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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tissue kallikrein and factor Xa were found to activate tissue plasminogen activator (t-PA) at a rate comparable with that of plasmin. During the activation reaction, the single-chain molecule was converted into a two-chain form. A slight t-PA activating activity was also found in plasma kallikrein. Other activated coagulation factors, factor XIIa, factor XIa, factor IXa, factor VIIa, thrombin and activated protein C had no effect on t-PA activation. t-PA was also activated by a tissue kallikrein-like enzyme that was isolated from the culture medium of melanoma cells. These results indicate that tissue kallikrein and factor Xa may participate in the extrinsic pathway of human fibrinolysis.
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PMID:Proteolytic activation of tissue plasminogen activator by plasma and tissue enzymes. 656 16

Alveolar lavage cells from normal sheep were found to be composed of over 95% macrophages. When the cells were cultured, fibrinolytic and thromboplastin-like activities could be detected within 2-4 hours of incubation. As the number of cultured cells was increased the two activities in the conditioned medium increased proportionately. The cells were separated into two distinct subpopulations by means of a sedimentation velocity cell fractionation technique. The macrophage subpopulations were examined for differences in size, morphology, esterase staining and ability to release plasminogen activator and procoagulant activity respectively. These activities were confined to the large cell subpopulation. The fibrinolytic activity was shown to be plasminogen-dependent and could be inhibited by DFP. On the basis of this the fibrinolytic activity has been designated as plasminogen activator. The procoagulant activity was shown to be thromboplastin in nature because it was Factor VII dependent, inactivated by phospholipase C and not inhibited by DFP. The procoagulant activity has been designated as macrophage thromboplastin. The two activities could be distinguished on the basis of DFP inhibition.
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PMID:Plasminogen activator and thromboplastin activity from sheep alveolar macrophages. 668 4

The fibrinolytic response to trauma was investigated in 23 patients. Patients were triaged upon arrival in the emergency center into three groups; group I-patients with significant trauma who maintained normal vital signs, had a good prognosis, and tolerated the trauma well (mean injury severity score 8, range 4 to 12); group II--patients with significant trauma and transient episodes of hypotension, hypoxia, or acidosis who recovered (mean injury severity score 22, range 9 to 38); and group III--patients with profound or continued hypoxia and hypotension who eventually died of the trauma (mean injury severity score 41, range 30 to 50). Serial measurements of prothrombin time, activated partial thromboplastin time, and platelet count; concentrations of fibrinogen, plasminogen, and fibrin degradation products; and assays of euglobulin fraction fibrinolytic activity on plasminogen-free and plasminogen-rich fibrin plates were obtained on all patients. Coagulation studies documented a trauma-related coagulopathy that correlated with the degree of trauma. Plasminogen concentrations were initially depressed in all three groups; however by 24 hours group III patients were noted to have significantly elevated plasminogen concentrations while group I and group II patients had normal plasminogen concentrations. Fibrinolytic activity measured on plasminogen-free and plasminogen-rich fibrin plates was initially increased in all three groups with group III patients demonstrating the greatest increase. Over the succeeding 14 hours fibrinolytic activity returned to baseline values in group I and group II patients while group III patients demonstrated no detectable fibrinolytic activity for the remainder of the study period. This absence of fibrinolytic activity and increase in plasminogen concentrations in group III patients is thought to be caused by depletion of the intravascular plasminogen activator with the subsequent development of a hypofibrinolytic state.
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PMID:Fibrinolytic response to trauma. 671 Mar 42

Chrysotile fibers injected into the peritoneal cavity of mice elicit a cellular exudate. Macrophages appearing in this exudate produce high levels of the neutral protease, plasminogen activator, when compared with the resident peritoneal macrophage population. In contrast, the levels of lysozyme and two lysosomal enzymes are the same for the two macrophage types. The asbestos-induced macrophages producing the plasminogen activator appear to have descended from recently divided precursors. Low concentrations of anti-inflammatory glucocorticoids inhibit macrophage plasminogen activator synthesis. Preliminary experiments indicate that different asbestos types induce hyperemia in skin, and also shorten the partial thromboplastin time of plasma and generate the release of kinins. These observations could be interrelated and are suggested as representing some aspects of the inflammatory response of the host to asbestos exposure.
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PMID:Macrophage stimulation and the inflammatory response to asbestos. 677 Nov 31

A new epithelial cell line derived from undifferentiated carcinoma of human renal pelvis, designated KP 1, was established in vitro. The cell line has been passaged 190 times in vitro for 5 years and 9 months. The predominant cell in KP 1 was a tear-drop-shaped cell. Doubling time of the cell line was 35 h. The malignant epithelial character of this line was verified by carcinogenicity in the subcuticular layer of nude mice and by karyotypic analysis which revealed the cells to be completely aneuploid with a model chromosome number in the hypertriploid range. KP 1 cells were shown to produce both tissue thromboplastin and plasminogen activator which was immunologically identical to urokinase, the plasminogen activator in urine.
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PMID:Establishment of a human renal pelvic cancer cell line producing tissue thromboplastin and plasminogen activator. 720 Feb 72

1. The time sequence of glomerular fibrin deposition, renal cortical fibrinolytic response and thrombocytopenia after thromboplastin infusion in rats has been established. 2. Fibrin clearance is rapid and is associated with markedly increased cortical fibrinolytic activity. 3. Plasma fibrinolytic activity was unchanged. 4. Experiments in which the dose-response relationship between thromboplastin dose, fibrin deposition and fibrinolytic response was examined showed that fibrinolytic response increased with fibrin deposition in glomeruli. 5. The dose-response experiments also provided data which suggested that the method of measurement of cortical fibrinolytic activity in the presence of deposited fibrin measures excess rather than total plasminogen activator production.
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PMID:Clearance of fibrin from glomeruli. Renal cortical fibrinolytic response after thromboplastin infusion in the rat. 723 23

A fibrinolytic agent purified from the haemolymph, hair secretion and whole body extract of Lonomia achelous (Cramer) cleaves various chromogenic peptide substrates. The best substrate were found to be pyro-Glu-Gly-Arg-pNA (S-2444) followed by D-Pro-Phe-Arg-pNA (S-2302) and Bz-Ile-Glu-(or) Gly-Arg-pNA (S-2222) designed for urokinase, plasma kallikrein and factor Xa, respectively. Using substrate S-2251 we also found a plasminogen activator.
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PMID:Studies of a fibrinolytic enzyme from the larvae of Lonomia achelous (Cramer) using chromogenic peptide substrates. 733 Aug 21

We had rare opportunities to examine changes in fibrin degradation products (FDP)-D-dimer (DD), thrombin-antithrombin III complex (TAT), plasmin-alpha 2-plasmin inhibitor complex (PIC) and other coagulation parameters during the clinical courses of living-related partial liver transplantation (LRPLT). In seven out of eight recipients without severe rejection and/or disseminated intravascular coagulation (DIC), FDP-DD values reached their maximum at 5 to 10 days after transplantation, then gradually decreased. On the other hand, TAT values rose to the maximum at anhepatic or reperfusion phase of liver transplantation. These data represent hypercoagulation in consequence of tissue thromboplastin activation after extensive operation. Changes in PIC, tissue-type plasminogen activator, and plasminogen activator inhibitor-1 (PAI-1) in the clinical course of case 1 suggested that fibrinolysis was suppressed by relatively elevated level of PAI-1 around the operation, but thereafter was adversely accelerated by relatively lower levels of PAI-1. In comparison with patients with DIC, TAT was much higher but PIC was significantly lower in recipients of LRPLT. These findings indicated that marked hypercoagulation and mild to moderate hyperfibrinolysis occurred in recipients of LRPLT.
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PMID:[Changes in coagulation parameters during the clinical courses of recipients of living-related partial liver transplantation]. 747 43

This retrospective analysis reviewed 183 patients with acute myocardial infarction who were given front-loaded recombinant tissue-type plasminogen activator (rt-PA) and r-hirudin (HBW 023) in 1 of 4 dose groups (bolus dose of 0.07, 0.1, 0.2, or 0.4 mg/kg, followed by an infusion of 0.05, 0.06, 0.1, or 0.15 mg/kg/hour over 48 hours). Activated partial thromboplastin time (aPTT) levels were determined at baseline and at 4, 8, 12, 16, 20, 24, 32, 40, and 48 hours. Of the 178 patients with r-hirudin treatment for > or = 12 hours, anticoagulation was optimal in 55.1% (all aPTTs > 2 x baseline), suboptimal in 33.7% (lowest aPTT > 1.5 but < 2 x baseline), and inadequate in 11.2% (> or = 1 aPTT but < 1.5 x baseline). Optimal anticoagulation was observed more frequently in the higher dose groups (dose 1, 15%; dose 2, 44.4%; dose 3, 63.4%; dose 4, 73.4%; p for trend < 0.0001). Patency (according to Thrombolysis in Myocardial Infarction trial grade 2 or 3) of the infarct artery after 36 to 48 hours was higher in the group with optimal anticoagulation compared with those with suboptimal or inadequate anticoagulation: 97.9%, 88.4%, and 85%, respectively (p = 0.03 optimal vs suboptimal or inadequate anticoagulation). In conclusion, r-hirudin in a dose of 0.1 or 0.15 mg/kg/hour achieves an optimal anticoagulation in about 63% or 74% of patients, which is associated with an enhanced patency 24 to 48 hours after rt-PA. A subsequent study revealed that this effective anticoagulation may be accompanied by an increased risk of severe bleeding complications after thrombolysis.
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PMID:Frequency of "optimal anticoagulation" for acute myocardial infarction after thrombolysis with front-loaded recombinant tissue-type plasminogen activator and conjunctive therapy with recombinant hirudin (HBW 023). ALKK Study Group. 748 79

Malignant mesothelioma (MM) is a locally aggressive tumor that spreads by poorly understood mechanisms. Because neoplastic spread has been linked to altered fibrin turnover, we used immunohistochemistry of nine MM and three fibrous tumors of the pleura to confirm in vivo fibrin deposition and expression of selected coagulation and fibrinolytic reactants in MM. Tumor-associated fibrin was readily detectable at site of tissue invasion. Little fibrin was distributed within the tumor, but tissue factor and tissue factor pathway inhibitor, urokinase, urokinase receptor, and plasminogen activator inhibitors 1 and 2 were all detected in either epithelioid or sarcomatous areas of MM. We used the MS-1 human pleural mesothelioma cell line to determine how expression of these reactants is regulated. Fibrinolytic activity of MS-1 is mainly due to urokinase and is responsive to cytokine stimulation. Functional extrinsic activation and prothrombinase complexes assemble at the cell surface. MM express procoagulants as well as fibrinolytic reactants in vivo and in vitro that promote local fibrin formation and remodeling. Fibrin deposition occurs primarily at areas of tissue invasion and could promote local extension of this neoplasm. Sparsity of fibrin within the central portions of the tumor stroma suggests that local resorption of transitional fibrin occurs at sites of established MM.
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PMID:Regulation of fibrin deposition by malignant mesothelioma. 748 95


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