Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A DEAE-Sephadex column chromatography step utilized to purify human Factor VII consistently yields a protein peak between the factor VII activity peak and prothrombin, factor X and factor IX activity peak (S.P. Bajaj, S.I. Rapaport, and S.F. Brown: J. Biol. Chem. 251, 253-259, 1981). We now report that this protein peak contains protein C and protein S. Preparative disc polyacrylamide gel electrophoresis of the proteins in this peak permitted a complete separation of protein C from protein S. Protein C at this step usually contained approximately 5-10% of Factor X, which could be removed by a goat anti-human Factor X antibody column. For a typical preparation, starting with 10L of plasma, the yield of Protein C was 5 mg and of protein S was 4 mg. Both proteins revealed apparent homogeneity in sodium dodecyl sulfate gel electrophoretic system. beta-Protein C and beta-protein S were not observed in our preparations starting with plasma collected directly into citrate anticoagulant containing benzamidine and soybean trypsin inhibitor, suggesting that these beta forms of protein C and protein S, isolated by other investigators, are slightly degraded forms of the native proteins. Antisera generated to these proteins were monospecific and could be used to monitor column fractions during purification. When examined by immunoelectrophoresis, the electrophoretic mobility of protein S in plasma was slower than that of isolated protein S. When exposed to plasmin, protein C was activated slightly and then rapidly degraded.
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PMID:A procedure for isolation of human protein C and protein S as by-products of the purification of factors VII, IX, X and prothrombin. 622 44

A 42-yr-old woman with systemic lupus erythematosus without bleeding diathesis developed a prolonged activated partial thromboplastin time that was not corrected by normal plasma. An inhibitor that acted rapidly and inactivated 0.5 U/ml plasma thromboplastin antecedent (PTA, factor XI) at a 1:200 plasma dilution was demonstrated. In addition to a low titer of PTA (less than 0.01 U/ml), plasma assayed at 20-fold dilution also showed low titers of Hageman (factor XII, 0.02 U/ml), Fletcher (plasma prekallikrein, 0.02 U/ml), and Fitzgerald (high molecular weight kininogen, less than 0.01 U/ml) factors. The titer of these factors, except PTA, returned to normal upon further plasma dilution or upon removal of the inhibitor by protein A adsorption. Thus, the inhibitor appeared to interfere with these clotting factor assays, possibly by inactivating PTA in the substrate plasmas in the test system. Its specificity was further confirmed. The inhibitor did not interfere with surface-induced proteolytic cleavage of Hageman factor. Surface-induced generation of plasma kallikrein activity (amidolysis of H-D-pro-phe-arg-pNa and cold-promoted factor VII activity enhancement) requires only Hageman, Fletcher, and Fitzgerald factors and was normal. Reactions requiring all 4 contact phase factors, including PTA, such as surface-induced generation of plasmin activity (amidolysis of H-D-val-leu-lys-pNa) and activated Christmas factor (factor IXa) activity, were defective. Furthermore, the inhibitor bound to agarose-protein A inactivated and removed PTA selectively from normal plasma. The inhibitor was an IgG-lambda autoantibody that precipitated PTA. The inactivated activated PTA (factor XIa) without the requirement for an additional cofactor. Furthermore, it inhibited surface-induced activation of PTA by interfering with its proteolytic cleavage upon glass surface exposure and with its binding onto the reactive surfaces.
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PMID:A unique precipitating autoantibody against plasma thromboplastin antecedent associated with multiple apparent plasma clotting factor deficiencies in a patient with systemic lupus erythematosus. 642 50

Experiments on animals in vitro showed that phosphatidylserine-containing anticoagulant (PhCA) inhibited factors X and VIII, restricted factor V activity and, to a less degree, that of factor VII, decreased the activity of fibrin-stabilizing factor, the degree of clot retraction and its tolerance to fibrinolysin. The activity of factor IX remained virtually unchanged under the influence of PhCA, whereas the contact phase was speeded up by 14%. Anticoagulant activity of PhCA was accounted for by the phosphatidyl molecule residue - glycerylphosphorylserine.
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PMID:[Mechanism of the hypocoagulemic effect and the active principle of a phosphatidylserine-containing anticoagulant]. 728

We investigated the relationship between fasting insulin level and various hemostatic factors, including fibrinolytic factors (active plasminogen activator inhibitor-1 (PAI-1), tissue type plasminogen activator (tPA)-PAI-1 complex, plasmin-alpha 2-plasmin inhibitor (PIC), and D-dimer), coagulation factors (activated factor VII, factor VII coagulant activity and antigen, factor VIII, factor X, and fibrinogen), coagulation inhibitors (antithrombin III, heparin cofactor II, and protein C), and an acute phase marker (sialic acid) in 102 healthy individuals aged > or = 75 years (46 men and 56 women). Active PAI-1 levels had a significant negative correlation with PIC levels (r = -0.342, P = 0.0006), indicating that PAI-1 influences in vivo fibrinolytic activity in the very elderly. Gender differences were found in the relationship between insulin and hemostatic abnormalities, with the insulin level being positively correlated with coagulation factors in men (factor VIII activity: r = 0.422, P < 0.01; factor VII activity: r = 0.386, P < 0.01) and with hypofibrinolysis in women (active PAI-1: r = 0.549, P < 0.0001). Insulin levels were positively correlated with the levels of factor VII antigen and factor VII activity in men (P < 0.01), but there was no correlation with activated factor VII levels. The fasting insulin level was also correlated with the levels of heparin cofactor II and sialic acid in men (P < 0.05). However, other hemostatic factors were not related to the insulin level in either sex.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gender differences of disturbed hemostasis related to fasting insulin level in healthy very elderly Japanese aged > or = 75 years. 757 76

With advancing age, an increasing number of healthy individuals have laboratory signs of heightened coagulation enzyme activity. Such biochemical hypercoagulability might be the basis of either the increased thrombotic tendency occurring with age or a harmless manifestation of this process. To see whether these alterations are also present in the very elderly who had aged successfully, 25 healthy centenarians were studied and results of coagulation and fibrinolysis measurements were compared with those obtained in two control groups of healthy adults, 25 ranging in age from 18 to 50 years and 25 from 51 to 69 years. Older controls had, in general, slightly higher values of several coagulation and fibrinolysis measurements than younger controls. Centenarians had striking signs of heightened coagulation enzyme activity, as assessed directly by measuring activated factor VII in plasma (P < .01, compared with either control group) or indirectly by measuring the plasma levels of the activation peptides of prothrombin, factor IX, factor X, and thrombin-antithrombin complexes (all P < .001). Heightened coagulation enzyme activity was accompanied by signs of enhanced formation of fibrin (high fibrinopeptide A, P < .001) and secondary hyperfibrinolysis (high D-dimer and plasmin-antiplasmin complex, P < .001). Plasma concentrations of fibrinogen and factor VIII were higher than in controls, whereas other coagulation factors were not elevated. In conclusion, this study shows the very elderly do not escape the state of hypercoagulability associated with aging, but that this phenomenon is compatible with health and longevity. Hence, high plasma levels of the coagulation activation markers in older populations do not necessarily mirror a high risk of arterial or venous thrombosis.
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PMID:Hypercoagulability in centenarians: the paradox of successful aging. 775 46

Remnants produced on the lipolysis of triglyceride-rich lipoproteins provide a contact surface that activates the contact system of coagulation and therefrom factor VII. New evidence is reviewed suggesting that increased levels of circulating activated factor VII (VIIa) initiates coagulation and produces thrombin at higher rate at the site of an atheromatous lesion or at an injury site. This may have profound significance for the propagation of thrombus and for the thrombin-induced inflammatory and proliferative responses. Vascular homeostasis is achieved by the regulated interaction of the coagulation and fibrinolytic systems. An imbalance in this equilibrium may lead to an increased risk of thrombosis or a bleeding diathesis. The role of PAI-1, a potent inhibitor of enzymes that generate plasmin, in the regulation of fibrinolytic activity, is discussed and the evidence linking the expression of its activity to hypertriglyceridaemia is reviewed. Moreover, the association between lipoprotein (a) and coronary heart disease is attributed to its interference in the normal activation of plasminogen to plasmin.
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PMID:Lipid-thrombosis interface. 780 33

The effect of two different regimens of hormone replacement therapy on coagulation and fibrinolysis was measured in 30 women taking Tibolone (Livial) and 30 taking oestradiol valerate, sequentially combined with cyproterone acetate (Climen). Blood samples were taken before the beginning of the medication, then six and twelve months afterwards. The Livial group showed a rise of fibrinolytic activity as measured by the alpha 2-antiplasmin-plasmin complexes. Tissue plasminogen activator antigen and plasminogen activator inhibitor-1 decreased simultaneously. No effect was seen in the coagulation variables. In the Climen group no significant alterations were noticed, either in the coagulation or in the fibrinolysis variables. In the direct comparison of both substances only factor VII appeared to be significantly higher in the Climen group after six months and one year of treatment.
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PMID:The effect of two regimens of hormone replacement therapy on the haemostatic profile in postmenopausal women. 791 43

Virally inactivated, high-purity factor XI concentrates are available for treatment of patients with factor XI deficiency. However, preliminary experience indicates that some preparations may be thrombogenic. We evaluated whether a highly purified concentrate produced signs of activation of the coagulation cascade in two patients with severe factor XI deficiency infused before and after surgery. Signs of heightened enzymatic activity of the common pathway of coagulation (elevated plasma levels of prothrombin fragment 1 + 2 and fibrinopeptide A) developed in the early post-infusion period, accompanied by more delayed signs of fibrin formation with secondary hyperfibrinolysis (elevated D-dimer and plasmin-antiplasmin complex). These changes occurred in both patients, but were more severe in the older patient with breast cancer when she underwent surgery, being accompanied by fibrinogen and platelet consumption. There were no concomitant signs of heightened activity of the factor VII-tissue factor mechanism on the factor Xase complex (plasma levels of activated factor VII and of factor IX and X activation peptides did not increase). The observed changes in biochemical markers of coagulation activation indicate that concentrate infusions increased thrombin generation and activity and that such changes were magnified by malignancy and surgery. Because some factor XI concentrates may be thrombogenic, they should be used with caution, especially in patients with other risk factors for thrombosis.
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PMID:Activation of the coagulation cascade after infusion of a factor XI concentrate in congenitally deficient patients. 804 46

To clarify age-related and lipid-related hemostatic abnormalities in the elderly, we measured the plasma levels of active PAI-1 antigen (aPAI-1), tPA-PAI-1 complex (TPC), plasminogen, alpha 2-plasmin inhibitor (alpha 2-PI), plasmin-alpha 2-PI complex (PIC), and D-dimer, together with the plasma levels of fibrinogen, factor VII (F VII), and thrombin-antithrombin III complex (TAT) and the serum lipid levels in 68 hyperlipidemic and 82 normolipidemic elderly subjects. The aPAI-1 ratio was calculated as aPAI-1/(aPAI-1 + TPC). In the normolipidemic elderly subjects, plasma PIC and D-dimer levels were much higher when compared with healthy young controls, and there was also a decrease in plasma plasminogen and alpha 2-PI levels, an increase in plasma TPC levels, and high plasma F VII and fibrinogen levels. In elderly subjects with type IIb hyperlipidemia, both the plasma aPAI-1 level and the aPAI-1 ratio were significantly increased, while the plasma PIC and D-dimer levels were reduced despite higher plasma F VII, fibrinogen and TAT levels. Both serum total cholesterol and triglyceride levels were correlated positively with plasma F VII and TAT levels and with the TAT/PIC ratio, while only serum triglyceride levels showed a positive correlation with plasma TPC and aPAI-1 levels and with the aPAI-1 ratio. Thus, an increase of fibrinolytic activity appears to occur as part of normal aging to balance the increase of procoagulant activity. However, an imbalance between thrombin activity (increased procoagulant activity) and plasmin activity (hypofibrinolysis) appears to occur in elderly individuals with hyperlipidemia, perhaps resulting in a predisposition to thromboembolic disease.
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PMID:Lipid-related hemostatic abnormalities in the elderly: imbalance between coagulation and fibrinolysis. 829 90

We measured factor VII activity and antigen levels in plasma of pregnant women and patients with elevated serum FDP including patients with DIC who were supposed to be in hypercoagulable state, and compared the values with normal subjects. Both FVII activities measured by human placenta thromboplastin (hTF/FVIIc) and bovine brain thromboplastin (bTF/FVIIc) in normal plasma were correlated well with the FVII antigen levels (FVIIag). Measured hTF/FVIIc, bTF/FVIIc and FVIIag in pregnant women were 163 +/- 44%, 205 +/- 49% and 175 +/- 44% respectively, and each value had correlation. Thrombin-antithrombin III complex in these subjects was increased (7.85 +/- 2.25 mg/ml). However, antithrombin III, plasmin-plasmin inhibitor complex and FDP D-dimer were within normal range. These observations indicated that pregnant women were in hypercoagulable state but not in hyperfibrinolytic state. hTF/FVIIc, bTF/FVIIc and FVIIag in plasma from patients with elevated serum FDP were 59.6 +/- 29%, 94 +/- 65% and 61.6 +/- 26% respectively. We divided these patients into 2 groups: Group A (both prolonged PT and APTT) and Group B (shortened APTT). hTF/FVIIc, bTF/FVIIc and FVIIag in plasma of Group A were 47 +/- 21%, 48 +/- 24% and 48 +/- 21% respectively. The corresponding values of Group B were 80 +/- 24%, 155 +/- 54% and 74 +/- 23% which were correlated each other. Low levels of FVII observed in Group A seemed to be due to increased consumption of coagulation factors. In Group B, the pattern of FVII activities and FVII antigen was similar to that of pregnant women, though FVII levels were lower.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Factor VII for a molecular marker in hypercoagulable state]. 835 13


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