Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.5 (thrombin)
 33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A noncovalent fluorescent probe that responded to changes in transmembrane potential was used to study the response of washed human platelets to aggregating agents. Concentration-dependent changes in the fluorescence were observed in response to ADP and to thrombin. No such changes were observed in response to collagen fibrils. Thus there was an indication that platelet membrane potential changed in response to aggregating stimuli, supporting the hypothesis that the mechanisms of platelet aggregation resembled the mechanisms of other systems that show stimulus-response coupling (e.g., muscle, adrenal chromaffin cells). The different responses to specific agents indicate that the agents may trigger platelet aggregation through different mechanisms.
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PMID:Probes of transmembrane potentials in platelets: changes in cyanine dye fluorescence in response to aggregation stimuli. 41 74

To determine whether the long-term feeding of dietary fats affect platelet functions in man, platelet aggregation (to thrombin ADP, collagen, epinephrine) and clotting activity of platelet-rich plasma (PRP), platelet-poor plasma and of washed platelets were studied in a mobile-laboratory in 44 healthy male farmers (40--45 years) from two French regions Var and Moselle, in relation to lipemia, glycemia, dietary nutriments, and platelet phospholipid composition. In the Moselle subjects, the platelet clotting activity of PRP and of washed platelets, the platelet aggregation to thrombin and ADP, were highly significantly (p less than 0.001) increased as compared to those of Var, but not the plasma cholesterol, which was identical in the two regions. In Moselle, the intake of total calories, total lipids and saturated fats was higher than in the Var. However, it was only with the saturated fat intake (mostly stearic acid) that the platelet clotting activity (p less than 0.01) and the platelet aggregation (p less than 0.001) were highly significantly correlated. The platelet clotting activity was also significantly (p less than 0.001) correlated with the fatty acid composition of the platelet phospholipid fractions phosphatidyl serine + phosphatidyl inositol.
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PMID:Platelet functions in relation to dietary fats in farmers from two regions of France. 42 66

Effect of Ticlopidine, 5-(2-chlorobenzyl)-4, 5, 6, 7-tetrahydro[3,2-C]pyridine hydro-chloride, on platelet aggregation was studied in the rat. Ticlopidine was found to be a potent, long-lasting inhibitor of platelet aggregation. It inhibited the aggregation induced by any of ADP, collagen, thrombin, arachidonic acid and prostaglandin endoperoxides and/or thromboxane A2-like substancee. Ticlopidine was effective at doses as low as 30 mg/kg when orally given to rats, and the effect lasted as long as the life span of the circulating platelets (half time: about 48 hours). Ticlopidine inhibited also nucleotide release from and prostaglandin synthesis in the platelets, but did not significantly affect platelet adhesiveness to glass, platelet factor 3 availability and clot retraction.
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PMID:Inhibition of platelet aggregation by a new agent, Ticlopidine. 42 67

The equilibrium between assembled and disassembled microtubules was studied in human platelets exposed to aggregating agents. Soluble and insoluble tubulin were "frozen" by addition of a glycerol-dimethyl sulfoxide-containing medium. The two pools were estimated by measuring the colchicine binding activities of total and polymerized tubulin. Resting platelets were found to contain an average of 56.2 mug tubulin/1 x 10(9) cells of which 56.7% was in polymerized form. Platelet aggregation induced by thrombin, ADP, epinephrine, or collagen produced a transient decrease in the pool of polymerized tubulin which was evident within 15 s after addition of the aggregating agent. A return to base-line values occurred within 1-4 min depending upon the specific aggregating agent used. Neither secretory release nor aggregation of platelets were found to be prerequisites for the temporary disturbance of the equilibrium between soluble and polymerized tubulin. With thrombin as the aggregating agent a clear threshold concentration could be demonstrated above with a dose-dependent dissociation response of microtubules was evident. We conclude that microtubules exist in a dynamic equilibrium between polymerized and depolymerized forms in human platelets, which is transiently disturbed by their interaction with aggregating agents.
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PMID:Quantitative assessment of polymerized and depolymerized platelet microtubules. Changes caused by aggregating agents. 42 63

Rabbit platelets were labeled in vivo with 35S for characterization of platelet sulfated glycosaminoglycan. When rabbit platelets were aggregated by ADP, sulfated proteoglycan was lost from the platelet surface although no release of granule contents occurred. The sulfated proteoglycan contained in the granules of platelets pretreated with ADP was subsequently released by treatment with thrombin. The 35S-labeled proteoglycan from both sources was isolated by gel filtration and the glycosaminoglycan portion of the proteoglycan was characterized as chondroitin 4-sulfate by examining the products of digestion with hyaluronidase, chondroitinase AC and ABC, and chondro-4- and 6-sulfatases; by identification of the hexosamine as N-acetylgalactosamine; by determination of a 1 : 1 : 1 molar ratio of N-acetylgalactosamine, uronic acid and inorganic sulfate; and by cetylpyridinium chloride cellulose chromatography. In these studies, the use of 35S-labeled proteoglycan made possible detection and quantification of much smaller amounts of material than would be possible with unlabeled material. Chondroitin 4-sulfate was the only sulfated glycosaminoglycan identified in the proteoglycan lost from the platelet surface during ADP-induced aggregation and in the proteoglycan released from the granules when the platelets were exposed to thrombin.
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PMID:Characterization of the sulfated glycosaminoglycan on the surface and in the storage granules of rabbit platelets. 44 61

Platelets lysed with Triton X-100 contain 3.44 +/- 1.27 (SD) microgram of fibronectin (cold-insoluble globulin) per 10(9) platelets. Fibronectin was partially released from washed whole platelets by collagen or thrombin, and its release by collagen was inhibited by aspirin. Analysis of subcellular fractions obtained by density-gradient centrifugation of disrupted platelets indicated that fibronectin was contained in the alpha granules. Fibrinogen depleted of fibronectin (less than 2 microgram/mg) supported ADP-induced aggregation as effectively as fibrinogen contaminated with this protein, thus reinforcing the generally held view that fibrinogen itself is the necessary protein cofactor in this reaction.
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PMID:Release of platelet fibronectin (cold-insoluble globulin) from alpha granules induced by thrombin or collagen; lack of requirement for plasma fibronectin in ADP-induced platelet aggregation. 44 75

Platelets from a patient with eosinophilic leukaemia were not aggregated by ristocetin. The defect was not corrected by normal human plasma and was due to a platelet abnormality. The patient's platelets also showed a diminished sensitivity to aggregation by bovine factor VIIIVWF. The defect was not associated with a prolonged bleeding time. No abnormalities were detected in ADP, collagen or thrombin-induced platelet aggregation. Biochemical studies showed that the platelets were deficient in sialic acid. This deficiency was associated with a reduced staining for glycoprotein I following SDS-polyacrylamide gel electrophoresis. The results suggest an acquired platelet surface abnormality.
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PMID:A platelet defect in a patient with eosinophilic leukaemia: absent ristocetin-induced platelet aggregation associated with a reduced platelet sialic acid content. 45 58

The minimal concentration of the platelet aggregation principle (Platelet Aggregoserpentin, PAS) necessary to induce platelet aggregation was 10 ng/ml, about one-hundredth of that of the crude venom. PAS induced the release of platelet factors 3 and 4 from platelets, but the released platelet factor 3 was easily inactivated by the anti-phospholipid effect of PAS. Pretreatment of platelets with neuraminidase potentiated PAS-induced platelet aggregation. PAS-induced platelet aggregation was independent on released ADP; it could occur in the ADP-removing systems, such as apyrase or a combination of phosphoenolpyruvate and pyruvate kinase. However, PAS-induced platelet aggregation could be inhibited by adenine nucleotides and adenosine. PAS-induced platelet aggregation was inhibited by some anti-inflammatory agents, antimalarial drugs, local anesthetics, antihistamine and smooth muscle relaxants. After deaggregation of PAS-treated platelets, thrombin and sodium arachidonate could further induce platelet aggregation, but ADP and second dose of PAS could not. It is concluded that PAS-induced platelet aggregation is due to prostaglandin synthesis. Recent literatures on the mechanism of platelet aggregation were surveyed and the actions of PAS were discussed.
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PMID:The action mechanism of the purified platelet aggregation principle of Trimeresurus mucrosquamatus venom. 46 15

Platelets provide a procoagulant activity for the conversion of prothrombin to thrombin during normal hemostatis. This activity designated as platelet prothrombin-converting activity (PPCA) was monitored as rate of thrombin production in a two-stage assay using gel-filtered bovine platelets, factor Xa, and prothrombin. Expression of PPCA was not associated with ADP-induced release or platelet shape change but was associated with aggregation. Release of the contents of dense bodies, measured by release of 14C-5-hydroxytryptamine, was not required for expression of PPCA during platelet aggregation. During the PPCA assay, 5-hydroxytrypamine was released, but only after onset of thrombin production. Furthermore, the release of 5-hydroxytryptamine was retarded during the assay by the addition of 2 mM theophylline and 100 nM prostaglandin E1 without a comparable reduction in PPCA. In addition, 125I-factor-Xa was bound in greater amounts to platelets (aspirin-treated) after ADP-induced aggregation (without detectable release) than to unactivated control platelets. Finally, the PPCA of the ADP-activated platelets was saturated with respect to factors Xa and Va at less than 1 nM concentrations, indicating that the aggregation induced by ADP leads to the exposure of specific procoagulant sites by some process other than dense body secretion.
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PMID:The effect of aggregation and release on platelet prothrombin-converting activity. 46 34

Normal rabbit peripheral blood neutrophils released a platelet-activating factor upon stimulation by opsonized zymosan. The liberation was Ca++ dependent and the time course of release was closely associated with phagocytosis. The material extracted into chloroform and exhibited an identical mobility by thin layer chromatography to basophil-derived, IgE-stimulated, platelet-activating factor (PAFb). It was similar to PAFb in its effect on platelets in both aggregation and release but was distinguished from ADP, thrombin, arachidonic acid, and thromboxanes. This factor appears to be responsible for some previously reported neutrophil-platelet interactions.
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PMID:The release of a platelet-activating factor by stimulated rabbit neutrophils. 46 47


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