Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Porcine urine, unlike human urine, does not contain detectable amounts of urokinase-type plasminogen activator (u-PA). The plasminogen activator present in porcine urine is of tissue-type (t-PA) as identified by the following criteria. (1) Porcine urine PA exhibits an Mr of 65,000 similar to the Mr of human t-PA (64-70,000) but distinct from the Mr of human u-PA (55,000). (2) Antibodies against human t-PA bind and inhibit crude and purified porcine urine PA, while human u-PA-specific antibodies do not react with porcine urine PA. (3) Plasminogen activation by porcine urine PA is markedly stimulated in the presence of fibrinogen fragments. (4) Porcine urine PA activity is not affected by concentration of amiloride substantially suppressing human u-PA activity.
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PMID:Characterization of a tissue-type plasminogen activator from porcine urine. 191 41

Fluid cadaveric blood is generally known as a characteristic of sudden death. However, it has been reported that soft blood clots have been observed in a number of cases of sudden death after alcohol drinking. Such a tendency was also recognized on autopsy cases in our laboratory. This study was carried out to reveal the effects on clotting and fibrinolytic system in golden hamsters under acute alcohol intoxication. Furthermore, the influences of ether anaesthesia were also observed. Activities of clotting and fibrinolytic factors were measured with fluorogenic peptide substrate. Prothrombin and factor X activities began to decrease 1 hr after administration of alcohol. But thrombin-like and factor Xa-like activities significantly increased after 1 hr and then returned to the initial value 4 hr after administration. Plasminogen activity began to decrease 1 hr after administration, whereas plasmin-like and t-PA-like activities increased after 1 hr and returned to the initial values or decreased after 4 hr. These results show that under acute alcohol intoxication clotting and fibrinolytic factors (prothrombin, factor X and plasminogen) in golden hamsters were converted temporarily to their active forms (thrombin, factor Xa and plasmin). No influence of only ether anaesthesia on clotting and fibrinolytic activities was observed. At 1 hr after administration of alcohol some effects of ether anaesthesia on prothrombin, prekallikrein and kallikrein were observed and then were not observed after 4 hr. But it seems that the influence of ether anaesthesia on clotting and fibrinolytic activities was negligible in the process after alcohol consumption.
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PMID:[Clotting and fibrinolytic activities in acute alcoholic golden hamsters with or without ether anaesthesia]. 192 Sep 21

The (Thrombolysis in Myocardial Infarction) TIMI-I trial led to the hypothesis that the greater reperfusion rate seen with recombinant tissue-type plasminogen activator (rt-PA) versus streptokinase would result in greater reductions in infarct size and mortality in patients with acute myocardial infarction. Despite extensive investigation, no trial comparing rt-PA with streptokinase (European Cooperative Study Group, Plasminogen Activator Italian Multicenter Study [PAIMS], Gruppo Italiano per lo Studio della Sopravvivenze nell'Infarto Miocardico [GISSI-2], International Study on Infarct Survival [ISIS-3], even TIMI-I itself) nor rt-PA and anisoylated plasminogen-streptokinase activator complex (APSAC or anistreplase) (Bassand, TEAM-3, ISIS-3), have confirmed this hypothesis. In a reversal of traditional scientific method, the studies, rather than the unconfirmed hypothesis, have been rejected. A lack of independent review of this subject may have contributed to this outcome. It is proposed that standards of review and editorial comment mandating true critical distance and independence be followed, permitting greater independence of scientific inquiry, review and debate.
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PMID:Thrombolysis: the need for a critical review. 193 63

Plasminogen activator inhibitor (PAI-I) rapidly inactivates tissue plasminogen activator (t-PA) and urokinase (UK) with nearly identical association rate constants. The contributions of Ser344, Ala345, and Arg346 (P3, P2, and P1 residues, respectively) in PAI-I to inhibition of UK and t-PA were evaluated using combinatorial mutagenesis of the human PAI-I cDNA. A bacteriophage lambda expression library potentially encoding the 8000 unique PAI-I species were screened for inhibitory activity against UK using a fibrin indicator gel. 390 plaques demarcated by zones of retarded fibrinolysis were analyzed to determine the DNA sequences of their associated active PAI-1 species. We found 134 unique PAI-1 variants that retained inhibitory activity towards UK; they contained a variety of amino acids in their P3 and P2 positions but only Arg or, infrequently, Lys in their P1 position. Each of the unique active PAI-1 were assayed for inhibitory activity towards UK or t-PA; many substitutions differentially affected the ability of the inhibitor to inactivate UK and t-PA. For example, replacement of Ser344 and Ala344 with Val and Pro, respectively, yielded a PAI-1 variant exhibiting an association rate constant that was unchanged for t-PA but decreased 23-fold for UK, relative to native PAI-1. In general, the PAI-1 variants were more potent inhibitors of t-PA than UK. Hence, t-PA appears more tolerant than UK of structural diversity present in the P3 and P2 positions of the PAI-1 variants.
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PMID:Combinatorial mutagenesis of the reactive site region in plasminogen activator inhibitor I. 202 63

Fetal rat calvaria cells (RC cells) grown in long term culture in the presence of ascorbic acid and organic phosphate proliferate and differentiate to form mineralized nodules of bone. Since transforming growth factor beta (TGF-beta), interleukin 1-alpha (IL-1 alpha) and epidermal growth factor (EGF) affect both bone resorption and bone formation, we have studied the ability of these growth factors to affect plasminogen activators and plasminogen activator inhibitors release by RC cells at different times throughout this proliferation/differentiation sequence. Cultures in log phase growth (day 4), when first multilayering (day 7) and when bone nodules were forming (day 13) were exposed to either TGF-beta, IL-1 alpha, EGF or vehicle. Conditioned medium was collected after 6 and 24 h and plasminogen activators and plasminogen activator inhibitors were analysed by fibrin autography and reverse fibrin autography. TGF-beta-mediated changes in plasminogen activator were apparent at day 4. By day 7 two molecular weight species of plasminogen activator were noted; a 65 kDa species, prominent at 24 h exposure was blocked by anti-tPA antibody, and a 38 kDa plasminogen activator, prominent after 6 h of stimulation was not blocked by anti-tPA antibody. Plasminogen activator-plasminogen activator inhibitor complexes are also increased. IL-1 alpha caused similar increases in plasminogen activator and plasminogen activator inhibitor with maximal activity measured at day 13, coincident with the time when bone nodules were forming. EGF-mediated changes were less by comparison. TGF-beta significantly decreased bone nodule formation after both a 6 and 24 h serum-free exposure, whereas IL-1 alpha and EGF decreased nodule number only after the 24 h exposure. The data suggest that the three factors influence the expression of plasminogen activator and plasminogen activator inhibitor by RC cells and their effect is different at different times of culture.
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PMID:Modulation of plasminogen activators and plasminogen activator inhibitors by TGF-beta, IL-1 alpha and EGF in fetal rat calvaria cells at different times of culture. 206 16

Plasminogen activator inhibitor-type 1 (PAI-1) was identified in extracts of Lewis lung carcinoma, and its immunohistochemical localization was studied together with that of urokinase-type (u-PA) and tissue-type (t-PA) plasminogen activators. All primary tumors (n = 11) contained heterogeneously distributed immunoreactivity against each of the three components. Most often, areas that contained u-PA immunoreactivity also contained PAI-1 immunoreactivity. However, several areas showed a strong u-PA immunoreactivity, but no or low PAI-1 immunoreactivity. The latter staining pattern was only found in peripheral areas, and usually in areas with histological signs of tissue destruction. Lung metastases always contained u-PA immunoreactivity, while PAI-1 immunoreactivity was found in most, but not all, metastases. t-PA immunoreactivity was found in a few scattered tumor cells, in primary carcinomas as well as metastases. Controls that included absorption with highly purified antigen preparations and immunoblotting, indicated that all the immunoreactivity represented genuine PAI-1, u-PA and t-PA, respectively. The results are consistent with an assumption that the plasminogen activation system, and particularly u-PA and PAI-1, plays a role in regulation of breakdown of extracellular matrix proteins during invasive growth in this carcinoma.
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PMID:Plasminogen activator inhibitor-type 1 in Lewis lung carcinoma. 210 45

Plasminogen activator (PA) was located in newborn rat osteoclasts using a single-cell assay. Immunohistochemistry using biotin-streptavidin-peroxidase indicated the presence of both tissue-type plasminogen activator (tPA) and urokinase (uPA) within the cytoplasm of osteoclasts isolated from newborn rat long bones. Electron microscopic immunohistochemistry using the biotin-streptavidin-colloidal gold system on L.R. Gold thin resin sections of undecalcified, newborn rat tibial metaphyseal trabecular bone identified these proteases in the lysosomal network of osteoclasts. uPA was also localized in marrow macrophage lysosomes, but tPA was not detected in these cells. The localization of these enzymes within osteoclasts may imply their involvement in bone resorption.
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PMID:Identification of plasminogen activator in osteoclasts. 211 31

The plasma level of tissue plasminogen activator antigen (t-PA-Ag) was examined in 86 patients with polycythemia (29 polycythemia vera, 11 secondary polycythemia and 46 with spurious polycythemia) and 24 healthy volunteers. Tissue plasminogen activator antigen was significantly decreased in patients with polycythemia vera in comparison with healthy controls. On the other hand, in patients with spurious polycythemia and secondary polycythemia t-PA-Ag concentration was significantly increased. There was no significant difference in t-PA-Ag levels in polycythemic patients with or without thromboembolic disease. A significant correlation was detected between t-PA-Ag level and hemoglobin or hematocrit concentration in patients with polycythemia vera (p = 0.02, r = 0.43). However, in patients with secondary polycythemia and spurious polycythemia, no significant correlation between t-PA-Ag and hemoglobin level was found. Plasminogen activator inhibitor (PAI) levels in patients with polycythemia vera and healthy volunteers did not differ significantly.
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PMID:Tissue plasminogen activator levels in different types of polycythemia. 211 15

Slow and fast contracting muscles differ in their innervation and electrophysiological properties as well as in their regenerating potentialities. The purpose of the present work was to investigate the expression of plasminogen activators and its possible relation to each type of muscle. Slow (Soleus) and fast (Extensor Digitorum Longus) muscles were obtained from white Wistar rats. Before sectioning the muscles, the euthanized rats were perfused with cold phosphate buffer saline to avoid interference by circulating proteases and inhibitors. Muscle extracts were pounded in an ice-cold Potter tube. Plasminogen activators (PAs) were assayed by fibrin zymography and by both liquid and solid-phase fibrin spectrophotometric assays for the detection of PAs activity. Both urokinase (uPA) and tissue-type plasminogen activator (tPA) activities corresponding to proteins of 38 kDa and 65 kDa molecular masses, were detected in the extracts. Slow muscles contained higher amounts of both activators than fast muscles, but the relative amount of uPA was higher in both types of muscles. In addition, the characteristics of each type of extracts differed somewhat: the fast muscle activity curve was typical of an accelerating process, while the slow muscle curve showed an activity probably related to already formed plasmin or to some other trypsin-like enzyme. These results suggest that the amount of plasminogen activators could be a new criterion of discrimination between slow and fast skeletal muscles.
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PMID:Slow and fast rat skeletal muscles differ in their plasminogen activator activities. 211 33

The fibrinolytic system of the peritoneum is important in the pathogenesis of adhesions. Plasminogen activator activity is depressed by serosal types of injury, which cause ischemia. Ischemic peritoneum induces fibrinous adhesions. When local fibrinolytic activity is impaired, persistence of fibrin and organisation of the fibrinous adhesions may occur. Peritoneal adhesion in rabbits were created by drying the serosa of the uterine horns and by introducing a small amount of blood intraperitoneally. In one group of rabbits tissue-type plasminogen activator (t-PA) was given intraperitoneally at the end of the operation: another group served as controls. 48 rabbits were operated on. The animals were killed 3 h, 1, 3 and 7 days postoperatively for evaluation of adhesions. All animals of the control group had adhesions. The animals of the t-PA group had less adhesions than the animals of the control group.
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PMID:Prevention of postoperative adhesions by tissue-type plasminogen activator (t-PA) in the rabbit. 212 63


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