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)

A family is described in which venous thrombosis developed in five members as early as 14 years of age. Routine coagulation studies, plasma antithrombin III, factor V, plasminogen, beta-thromboglobulin, fibrinopeptide A, prothrombin fragment F1+2, and thrombin-antithrombin III complex were all within normal limits. However, defective release of vascular plasminogen activator was observed on several occasions in all five subjects as compared with a control population of 125 persons (0.04 Committee on Thrombolytic Agents [CTA] units/ml plasma as compared with 0.21 CTS units/ml). In addition, levels of factor VII/von Willebrand's factor were significantly elevated above the normal range in this pedigree.
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PMID:Venous thrombosis in a family with defective release of vascular plasminogen activator and elevated plasma factor VIII/von Willebrand's factor. 640 91

Studies on the effect of DDAVP both in vitro and in vivo are reported. In order to define the extent of the DDAVP induced rise of circulating endothelial cell proteins in normal individuals and the endothelial cell defect in von Willebrand's disease (vWd) we have measured the effect of intravenous DDAVP on a range of possible endothelial cell markers in normal subjects and in patients with mild haemophilia and vWd. In a series of double blind cross over studies on normal volunteers we have tested the effect of naloxone, DDAVP or saline on circulating levels of factor VIII related activities (VIIIR) and plasminogen activator (PA). The results confirmed the effect of DDAVP on circulating levels of VIIIR and PA but showed that it did not induce release of these activities from cultured endothelial cells in vitro nor did it influence circulating levels of other endothelial cell markers including fibronectin, antithrombin III and platelet factor 4. Infusion of nalaxone did not significantly alter circulating levels of VIIIR or PA nor the response of these to DDAVP suggesting that normally these activities are not subjected to a vasopressin drive.
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PMID:The effect of desamino-D-arginine vasopressin (DDAVP) and naloxone infusions on factor VIII and possible endothelial cell (EC) related activities. 643 Mar 37

We have studied vessel wall function in two groups of patients with chronic renal failure - 1) conservative treatment only and 2) maintenance hemodialysis. Three proteins synthesized by vascular endothelium-plasminogen activator (PA), factor VIII related antigen (VIII:RAg) and antithrombin III (ATIII) - were assayed before and after a fifteen minute period of venous occlusion. The release of PA was significantly reduced in patients on maintenance hemodialysis as compared to both undialyzed uremics and controls. Lesser amounts of VIII:RAg were also released by hemodialysis patients than by undialyzed uremics. These defects, which are suggestive of vessel wall dysfunction on maintenance hemodialysis, may contribute to the high incidence of arteriopathy and thrombotic disease observed in this group of patients.
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PMID:Impaired vessel wall response to venous occlusion in patients with chronic renal failure on maintenance hemodialysis. 644 60

Fibrinolytic and coagulation components were assayed in six patients with pheochromocytoma. Blood samples and a specimen from a superficial hand vein were obtained before, and six months after removal of the tumour. Vascular plasminogen activator (PA) activity in the vein wall was significantly increased in all patients who all had increased concentrations of urinary adrenaline, or noradrenaline, or of both. After adrenalectomy catecholamines were normalized and the PA activity was within normal range in all patients. There were no significant differences in factor VIII, antithrombin III, fibrinolytic activity, plasminogen or inhibitors of the plasminogen activation in plasma.
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PMID:Increased vascular plasminogen activity in patients with pheochromocytoma. 666 93

We have characterized the molecular properties of the plasminogen activators in different cell types comprising the immature and the estrogen-stimulated rat uterus and in rat uterine luminal fluid. There were two plasminogen activators in the immature (day 20) rat uterus with apparent molecular weights, determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, of 70,000 and 46,000. Both plasminogen activators were present in epithelial and in stromal plus myometrial cell fractions of the immature uterus, and after stimulation by 17 beta-estradiol, no new plasminogen activators were detected in either cell fraction. The Michaelis constants (Km) for the activation of dog plasminogen by extracts from epithelial cells and from stromal plus myometrial cells obtained from either immature or 17 beta-estradiol-stimulated uteri were similar (approximately 11 microM). The maximal velocity (Vmax), normalized to protein concentration, increased 2.5-fold in the stromal plus myometrial cell fraction and 6.5-fold in the epithelial cell fraction, upon hormone stimulation (2 micrograms 17 beta-estradiol/day X rat for 3 days). The greatest concentration of plasminogen activator activity was found in the luminal fluid from estrogen-stimulated uteri, where the Vmax per mg protein was more than 10-fold greater than that in the cell fractions from estrogen-stimulated uteri. The plasminogen activator activity of luminal fluid was inhibited by diisopropyl fluorophosphate and rho-nitrophenyl rho-guanidinobenzoate, was not inhibited by human alpha-1-proteinase inhibitor and human antithrombin III, and was inhibited by high, but not low, concentrations of soybean trypsin inhibitor and bovine pancreatic trypsin inhibitor. These studies indicate that the plasminogen activators in different cell types comprising the uterus are similar and show that the estrogen enhancement of uterine plasminogen activator activity is the result of an increase in Vmax. The presence, upon hormone stimulation, of an apparent concentration gradient of increasing plasminogen activator activity through the uterus from myometrium to epithelium to luminal fluid may be a reflection of the dynamic role of this protease in the physiology of the uterus.
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PMID:Plasminogen activators in tissues of the immature and estrogen-stimulated rat uterus and in uterine luminal fluid: characterization and properties. 668 1

It has been shown that physical exercise increases blood fibrinolytic potential, primarily by inducing a release of extrinsic plasminogen activator from the vessel wall. Synthetic estrogens have also been reported to influence fibrinolytic activity. The effect of exercise and the possible additional effect of oral contraceptive agents (OCA) on the fibronolytic system were studied in 20 competitive female rowers. Ten females used OCA (users), and 10 others did not (nonusers). All participants were subjected to standardized exhaustive exercise. Preexercise data revealed higher factor XII, total plasminogen, and free plasminogen levels together with a significantly lower C1-inactivator level in the group of users. No differences were observed in prekallikrein, high-molecular-weight kininogen, alpha 2-antiplasmin, alpha 2-macroglobulin, antithrombin III, and histidine-rich glycoprotein plasma levels. The factor XII-dependent fibrinolytic activator activity and the extrinsic (tissue-type) plasminogen activator were significantly higher; however, the urokinase-like fibrinolytic activator activity was significantly lower. These observations suggest a greater susceptibility to activation of the fibrinolytic pathways during OCA medication. Exercise resulted in a decrease of all factors under study but an increase in all fibrinolytic activities. No differences were observed between the two groups in the percentages of change that occurred with exercise.
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PMID:Effect of exercise and oral contraceptive agents on fibrinolytic potential in trained females. 672 68

The effect of orally-administered stanozolol, 5 mg b.d. on fibrinolysis, coagulation and on various haematological and biochemical parameters have been studied in 16 healthy adults, 8 males and 8 females. Statistically significant enhancement of extrinsic (tissue-type) plasminogen activator activity was detected in all subjects studied. This was associated with significant increases in plasma plasminogen and a concomitant reduction in histidine-rich glycoprotein. There were no changes in plasma urokinase activity. Changes in the coagulation system included significant reduction in plasma fibrinogen and elevation of protein C and antithrombin III. Changes in plasma lipids included significant reduction of HDL cholesterol associated with an increase in LDL triglycerides. No change occurred in total cholesterol. There were no major differences between the sexes, nor were there serious side effects. The effects of stanozolol on extrinsic (tissue-type) plasminogen activator activity, "free" plasminogen, protein C and antithrombin III, argue strongly in favour of its therapeutic potential.
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PMID:Stanozolol-induced changes in fibrinolysis and coagulation in healthy adults. 674 May 47

We prospectively studied the hemostatic system of ten persons bitten by the Eastern diamondback rattlesnake (Crotalus adamanteus) during 1978-1980. Blood was drawn when the patients arrived in the emergency room and every 6 hr thereafter. All envenomated victims developed incoagulable blood (defined by a thrombin time greater than or equal to 120 sec, normal less than 20 sec). Platelet counts and plasma levels of antithrombin III and factors II and VIII were not drastically altered, which distinguished this disorder from classic disseminated intravascular coagulation. Fibrinogen levels were markedly decreased (mean coagulable level of 0 mg/dl and antigenic levels of 99 mg/dl). Plasminogen levels were 20% of normal, alpha-2-plasminogen inhibitor was 17% of normal, and plasminogen activator was 20 times normal. Levels of fibrin degradation products peaked at a mean of 7,680 micrograms/ml. The magnitude and duration of the coagulopathy were proportional to the clinical severity of envenomation. Treatment with antivenin blunted the coagulopathy. Because venom from the Eastern diamondback rattlesnake does not directly activate plasminogen, we conclude that coagulopathy following envenomation by that reptile appears to be due to partial proteolysis of fibrinogen with secondary activation of plasminogen by released plasminogen activator, probably of endothelial origin.
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PMID:Mechanism of defibrination in humans after envenomation by the Eastern diamondback rattlesnake. 685 33

The role of the microvascular endothelium in the integration of inhibitory and catabolic pathways of hemostasis is discussed in light of recent findings of direct biochemical links between endothelium and regulatory plasma proteins. These findings include the following: (1) On the vascular endothelium, a cofactor for antithrombin III (with an activity comparable to stationary phase heparin) catalyzes thrombin inhibition in vivo. (2) A second cofactor on endothelium binds thrombin in a manner that enhances by several orders of magnitude the ability of thrombin to activate protein C. (3) Activated protein C has both anticoagulant and catabolic activities; anticoagulant activity results from the susceptibility of factors Va and VIIIa to inactivation by activated protein C, whereas catabolic activity arises from the stimulation by activated protein C of the release from endothelium of fibrin-dependent plasminogen activator. (4) Because it requires fibrin as a cofactor, the plasminogen activator lyses clots without provoking fibrinogenolysis. Location of these activities on endothelium separates coagulation in time and space from catabolic pathways, and provides for their expression after the initiation of hemostasis.
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PMID:The control of hemostasis. Role of endothelium in the regulation of inhibitory and catabolic pathways. 689 31

Experiments were initiated to gain an understanding of the environmental factors that may regulate injury-induced mitosis and wound healing in the mammalian lens. The addition of thrombin or trypsin to a completely defined serum-free medium stimulated cell proliferation and migration in the cultured mammalian lens. A 30 min exposure of the rabbit lens to highly purified thrombin induced DNA synthesis and mitosis throughout the normally amitotic central region of the lens epithelium. Lenses exposed to thrombin for 24 or 52 hr exhibited cell migration and mitosis. The mitotic response brought about by thrombin was totally curtailed by hirudin and antithrombin III. Prothrombin, papain, or pepsin were not mitogenic toward the cultured lens. A 30 min exposure of the lens to trypsin induced cell division and migration, a response that did not occur in the presence of trypsin inhibitors. Lenses cultured in a trypsin-containing medium for 24 hr showed extensive cell death throughout the entire central region of the epithelium. In addition, an endogenous serine protease, plasminogen activator, was detected in cultured rabbit lens epithelial cells. Wound healing in the lens in vivo is accompanied by cellular migration and mitosis. The present experiments demonstrate that a highly purified serine protease, thrombin, which is present at the site of lenticular injury in vivo, is capable of inducing mitosis and migration in lens epithelia. The results suggest that thrombin or other exogenous and endogenous serine proteases might contribute to the process of wound healing in the ocular lens.
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PMID:Thrombin induces cell division in rabbit lenses cultured in a completely defined serum-free medium. 719 16


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