Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.4.3 (phospholipase C)
 18,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association between the concentration of different plasma lipoproteins and plasma factor VII (F VII) was analysed by isolating plasma very low density lipoprotein (VLDL), low density lipoprotein (LDL), and high density lipoprotein (HDL) lipoproteins and assessing their in vitro interaction with F VII by immunoenzyme assay using peroxidase labelled anti-factor VII immunoglobulins to determine whether F VII coagulant activity is prognostic for cardiovascular mortality. F VII bound to triglyceride rich lipoproteins, the fixation being stronger on chylomicrons and VLDL fractions than on LDL fractions. In our experiments HDL did not bind to F VII. The fixation of coagulation factor X (FX) tested by the same method is comparable with that of F VII. The nature of this fixation seemed to arise from hydrophobic interaction as calcium was not necessary and the use of Tween 20 inhibited the interaction. The binding of factors VII and X was increased when lipids were previously treated by phospholipase C and the interaction seemed to be completely dependent on the lipid part of the lipoproteins. Hyrophobic fixation is a possible mechanism of interaction of plasma lipoproteins and F VII and X, and it may be of importance in the covariance of triglyceride concentrations and the activity of vitamin K dependent coagulation factors.
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PMID:Association between coagulation factors VII and X with triglyceride rich lipoproteins. 305 86

We have reported the existence of a novel form of coagulation factor VII - probably a factor VII-phospholipid complex - in plasma from pregnant women and men at risk for cardiovascular disease. We report here further observations on the presence and characteristics of this complex. Some apparently healthy individuals who, on testing by standard methods, have normal levels of factor VII activity achieve such levels by means of a phospholipase C-sensitive modification of (some of) their factor VII molecules. Their residual factor VII activity after phospholipase C treatment of plasma may be as low as 10-20 U/ml. Antiserum to the protein component of thromboplastin (apoprotein III) had no effect on the factor VII activity, whereas antiserum to factor VII effectively blocked both the total factor VII activity and the residual activity of factor VII after treatment of plasma with phospholipase C. These factor VII complexes precipitate with the VLDL/LDL fraction in lipoprotein precipitations.
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PMID:A new form of coagulation factor VII in plasma. 309 Jun 80

In a recent study, Dalaker et al. (Br J Haematol 1985; 61:315-22) reported that men at high risk for cardiovascular disease had an increased mean level of factor VII procoagulant activity that was apparently attributable to an increase of a phospholipase C-sensitive form of factor VII in their plasma. We chose to investigate this phenomenon further by observing patients at high risk of coronary artery disease with assays that reflect the activity state of factor VII. We measured factor VII levels in patients before coronary arteriography and in normal subjects by an amidolytic assay (FVIIam assay) and by a standard clotting assay (FVIIc-A assay), both of which reflect the total amount of factor VII and are insensitive to activated factor VII, and by the method of Seligson et al. (Blood 1978;52:978-88) (FVIIc-B assay), which is sensitive to the presence of activated factor VII. In the FVIIc-A and FVIIam assays, the patients had a significantly higher mean value than the normal subjects; in the FVIIc-B assay, the patients had a significantly lower mean value than did the normal subjects. Moreover, the ratio of FVIIc-B to FVIIam, which is an indicator of the factor VII activity state, was much lower for the patients (0.70) than for the normal subjects (0.99). Thus, patients at high risk for coronary artery disease have an increased mean level of total factor VII that is not associated with an increase in activated factor VII and therefore presumably reflects an increase in zymogen factor VII.
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PMID:Factor VII activity state in coronary artery disease. 335 80

Cell-free supernatants (sol phases), obtained after centrifugation (50,000 x g for 45 minutes) of respiratory tract secretions from horses with chronic pulmonary disease, were assayed for procoagulant activity (PCA) in a one-stage clotting assay. Of the 103 specimens tested, 59% (61) contained PCA. Procoagulant activity was detected most often in respiratory tract secretions of severely affected horses and was correlated with the quantity of neutrophils in the respiratory tract secretions. In 12 of the 17 secretions tested, the clotting time was decreased in a dose-dependent manner. However, in the coagulation assay, some reversal of PCA or inhibition of coagulation was observed in 4 secretion specimens when greater volumes of sol phase were added. Procoagulant activity was characterized tentatively as tissue factor, because it was temperature stable and was inhibited by phospholipase C and by concanavalin A. Clotting was induced in factor VIII-deficient human plasma; however, with the exception of 1 respiratory secretion specimen, clotting was not enhanced in factor VII-deficient human plasma. Procoagulant activity is a useful indicator of airway inflammation.
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PMID:Procoagulant activity in respiratory tract secretions from horses with chronic pulmonary disease. 339 15

Disseminated intravascular coagulation invariably accompanies placement of peritoneovenous (LeVeen) shunts, which suggests that ascitic fluid contains procoagulant material capable of activating blood coagulation. In this study, we identified thrombogenic activity in human ascites and the hemostatic pathway by which it acts. Peritoneal fluid was removed percutaneously from patients with ascites due to various causes. Four fractions were prepared by centrifugation: cells, a low-speed, cell-free fluid, a high-speed supernatant, and the precipitate from the high-speed centrifugation. Cellular fractions from all ascitic fluids shortened a one-stage clotting time of normal pooled plasma by 68% in comparison with saline solution and endotoxin controls. Similarly, the cell-free fluids also shortened the clotting time of normal pooled plasma by 41%. The cellular and cell-free fractions shortened the clotting time of factor VIII-deficient plasma but failed to demonstrate procoagulant activity in factor VII-deficient plasma. These fractions had no effect on platelet aggregation or the platelet release reaction. The high-speed precipitate was dissociated by ethylenediaminetetra-acetate (EDTA) into fluid phase and precipitate, both of which demonstrated procoagulant activity. Furthermore, high-speed precipitate contained protein, phospholipid, and sterol in proportions similar to those of plasma membranes and contained membrane-bound vesicles as identified by means of electron microscopy. This material could be rendered inactive by heating to 100 degrees C for 2 minutes or by incubation with phospholipase C for 15 minutes. Finally, the ability of the high-speed precipitate to shorten the clotting time was prevented by preincubation with a monoclonal antibody, which is known to inhibit the procoagulant activity of human tissue factor. We suggest that several entities contribute to the procoagulant properties of human ascites, with procoagulant material deriving at least in part from peritoneal cells. The sedimentable procoagulant factor appears to be associated with cellular membranes or membrane fragments and is thromboplastin-like in its chemical composition, immunoreactivity, and substrate specificity.
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PMID:Preliminary characterization of the procoagulant material in human ascites. 358 68

We report here a highly significant positive correlation observed when the factor VII-phospholipid complex (the phospholipase-C sensitive component of factor VII) in plasma was tested in a specific factor VII system and in Normotest (p less than 0.0001). The Normotest system, which is sensitive to variations in coagulation activity within the normal range, was not influenced by phospholipase C when the enzyme was added immediately before the start of the coagulation assay. Normotest is well suited for determination of the factor VII-phospholipid complex in plasma.
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PMID:A simple method for determination of the factor VII-phospholipid complex using Normotest. 362 56

Partially purified Amniotic Fluid Factor (AFF) is found to directly activate human factor X, with a Km for factor X of 0.37 +/- 0.06 M. Added phospholipid has only a slight effect on the activation at low concentrations, and inhibits the reaction at higher concentrations. Both DIPF and PMSF inhibit AFF factor X activation. Although added phospholipid is not required for AFF-activity, phospholipase C rapidly destroys it, indicating the presence of intrinsic phospholipid. Phospholipase C treated AFF releases factor VII activity, which leads to the conclusion that AFF is in fact a thromboplastin: factor VII complex. Both AFF and a human brain thromboplastin factor VII complex prepared in vitro were inhibited by Zn++ ion, while human brain thromboplastin alone is not. AFF is markedly larger than the human brain thromboplastin-factor VII complex as judged by gel filtration.
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PMID:Studies on the procoagulant activity of human amniotic fluid. II. The role of factor VII. 393 21

During pregnancy the activity of coagulation factor VII in plasma increases up to 248% (SEM 16) (n = 18) at 40 weeks even when all precautions to avoid cold activation are taken. This increase is at all times during pregnancy, delivery and puerperium entirely due to the presence in vivo of what is most likely a phospholipid-factor VII complex. This complex is sensitive to phospholipase C, so that treatment with the enzyme reduces the activity of pregnant plasma down to that of non-pregnant controls. When present in the complex factor VII has a higher specific activity and an altered conformation with a more accessible active site as demonstrated by increased susceptibility to inactivation by diisopropylfluorophosphate. Factors II and X are increased to 136% (SEM 4) and 171% (SEM 6) (n = 18) without being sensitive to phospholipase C. The increase during pregnancy and the decrease after delivery of the phospholipase-sensitive factor VII activity have been followed.
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PMID:Clotting factor VII during pregnancy, delivery and puerperium. 394 1

Various n-formylated peptides function as receptor-specific chemoattractants for both granulocytes and monocytes. Because these agents are important tools in the study of leukocyte function in vitro, we chose to examine their effects on leukocyte procoagulant activity. The synthetic chemotactic peptide N-formyl-methionyl-leucyl phenylalanine (FMLP) induces a fourfold increase in procoagulant activity (PCA) in cultured human monocytes at an optimal dose of 5 X 10(-9) mol/L, whereas higher doses inhibit PCA response. Although nonadherent lymphocytes are not absolutely required for PCA expression, their presence significantly amplifies monocyte PCA. Irradiation of nonadherent lymphocytes before mixing them with FMLP and adherent cells abolishes their ability to amplify PCA. Kinetic studies demonstrate an increase in optimal dose FMLP-stimulated PCA over time whereas high-dose inhibition of PCA generation occurs at various incubation times. Cell viability is unaffected by inhibitory concentrations of FMLP. Supernates from high-dose FMLP-stimulated cells fail to inhibit later expression of PCA by cells exposed to endotoxin. The cellular procoagulant remains cell-bound and exhibits characteristics of thromboplastin (tissue factor), including inhibition by concanavalin A and phospholipase C as well as the ability to shorten the clotting times of factor VIII but not factor VII-deficient substrate plasmas. These results suggest a complex system of lymphoid cell regulation of procoagulant generation by monocytes exposed to various chemotactic peptides in vitro.
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PMID:Regulation of monocyte procoagulant by chemoattractants. 397 Oct 40

Leukocytes can generate procoagulant (tissue factor) activity when incubated with endotoxin. These studies were undertaken to determine whether platelets could influence the procoagulant activity generated by leukocytes. Intact or disrupted platelets (rabbit or human) enhanced the clot-promoting properties of rabbit leukocytes. The enhancing effect of human platelets on human leukocytes required the presence of human serum (devoid of factor VII and X activities). When platelets were incubated with endotoxin in the absence of leukocytes, no increase in their clot-promoting properties was discernible. However, a mixture of platelets, leukocytes, and endotoxin generated procoagulant activity which appeared rapidly and was fivefold greater than that produced by leukocytes incubated with endotoxin alone. The enhancement produced by platelets was even more pronounced if homogenates were used. The platelet effect was examined in more detail by the substitution of membranes, granules, and the "soluble" fraction for whole platelets in the test system. The stimulating activity was localized to the particulate fractions, i.e., membranes and granules. Prior treatment of platelet membranes with phospholipase C or gangliosides or by extraction of lipid resulted in loss of enhancing activity, whereas no inhibition was observed after exposure to neuraminidase or trypsin. It is proposed that platelets contribute a membrane lipoprotein surface which enhances the procoagulant activity generated by leukocytes in the presence of endotoxin. This mechanism may be involved in some of the clinical and pathologic manifestations of gram-negative sepsis with disseminated intravascular coagulation.
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PMID:The stimulatory effect of platelets and platelet membranes on the procoagulant activity of leukocytes. 461 59


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