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)

To evaluate the toxicity of lead on the blood fibrinolytic system, vascular endothelial cells from human umbilical vein were cultured in the presence of lead and the content of tissue plasminogen activator antigen (t-PA:Ag) released into the medium was determined by enzyme immunoassay. It was found that lead significantly decreased the t-PA:Ag release from the cells. Although heavy metals including cadmium, mercury, cobalt, manganese, nickel, zinc and copper as well as lead each had an inhibitory effect, lead was the potent inhibitor. Lead significantly disturbed thrombin up-regulation of t-PA:Ag release and significantly amplified endothelin-1 down-regulation of it. Incorporation of [3H]thymidine into the acid-insoluble fraction of the cell layer was significantly increased by lead; however, that of [14C]leucine was unchanged by the metal. In lead-treated cells, a significant accumulation of lead was observed but calcium content was increased slightly. From these results, it was suggested that lead decreased the release of t-PA:Ag from cultured endothelial cells without nonspecific inhibition of protein synthesis; lead may stimulate the calcium-dependent down-regulation of endothelial cell t-PA:Ag release by calcium or by mimicking calcium.
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PMID:Inhibitory effect of lead on the release of tissue plasminogen activator from human vascular endothelial cells in culture. 160 31

A previous study from this laboratory, using morphological and biochemical (LDH release) parameters, has shown that tungsten carbide-cobalt dust exhibits a greater cytotoxicity toward isolated macrophages than cobalt metal powder alone. The present study extends this comparison by examining additional biological parameters. Glucose uptake and superoxide anion production by isolated macrophages were significantly more depressed by the tungsten carbide-cobalt mixture (WC-Co) than by cobalt alone (Co) while pure tungsten carbide (WC) had no effect or even stimulated the cells. For glucose-6-phosphate dehydrogenase and cell-associated plasminogen activator (PA) activities, no difference between Co and WC-Co dusts was observed. These observations add further evidence to our previous findings regarding the different biological reactivity of cobalt metal alone or mixed with tungsten carbide.
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PMID:Biological responses of isolated macrophages to cobalt metal and tungsten carbide-cobalt powders. 165 97

We investigated the effect of cadmium (0.5, 1.0 or 2.0 microM) on the release of plasminogen activator inhibitor-1 antigen (PAI-1:Ag) from cultured human vascular endothelial cells. It was found that cadmium at 1.0 and 2.0 microM significantly increased the PAI-1:Ag release from the cells after a 24-h incubation. However, the tissue plasminogen activator antigen (t-PA:Ag) release was not changed by the metal. Although nickel as well as cadmium increased the PAI-1:Ag release, the other heavy metals including cobalt, zinc and copper did not exhibit such a stimulatory effect. The incorporation of [3H]leucine into the acid-insoluble fraction of the cell layer was unchanged by cadmium, suggesting that the metal may stimulate the synthesis of PAI-1 without association with generalized increase in protein synthesis. Cadmium at 1.0 and 2.0 microM significantly decreased the t-PA activity in the medium. The present study showed that cadmium increases the release of PAI-I:Ag from cultured endothelial cells without non-specific stimulation of protein synthesis. The decrease in the t-PA activity suggests an implication of cadmium in vascular lesion which is mediated by anti-fibrinolytic activity.
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PMID:Cadmium stimulation of plasminogen activator inhibitor-1 release from human vascular endothelial cells in culture. 824 47

Hypoxia underlies a number of biologic processes in which cellular migration and invasion occur. Because earlier studies have shown that the receptor for urokinase-type plasminogen activator (uPAR) may facilitate such events, we studied the effect of hypoxia on the expression of uPAR by first trimester human trophoblasts (HTR-8/SVneo) and human umbilical vein endothelial cells (HUVEC). Compared with control cells cultured under standard conditions (20% O2), HTR-8/SVneo cells and HUVEC cultured in 1% O2 expressed more uPAR, as determined by flow cytometric and [125I]-prourokinase ligand binding analyses. Increased uPAR expression paralleled increases in uPAR mRNA. The involvement of a heme protein in the hypoxia-induced expression of uPAR was suggested by the observations that culture of cells with cobalt chloride, or sodium 4, 5-dihydroxybenzene-1,3-disulfonate (Tiron), an iron-chelating agent, also stimulated uPAR expression, and that the hypoxia-induced uPAR expression was inhibited by adding carbon monoxide to the hypoxic atmosphere. Culture of HTR-8/SVneo cells with vascular endothelial growth factor (VEGF) did not increase uPAR mRNA levels, suggesting that the hypoxia-mediated effect on uPAR expression by these cells did not occur through a VEGF-dependent mechanism. The functional importance of these findings is suggested by the fact that HTR-8/SVneo cells cultured under hypoxia displayed higher levels of cell surface plasminogen activator activity and greater invasion through a reconstituted basement membrane. These results suggest that hypoxia may promote cellular invasion by stimulating the expression of uPAR through a heme protein-dependent pathway.
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PMID:Hypoxia stimulates urokinase receptor expression through a heme protein-dependent pathway. 955 86

The aim of this study was to evaluate the characteristics of resorption and the pattern of bacterial collonisation of polyglycolic and polylactic resorbable membranes under controlled experimental conditions. A removable cobalt-chromium device was applied to the lower jaw of 5 students for a period of 4 weeks. 8 composite resin chambers were glued to the device, 4 on each side of the mouth. A small piece of PLA/PGA membrane separated the composite chambers into 2 parts. The subjects wore the devices 24 h a day, except for the time necessary for oral hygiene procedures, during which time, the structure was submerged in a 0.2% chlorexidine solution. Every week, 2 of the chambers were removed; one was processed for scanning electron microscopy, to be observed both on the external and internal surface, and the other one for light microscopy examination. Both the electron microscopic and histologic observations showed a progressive increase in the plaque layer on the external surface of the membrane during the period of observation. The light microscopy showed an early invasion of the membrane, starting about 1 week after the exposure. On all the 3- and 4-week specimens, a complete bacterial invasion over the whole thickness of the membrane was visible. After 3 weeks of plaque accumulation, bacterial colonisation of the inner portion of the membrane was detectable in all the specimens. At 3-weeks, we observed in the light microscopy group in 4 out of 5 specimens, a large reduction of the thickness of the material and small voids in the membrane structure. In 1 specimen, the membrane was no more detectable. Only in 5 specimens of the 4-week group was the membrane still recognizable, though reduced to fragments. In conclusion, once exposed to the oral cavity, the PLA/PGA membranes start to resorb in the early stages: this process concludes itself between the 3rd and 4th weeks of exposure. However, the particular conditions of the experimental design nevertheless classify this study as an in vitro, more than as an in vivo experimentation.
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PMID:Bacterial penetration through Resolut resorbable membrane in vitro. An histological and scanning electron microscopic study. 958 53

In review the results of investigation of plasminogen(Pg) activation by antiplasminogen monoclonal antibody IV-1c have been presented. Antigenic determinant of IV-1c was localized in Val709-Gly718 site of Pg protease domain. IV-1c completely inhibited the Pg activation by streptokinase, but increased the rate of Pg activation by t-PA and urokinase. Catalytic properties of plasmin in complex with IV-1c were studied. It was found that IV-1c induced catalytic activity in Pg-IV-1c complex. It was shown that Pg and IV-1c interacts in complex by two-centre mechanism: IV-1c binds with Pg by paratope and by N-terminal lysine of gamma-chain and Pg binds to IV-1c by one of the lysine binding sites and by V709-G718 site of protease domain. The influence of pH, temperature, 1.5 mM Ca2+, Mg2+, Sr2+, Ba2+, Co2+, Ni2+ cations and 10 mM Cl-, F-, Ac-, SO4(2-), HPO4(2-) anions on lag and fast phases of Pg activation by VI-1c was investigated. It was revealed that Val709-Gly718 site was determining in Pg activation by IV-1c and streptokinase.
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PMID:[Plasminogen activation by antiplasminogen monoclonal antibody IV-1C. Properties and mechanism of reaction]. 1120 Apr 60

We investigated the effect of cholesterol and the metalloporphyrins cobalt mesoporphyrin (CoMP) and chromium protoporphyrin (CrPP) on phospholipase A(2) (PLA(2)) activity and the consequent hepatic mitochondrial stability as well as on lipid concentrations. Our studies revealed that on administration of cholesterol, CrPP, CoMP as well as simultaneous adminstration of cholesterol and CrPP, there was an inhibition of PLA(2) activity. These moieties may therefore, be agents for preventing destabilisation of the mitochondrial membrane and the consequent pathological conditions which may arise due to membrane lysis. Our results revealed that cholesterol administration increased phospholipid concentration, albeit by modest amounts. Although the independent administration of metalloporphyrins led only to minor elevations in phospholipid concentration, the simultaneous administration of cholesterol and CrPP generated a steep elevation in the concentration of total phospholipid. Since cholesterol inhibits PLA(2) activity it has the potential of being therapeutic agent for preventing the pathological conditions which may arise due to membrane lysis.
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PMID:Inhibitory effect of metalloporphyrins in conjunction with cholesterol on hepatic phospholipase A(2) activityin vivo in rats. 2310 57

Just add water: The copolymerization of propylene oxide and CO2 catalyzed by a cobalt complex is tolerant to the addition of water as chain-transfer reagent to afford polyols (HO-(PPC)-OH) with narrow molecular weight distributions (see picture; PPC=poly(propylene carbonate); PLA=polylactide). The addition of an organocatalyst to these polyols in the presence of lactides produces well-defined triblock copolymers (PLA-b-PPC-b-PLA).
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PMID:A one-pot synthesis of a triblock copolymer from propylene oxide/carbon dioxide and lactide: intermediacy of polyol initiators. 2394 53

Hodological and genetic differences between dorsal (DH) and ventral (VH) hippocampus may convey distinct behavioral roles. DH is responsible for mediating cognitive process, such as learning and memory, while VH modulates neuroendocrine and emotional-motivational responses to stress. Manipulating glutamatergic NMDA receptors and nitric oxide (NO) systems of the hippocampus induces important changes in behavioral responses to stress. Nevertheless, there is no study concerning functional differences between DH and VH in the modulation of behavioral responses induced by stress models predictive of antidepressant effects. Thus, this study showed that reversible blockade of the DH or VH of animals submitted to the forced swimming test (FST), by using cobalt chloride (calcium-dependent synaptic neurotransmission blocker), was not able to change immobility time. Afterwards, the NMDA-NO system was evaluated in the FST by means of intra-DH or intra-VH administration of NMDA receptor antagonist (AP7), NOS1 and sGC inhibitors (N-PLA and ODQ, respectively). Bilateral intra-DH injections after pretest or before test were able to induce antidepressant-like effects in the FST. On the other hand, bilateral VH administration of AP-7, N-PLA and ODQ induced antidepressant-like effects only when injected before the test. Administration of NO scavenger (C-PTIO) intra-DH, after pretest and before test, or intra-VH before test induced similar results. Increased NOS1 levels was associated to stress exposure in the DH. These results suggest that the glutamatergic-NO system of the DH and VH are both able to modulate behavioral responses in the FST, albeit with differential participation along time after stress exposure.
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PMID:NMDA-NO signaling in the dorsal and ventral hippocampus time-dependently modulates the behavioral responses to forced swimming stress. 2701 28