Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.7 (plasmin)
9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factor VIII/von Willebrand factor (FVIII/vWF) is a glycoprotein with a molecular weight greater than one-million daltons. Two activities are associated with this large molecule: FVIII procoagulant activity and vWF activity. Incubation of FVIII/vWF with proteolytic enzymes causes rapid inactivation of the FVIII procoagulant activity but has little effect on the vWF activity or antigenicity. In an attempt to gain insight into the structural features required for these two activities, antisera were raised in rabbits to normal, thrombin-inactivated, and plasmin-inactivated FVIII/vWF. All of these proteolytically modified forms of FVIII/vWF cross-reacted with each of the rabbit antisera; each blocked the ability of a human inhibitor to inactivate native active FVIII/vWF. Each of the antisera was a potent inhibitor of vWF activity and inactivated vWF activity at the same titer. The antisera were much less potent inhibitors of FVIII activity than of vWF activity. Antibodies to thrombin-inactivated FVIII/vWF or normal FVIII/vWF had about the same ability to inactivate FVIII procoagulant activity. Surprisingly, those to plasmin-inactivated FVIII/vWF still retained about 50% of this inhibitory capacity. A comparison of the three types of antigens by polyacrylamide gel electrophoresis in sodium dodecyl sulfate-6 M urea demonstrated that the structure of thrombin-inactivated FVIII/vWF was indistinguishable from that of normal FVIII/vWF, while plasmin-inactivated FVII/vWF was completely cleaved to lower molecular weight fragments. Some of the reported variations in the ability of rabbit antibodies to inhibit procoagulant activity may be due to partial degradation of the starting antigen. The retention by FVIII/vWF protein of its immunologic properties even after extensive proteolytic degradation suggests that under nondenaturing conditions, the conformation of the native and degraded molecules are very similar.
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PMID:Immunologic studies of native and modified human factor VIII/von Willebrand factor. 8 37

The intraindividual variability in terms of coagulation analyses was explored in 10-16 samples collected from each of 15 women during one menstrual cycle. For comparison, six men were sampled six times during a period of 30 days. The following variables were analysed: FVII, FVIII, FX, vWF:Ag, vWF:ristocetin cofactor, fibrinogen, antithrombin, plasminogen and anti-plasmin. The results demonstrated mean coefficients of variation ranging between 4.5 (plasminogen) and 20.7 (vWF:Ag). In certain individuals, the intraindividual variability amounted to nearly 40%, in particular in the assays of FVIII and vWF:Ag. No direct relation between these two factors and oestradiol, progesterone or testosterone levels could be observed in our individuals. The implications of these variations are discussed in terms of disease prediction and diagnosis of coagulation disorders.
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PMID:On the intraindividual and gender variability of haemostatic components. 161 87

Urokinase immobilized polymer is highly antithrombotic, which cannot be explained only by fibrinolysis. We immobilized 10 IU/cm2 of urokinase to polyurethane by using maleic anhydride methylvinyl ether copolymer as a carrier. Then we incubated blood in circular tubes made of this material, measured the clotting factors and observed the surface of the tubes after incubation by scanning electronmicroscopy and immunofluorescence microscopy. After 5 min incubation, the relative activities of factors V, VIII, IX, X and XII, fibrinogen, plasminogen and alpha 2 plasmin inhibitor decreased, but the activity of factor VII increased. No platelet adhesion to the surface of the urokinase immobilized polyurethane was observed and there was no significant adsorption of serum proteins, including fibrinogen, fibronectin and vWF antigen, on the surface. Urokinase-immobilized polyurethane catalyzed the digestion of clotting factors as well as fibrinolysis and also inhibited platelet adhesion on its surface probably by inhibiting protein adsorption and its clinical application including vessel prosthesis should be developed further.
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PMID:Antithrombotic mechanisms of urokinase immobilized polyurethane. 202 41

We determined the following coagulo-fibrinolytic activities in 24 patients with systemic lupus erythematosus (SLE) and 20 healthy adults: prothrombin time (PT), activated partial thromboplastin time (A-PTT), factor VIII: coagulant activity), von Willebrand factor antigen (vWF: Ag), antithrombin-III (AT-III), plasminogen (PLG), alpha 2 plasmin inhibitor (alpha 2 PI), alpha 2-plasmin inhibitor-plasmin complex (PIC), protein C (PC: activity and antigen concentration), and protein S (PS: total PS and free PS). PLG, AT-III, PC antigen concentration and total PS were significantly decreased in ten female controls as compared with ten male controls. Therefore, we used the ten healthy females as controls and excluded two male SLE patients in the analysis of the correlations of coagulo-fibrinolytic activities with lupus anticoagulant (LA), clinical and laboratory features in 22 female patients with SLE. In the SLE patients, PT was significantly shortened, while A-PTT was prolonged. PLG, PC activity and antigen, and total PS were significantly increased, and free PS levels were decreased in SLE. The shortened PT and decreased free PS suggest hypercoagulable states in SLE patients. A significant prolongation of A-PTT and a decrease of F VIII activity were observed in the six LA-positive SLE patients, and the results were considered as known effects of LA. Furthermore, vWF: Ag, AT-III and PC antigen levels were significantly increased in the LA-positive patients as compared with LA-negative patients. These changes indicate both vascular endothelial cell damages and a compensatory increase in coagulation inhibitors in the LA-positive patients.
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PMID:[Regulation of coagulo-fibrinolytic activity and lupus anticoagulants in systemic lupus erythematosus]. 212 31

Plasma levels of thrombin-antithrombin III complex (TAT), plasmin-alpha 2-plasmin inhibitor complex (PAP), von Willebrand factor antigen (vWF:Ag) plasminogen activator antigen (PA) and plasminogen activator inhibitor-1 antigen (PAI-1), were determined in 110 patients with arterial thromboembolic diseases within 4 weeks after attack (Th; 41 cases with myocardial infarction and 69 with cerebral infarction), 67 patients with various types of carcinoma (Ca; 31 cases without metastasis and 36 with metastasis) and 50 age-matched healthy individuals (Co). The following results were obtained: 1) Mean plasma levels of TAT, PAP, vWF:Ag, PA and PAI-1 were significantly higher in Th than Co. 2) Mean plasma levels of TAT, PA and PAI-1 were significantly higher in Ca than Co regardless of metastasis but those of PAP and vWF:Ag were significantly higher only in Ca with metastasis than Co. 3) Significant relationship was observed between plasma levels of TAT and PAP both in Th and Ca. 4) Significant relationship was also observed between plasma levels of TAT and vWF:Ag, PA or PAI-1 in Th, but not in Ca. It is suggested from these results that the coagulopathies observed in these patients result from the activation of intravascular blood coagulation and fibrinolysis, and that vascular endothelial cell damage may play an important role in the activation in Th.
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PMID:Studies on the pathogenesis of coagulopathy in patients with arterial thromboembolism and malignancy. 214 28

Alteration of the coagulation-fibrinolysis system was examined in patients on maintenance hemodialysis. The mean values of fibrinogen, factor V, factor VII, factor VIII, vWF (activity and antigen), factor IX and factor XI were significantly higher in these patients than in control subjects (p less than 0.01), but factor XII alone was significantly lower. Fibrinolytic parameters (euglobulin lysis time, fibrin plate lysis, fibrin degradation products and alpha 2-plasmin inhibitor-plasmin complex) suggested a hyperfibrinolytic state and plasmin generation in the patients' circulation. These findings suggest that the alteration of the coagulation-fibrinolysis system is aggravated by repeated hemodialysis, either by the influence of the dialyzer itself or heparin.
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PMID:Coagulation and fibrinolysis in patients with chronic renal failure on maintenance hemodialysis. 274 46

Bovine von Willebrand factor was digested with human plasmin in order to isolate and characterize a fragment that can bind to human platelets. A terminal plasmin digest of bovine von Willebrand factor is composed of five fragments, ranging in relative molecular weight (Mr) from 250,000 to 35,000. The major fragment has a Mr of 250,000 and consists of four disulfide-linked polypeptide chains with Mr from 69,000 to 35,000. The Mr 69,000 and 49,000 polypeptides possess carbohydrate moieties, as indicated by their reaction with periodate-Schiff reagent. Gel filtration studies suggest that, at physiological ionic strength, four of the Mr 250,000 fragments associate into a limited noncovalent oligomer. Monoclonal antibodies were prepared against native von Willebrand factor and used to characterize the distribution of epitopes on native vWF and the Mr 250,000 major fragment. Two of the monoclonal antibodies that recognize the major fragment (2 and H-9) inhibit platelet agglutination. The Mr 250,000 fragment binds to human platelets, and the binding is inhibited by monoclonal antibodies 2 and H-9. The Mr 250,000 fragment does not agglutinate platelets, consistent with a requirement for high molecular weight oligomers of von Willebrand factor for platelet agglutination. The Mr 250,000 fragment can compete with intact, bovine von Willebrand factor for binding to human platelets. However, its affinity is one-tenth that of intact von Willebrand factor.
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PMID:Characterization of a fragment of bovine von Willebrand factor that binds to platelets. 302 6

Thrombus formation is recognized pathologically in the affected arteries and is supposed to play a major role in the pathogenesis of Takayasu's arteritis; however, hemostatic conditions in this disorder have not been elucidated fully. We determined plasma levels of molecular markers for platelet activity (platelet factor 4; PF4, beta-thromboglobulin; beta TG), thrombotic status (thrombin-antithrombin III complex; TAT, fibrinopeptide A; FPA), fibrinolytic status (plasmin-alpha 2-plasmin inhibitor complex; PIC, D-dimer), and endothelial injury (von Willebrand factor antigen; vWF:Ag, thrombomodulin; TM) in 30 patients with Takayasu's arteritis and 20 age-matched control subjects. Plasma levels of PF4, beta TG, TAT, FPA and D-dimer, but not PIC, in patients with Takayasu's arteritis were substantially higher than those in normal control subjects. The levels of these markers were not different between the active and inactive stages of the disease. Plasma levels of vWF:Ag in patients with Takayasu's arteritis did not differ significantly from those in normal subjects, and plasma levels of TM were significantly lower than those in normal subjects. In patients with Takayasu's arteritis, platelet and coagulation activities are significantly increased, leading to hypercoagulable state and thrombus formation, although there is little, if any, endothelial damage.
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PMID:Hypercoagulable state in patients with Takayasu's arteritis. 872 10

Hemostasis is the system of generation and destruction of thrombi. It consists of coagulation and thrombolysis and has a plasmatic part and a cellular one, the latter being the thrombocytes and endothelial cells for coagulation and the polymorphonuclear granulocytes (PMN) for thrombolysis. Main products of PMN are oxidants of the hypochlorite/chloramine-type that can generate the nonradical excited oxidant singlet molecular oxygen ((1)DeltaO(2)(*)). Physiologically, (1)DeltaO(2)(*) reacts with methionine and cysteine residues and with carbenic structures in lipids, generating dioxetanes, which upon disruption emit photons in the blue spectrum of light (380-450 nm). It modifies some important hemostasis components in blood: (1)DeltaO(2)(*) inactivates the factors I (fibrinogen), V, VIII, vWF, X, plasminogen activator inhibitor-1 (PAI-1), and alpha2-antiplasmin. (1)DeltaO(2)(*) oxidation of plasminogen and fibrin facilitates their specific cleavage by plasminogen activators and plasmin. Furthermore,(1)DeltaO(2)(*)downregulates thrombocyte-function and upregulates PMN-function. Chloramines seem to be the main physiologic generators of (1)DeltaO(2)(*): in concentrations of 0.1-2 mM in blood they strongly inhibit coagulation and enhance thrombolysis. The biogenesis and reaction pattern of (1)DeltaO(2)(*) is of importance to understand the PMN-physiology in hemostasis, giving rise to new therapy forms of thromboatherothrombosis in man.
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PMID:Regulation of hemostasis by singlet-oxygen (1DeltaO2*). 1532 Aug 15

Systemic thromboembolism is a major complication of mitral stenosis (MS), especially in those patients having atrial fibrillation (AF). Recent evidence has suggested that regional left atrial coagulation activity may be increased in MS and may contribute to the pathophysiology of left atrial thrombus. However, the relation of left atrial coagulation activity to factors that predispose to left atrial thrombus formation is unknown. Also, the relations between left atrial and systemic coagulation activity, fibrinolysis, and platelet activation remain unresolved. Left atrial and peripheral venous levels of fibrinogen, antithrombin III, factor VII and factor VIII for coagulation, D-dimer, tPA and PAI-I, plasmin and antiplasmin for fibrinolysis, and platelet factor 4 and vWF for platelet activation, and endothelial dysfunction were measured in 46 patients with MS and normal clotting times who were undergoing percutaneous mitral valvuloplasty. Left atrial tPA, plasmin, PAI-I, antiplasmin, PF4, and vWF levels exceeded the corresponding peripheral venous levels (P < 0.05) in patients with MS, being more significant in the AF subgroup. There were no significant differences between left atrial and peripheral venous levels of fibrinogen, D-dimer, factor VII, and factor VIII within the patient group (P > 0.05). The results suggest that there are significant variations in the indices of coagulation, fibrinolytic system and platelet activation, and endothelial dysfunction between left atrial and peripheral venous blood samples of patients with MS that may be due to limited spillover from the left atrium to the systemic circulation.
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PMID:Regional left atrial coagulation and fibrinolytic activities in patients with mitral stenosis. 1555 19


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