic mutations have been described in the PS gene (14,15). On the other hand, PS deficiency can also be acquired throughout life by conditions such as oral contraceptive use and liver disease (16). To better understand the different functions of PS and the possible causes of PS deficiency, more information is needed on the regulation of the PS gene, mRNA, and protein.The major source of circulati...

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“…Standard laboratory procedures were used for the following tests: activated protein C ratio, protein C activity, von Willebrand factor, lupus anticoagulant (Behring Coagulation System, Dade Behring Inc), factor VIII, antithrombin III (STA, Diagnostica Stago), and protein S with the use of an enzymelinked immunosorbent assay. 7 The factor V Leiden mutation was determined only if the activated protein C ratio was abnormal. 8 Factor II mutation was determined according to a technique as previously described.…”

Section: Methodsmentioning

confidence: 99%

Spinal Dural Arteriovenous Fistulas Are Not Associated With Prothrombotic Factors

Jellema

Tijssen

Fijnheer

et al. 2004

Stroke

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Background and Purpose-The cause of spinal dural arteriovenous fistulas (SDAVF) is unknown. In intracranial dural arteriovenous fistulas, an association with factor V Leiden mutation has been found. Therefore, we studied the association between prothrombotic factors and SDAVF. Methods-Factor V Leiden mutation, factor II mutation, protein S, protein C, factor VIII, von Willebrand factor, antithrombin III, and lupus anticoagulant were determined by means of standard laboratory tests in 40 patients and 119 control subjects matched for sex and age. Results-Factor V Leiden mutation was not found in the patient group and was found twice in the control group. Factor II mutation was found in 1 patient and in none of the control subjects. There was no decreased activity of protein S, protein C, factor VIII, von Willebrand factor, or antithrombin III in patients in comparison with controls. Lupus anticoagulant was not found in the patient group and once in the control subjects. Conclusions-We conclude that it is unlikely that prothrombotic factors are involved in the pathogenesis of spinal dural arteriovenous fistulas, but subtle associations are not ruled out. Key Words: arteriovenous fistula Ⅲ spinal cord Ⅲ thrombophilia T he cause of spinal dural arteriovenous fistulas (SDAVF) is unknown. Infection 1 and trauma 2 are among the factors that have been proposed as possible factors in the course of events leading to this condition. In intracranial dural arteriovenous fistulas, an association with factor V Leiden mutation has been found, 3,4 whereas venous (sinus) thrombosis has also been implicated in the pathogenesis of that condition. 5 Because of the similarities between cerebral and spinal fistulas, thrombophilia might also operate in patients with SDAVF. Therefore, we investigated the association between prothrombotic factors and SDAVF. Patients and MethodsBetween 1990 and 2002, 68 patients had SDAVF diagnosed and treated in the 4 hospitals mentioned in this article. Of these 68 patients, 12 had died (5 from cardiovascular disease, 2 from cancer, 2 from pneumonia, and 3 from unknown causes). Of the 56 survivors, 3 patients could not be traced, 4 patients did not respond, and 7 refused to participate in the study. In 2 patients no blood could be drawn. In 1 patient who died of an unknown cause, the medical history revealed pulmonary embolism; the medical history did not contain information about presence or absence of prothrombotic factors. The patient characteristics of the 28 patients who did not participate in this study did not differ from those of the 40 patients who participated.The 40 patients were included in the current study between May and July 2002. The diagnosis of SDAVF was confirmed by angiography in all patients. From the medical records, we collected information on medical history, clinical features, time to diagnosis, and level of fistula. The clinical features of these patients have been described in more detail in a previous article. 6 The patients had been treated in the Elisabeth Hospital Tilburg ...

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Two ELISA's for measurement of protein S, and their use in the laboratory diagnosis of protein S deficiency

Cited by 44 publications

References 13 publications

Coagulation Abnormalities in Dengue Hemorrhagic Fever: Serial Investigations in 167 Vietnamese Children with Dengue Shock Syndrome

Coagulation Abnormalities in Dengue Hemorrhagic Fever: Serial Investigations in 167 Vietnamese Children with Dengue Shock Syndrome

The Constitutive Expression of Anticoagulant Protein S Is Regulated through Multiple Binding Sites for Sp1 and Sp3 Transcription Factors in the Protein S Gene Promoter

Spinal Dural Arteriovenous Fistulas Are Not Associated With Prothrombotic Factors

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