Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
 47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prostaglandin E2 (PGE2)-like activity was measured in osteonecrotic femoral heads caused by high doses of methyl prednisolone acetate in rabbits. Serum levels of cholesterol, total lipids, free fatty acids, alkaline phosphatase, SGOT and lipase were also determined. There were increases in local tissue PGE2-like activity, serum cholesterol, total lipid and free fatty acid levels in rabbits with steroid-induced osteonecrosis as compared to the controls. The rabbits given aprotinin together with the steroid showed significant decreases in serum cholesterol and lipid levels coupled with a marked increase in the local PGE2-like activity. Aprotinin prevented osteonecrosis induced by steroids. The results are discussed in the light of the relevant literature.
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PMID:Isolation of prostaglandin E2-like material from osteonecrosis induced by steroids and its prevention by kallikrein-inhibitor, aprotinin. An experimental study in rabbits. 620 27

To explore the possible vasoregulatory role of renal prostaglandins during liver disease, excretory rates of PGE2, PGF2 alpha, and a metabolite of PGI2, 6k-PGF1 alpha, were determined before and after chronic ligation of the common bile duct in 23 dogs. Bile duct ligation for 50 +/- 3.7 days (mean +/- SEM) significantly increased serum bilirubin and alkaline phosphatase. PGE2, PGF2 alpha, and 6k-PGF1 alpha excretion rates were significantly (p less than 0.01) increased following chronic bile duct ligation, by approximately 100%, 80%, and 500%, respectively, with similar increments in both ascitic and nonascitic animals. In 10 sham-ligated animals, PGE2, PGF2 alpha, and 6k-PGF1 alpha excretion rates were unchanged. In 6 dogs sequential measurements of urine prostaglandins indicated that PGE2 and 6k-PGF1 alpha excretion were significantly increased at 2, 4, and 6 weeks after ligation, whereas the increase in PGF2 alpha excretion was not significant until 6 weeks. Indomethacin (2 mg/kg) reduced prostaglandin excretion by 65% to 90% and significantly increased arterial pressure, decreased glomerular filtration rate and renal blood flow, and increased renal vascular resistance from 0.53 +/- 0.09 to 0.90 +/- 0.13 mm Hg/ml/min. Fractional renal blood flow, assessed by microspheres, was disproportionately reduced in the inner cortex after prostaglandin inhibition in the chronic bile duct ligation group. Indomethacin did not significantly alter renal function in sham animals, despite comparable reductions in prostaglandin excretion. These data demonstrate that, in dogs with experimental liver disease produced by chronic bile duct ligation, renal prostaglandin synthesis is increased, and the enhanced synthesis of vasodilatory prostaglandins serves to maintain renal blood flow and glomerular filtration rate.
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PMID:Importance of renal prostaglandins in control of renal function after chronic ligation of the common bile duct in dogs. 654 81

A procedure was developed to investigate the electrolyte metabolism of human trabecular bone and its regulation in vitro, in particular the influence of prostaglandins. Trabecular bone was prepared from femoral heads of patients who had undergone hip replacement surgery for coxarthrosis. 500 mg samples were incubated in modified EAGLE's minimal essential medium. Net electrolyte movements between bone and incubation medium were measured. During 6 hours of incubation PGE2 caused an increase in the release of calcium and magnesium from bone into incubation medium as compared to controls. The effect of PGE2 was dose-dependent and comparable to that of human parathyroid hormone 1-34 (hPTH 1-34) whereas hPTH 3-34 had no effect. Human calcitonin (hCT) caused a decrease in the release of calcium and magnesium. PGE2 was found to be the most potent prostaglandin. PGE1 and PGF2 alpha had about 50% and PGF1 alpha about 40% of the potency of PGE2. PGA1 and PGA2 had no effect. The effect of PGE2 could be completely inhibited by hCT and was not further enhanced by hPTH 1-34. Magnesium movement was affected in the same way as calcium movement, while phosphate movement and release of alkaline phosphatase and hydroxyproline from bone into incubation medium were not affected by prostaglandins.
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PMID:Influence of prostaglandins on electrolyte metabolism of human trabecular bone in vitro. 659 50

Prostaglandins seem to be involved in the pathogenesis of juxtaarticular osteopenia in rheumatoid arthritis. Therefore the influence of prostaglandins on in vitro electrolyte metabolism of human trabecular bone was tested. Trabecular bone was prepared from femoral heads of patients who had undergone hip replacement surgery for coxarthrosis. 500 mg samples of trabecular bone were incubated in modified Eagle's minimal essential medium. Net electrolyte movements between bone and incubation medium were measured. PGE2 caused an increase in the release of calcium (Ca) and magnesium (Mg) from bone into incubation medium as compared to controls (PGE2 1 micrograms/ml: Ca = 0.87 +/- 0.09 mmol/l*, Mg = 0.44 +/- 0.03 mmol/l*; controls: Ca = 0.81 +/- 0.09 mmol/l, Mg = 0.41 +/- 0.05 mmol/l; n = 15, *p less than 0.001). The effect of PGE2 was dose-dependent and comparable to the effect of human parathyroid hormone 1-34 (hPTH 1-34). PGE2 turned out to be the most potent prostaglandin on human trabecular bone. PGE1 and PGF2 alpha had about 50% and PGF1 alpha about 40% of the potency of PGE2. PGA1 and PGA2 had no effect. The effect of PGE2 could be completely inhibited by human calcitonin (hCT), similar to the inhibition of the effect of hPTH 1-34 by hCT. The effect of PGE2 was not further enhanced by hPTH 1-34. Magnesium metabolism was affected in all experiments in the same way as calcium metabolism. Phosphate metabolism, release of alkaline phosphatase and hydroxyproline from bone into incubation medium were not affected by prostaglandins.
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PMID:[Effect of prostaglandins on in vitro electrolyte metabolism in human spongiosa]. 659 15

Prostaglandin E2, colchicine and imidazole, known to enhance and inhibit thromboxane A2 (TxA2) synthesis respectively and chloroquine, a PGE1 synthesis enhancer and PGE2 antagonist can alter the leukocyte alkaline phosphatase (LAP) enzyme activity. Thromboxane A2 and other related prostaglandins (PGs) are known to bind to DNA and thus possibly regulate DNA action. It is proposed here that prostaglandins are able to modify LAP activity by their action on the DNA and thus the Gene that codes for LAP. This hypothesis envisages that normally there are specific receptors on the genes for PGs. Taking LAP enzyme system as the model, it is proposed that the affinity of TxA1, TxA2, PGE2 and PGE1 to the operator is more than to that of the repressor. But when the levels of TxA2, PGE2 and PGE1 are in excess, all the receptors on the operator are not only completely occupied but they are also able to bind to repressor in sufficient amounts to transiently switch off the LAP synthesis by the structural gene. It is further envisaged that the affinity of the PG receptors on the operator and repressor systems of the operon is greatest for TxA1 and least for PGE2 (TxA1 greater than TxA2 greater than PGE1 greater than PGE2). This hypothesis though simply in its model explains all the variables obtained in our studies on the effect of PGs on the LAP activity. This concept by itself or a suitable modification, may explain the role of PGs in the pathogenesis of cancer. It will be interesting to study, in the light of this hypothesis, the role of the PG system on DNA repair mechanism, m-RNA and t-RNA synthesis and gene action in several systems.
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PMID:Prostaglandins and gene action: possible relevance to the effect of PG system on leukocyte alkaline phosphatase enzyme activity. 668 5

Male rats were treated with subcutaneous vehicle or 16,16-dimethyl-PGE2 (dmPGE2, 100 micrograms per kg), 24, 18 and 0.5 hr prior to and 6, 24 and 30 hr after challenge with oral alpha-naphthylisothiocyanate (ANIT, 30 mg per kg). Forty-eight hours after challenge, rats were sacrificed by decapitation; serum and liver samples were taken for biochemical and histological analysis, respectively. Rats treated with vehicle (2% ethanol in saline) and ANIT exhibited elevations in alkaline phosphatase, SGPT and bilirubin as well as cholangitis and mild parenchymal necrosis. Rats treated with dmPGE2 and ANIT had normal serum biochemical findings, no necrosis and only mild proliferation of bile duct epithelium. Thus, dmPGE2 may be able to protect the rat liver against the deleterious effects of orally administered ANIT.
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PMID:16,16-dimethyl-PGE2 protection against alpha-naphthylisothiocyanate-induced experimental cholangitis in the rat. 674 53

Prostaglandins (PGs) are naturally occurring, cyclic, unsaturated fatty acids which possess a wide range of potent biological activities. PGs have been found in human middle ear effusions and might have implications for understanding the inflammation and possibly the bone resorption seen in chronic otitis media. We have measured PGs by radioimmunoassay in middle ear effusions (MEE) from experimentally induced serous otitis media (SOM) and purulent otitis media (POM) in chinchillas. PGE2 levels were significantly higher in the POM group compared to the SOM group. We have also demonstrated that chinchilla middle ear mucosa can convert arachidonic acid (AA), a precursor of PGs, to PG by injecting 14C-AA into bullae and assaying using radiochromatography. This conversion was completely blocked by both indomethacin and aspirin given orally or by direct injection into the middle ear. We then injected 50 microgram of PGE2 into chinchilla bullae to assess its effect on the composition of MEE. First, the time course of PGE2 metabolism after its injection into the middle ear (ME) was determined by thin-layer chromatography (TLC) of labelled and unlabelled PGE2. Following this, serial daily injections of PGE2 and normal saline as control were made for one, three, and seven days. MEE and serum were collected and assayed for lactate dehydrogenase (LDH), acid and alkaline phosphatase, calcium, protein and hexosamine. Compared to the control, the levels of LDH, acid and alkaline phosphatase, calcium and protein were significantly elevated. Hexosamine levels were higher than the control at one and three days but did not differ significantly at seven days from the control. We have therefore demonstrated that chinchilla middle ear mucosa has the ability to synthesize PG from AA and suggest an active role for PGs in the inflammation and in the bone resorption seen in otitis media.
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PMID:Effect of prostaglandin on the composition of chinchilla middle ear effusion. 677 99

Bone remodelling is regulated at the local level by an incompletely elucidated cytokine network. In the present study we have determined the effect of interleukin-4 (IL-4), a cytokine produced by T lymphocytes and other cells, on the activity of murine osteoblasts. IL-4 (0.1-10 ng/ml) did not influence the proliferation rate of the osteoblast-like cell line MC3T3, but inhibited the expression of alkaline phosphatase. In long-term cultures supplemented with ascorbic acid and glycerophosphate such an effect was accompanied by a retardation of matrix mineralization. IL-4 also stimulated M-CSF expression by MC3T3 cells, both at the RNA and bioactivity levels. However, no stimulation of IL-1, IL-6, GM-CSF or PGE2 production was observed. An IL-4-induced inhibition of alkaline phosphatase expression and retardation of mineralization was also found in cultures of primary osteoblast-like cells isolated from neonatal mice calvariae. These results suggest that IL-4, probably released by cells within the bone marrow, may locally influence the activity of bone-forming cells.
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PMID:Interleukin-4 as a bone regulatory factor: effects on murine osteoblast-like cells. 754 94

1. We examined the factors which mediate the decrease of alkaline phosphatase (ALP) activity in human peridontal ligament (PDL) cells in response to cyclic tension-force. 2. ALP activity in human PDL cells obtained from three donors in response to cyclic tension-force (24% elongation) was 43% lower than that of the corresponding control. 3. ALP activity was decreased by the addition of conditioned medium obtained from the culture of the cells exposed to tension-force. 4. The inhibitory effect of the conditioned medium on ALP activity was partially abolished in the presence of indomethacin (10(-6) M) and IL-1 beta antibody (10 ng/well). Moreover it was almost completely abolished in the presence of both indomethacin and IL-1 beta antibody. 5. Treatment of PDL cells with exogenous PGE2 or IL-1 beta for 24 hr caused a dose-dependent decrease in ALP activity. Treatment with both PGE2 (10(-8) M) and IL-1 beta (1.25 x 10(-10) M) together decreased ALP activity by 47% compared with the non-treated control. 6. These findings suggest that ALP activity in PDL cells was decreased in response to the cyclic tension-force and that the decrease in ALP activity was mainly mediated by PGE2 and IL-1 beta produced by PDL cells in response to cyclic tension-force.
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PMID:Identification of factors mediating the decrease of alkaline phosphatase activity caused by tension-force in periodontal ligament cells. 787 49

The effects of PGE2 on mineralized bone nodule formation were studied in fetal rat calvarial (RC) cells in vitro. Continuous exposure of RC cells to 3 x 10(-8) M PGE2 induced a twofold increase in mineralized bone nodule formation and a 1.5-fold increase in alkaline phosphatase (ALPase) activity without affecting RC cell growth. These stimulatory effects were evoked by concentrations of 3 x 10(-9)-3 x 10(-6) M PGE2 and the maximal effect was observed with 3 x 10(-8) M PGE2. The in vitro effects of PGE2 were evident when RC cells were exposed to it on days 8-14 and 8-21, which correspond to the post-confluent culture stage, but no effects were observed when the cells were exposed on days 1-7, the growth stage. The ALPase activity was also higher (1.2-1.4-fold) when 3 x 10(-8) M PGE2 was added during the post-confluent stage. In order to determine the effect of PGE2 during the mineralization phase of bone nodules in the presence of a large population of osteoprogenitor cells, RC cells were exposed to dexamethasone for 7 days before PGE2 was added during the post-confluent stage. A significantly higher percentage of nodules mineralized were observed with 3 x 10(-8)-3 x 10(-9) M PGE2 (1.6- and 1.4-fold, respectively), than in control cultures. Analysis of the mineral-related proteins by EDTA extraction of bone nodules followed by electrophoresis and Stains-All staining revealed an increased total amount of osteopontin extracted from the mineralized matrix after PGE2 treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostaglandin E2 on mineralization of bone nodules formed by fetal rat calvarial cells. 789 84


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