Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.6.4 (chondroitinase)
 2,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been found that dermatan polysulfates (DPS) I, II and III isolated from hagfish notochord, hagfish skin and shark skin, respectively, and chemically sulfated dermatan sulfate exhibit considerable anticoagulant activity in the "activated partial thromboplastin time (APTT)" system. On comparing the activities with the various compositions, including disaccharide units produced by the digestion with chondroitinase-ABC, it was shown that the activity of these dermatan polysulfates depends not only on the total sulfate content but also on the content of sulfated L-iduronic acid residues. The activity seemed to decrease for molecular weight of below 10,000. The effect of these dermatan polysulfates on th inactivation of the clotting enzymes, factor Xa and thrombin, by antithrombin II (AT-III) was also studied using chromogenic substrates for the assay of the enzyme activities. The dermatan polysulfates showed an inhibitory effect on thrombin-AT-III, as estimated by the APTT assay, in contrast with the effect on factor Xa-AT-III which was found to be very small.
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PMID:Anticoagulant activity of dermatan polysulfates. 680

We examined the ability of unfractionated heparin to modulate the procoagulant activities of stimulated endothelial cells (EC). Confluent human venous umbilical EC were incubated with heparin before or after stimulation, then rinsed extensively to eliminate any heparin in the solution. EC, stimulated for 4 h with endotoxin and interleukin 1 beta, expressed tissue factor and prothrombinase activities. When EC were treated with heparin (6 and 60 micrograms/ml) during the last 10 min of the stimulation period, EC-related procoagulant activities were inhibited in a dose-dependent manner (80-90% inhibition at 60 micrograms/ml). The inhibition was antithrombin-dependent and it disappeared after heparin removal in less than 15 min at 37 degrees C but persisted at 4 degrees C. When EC were treated with heparin (60 micrograms/ml) for 24 h then extensively washed before stimulation, the anticoagulant effect was more modest (50% inhibition). The effect was antithrombin-dependent. Inhibition was maximum after 18-24 h of pretreatment of EC with heparin and was stable for at least 7 h. The cell surface displayed a "heparin-like" activity: treatment by heparin doubled the rate of thrombin-antithrombin complex formation and this effect was heparinase sensitive and chondroitinase ABC insensitive. Thus, heparin modulates the procoagulant properties of stimulated EC according to two distinct mechanisms. The first one is rapid and transient, probably related to the presence of heparin molecules bound at the membrane surface. The second is delayed and persistent, and our results suggest that it is mediated by an increase in the membrane heparan sulfate molecules.
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PMID:Heparin reverses the procoagulant properties of stimulated endothelial cells. 871