Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Protein kinase C (PKC) isoforms are altered in colon tumors and upon exposure of intestinal mucosa to nutrients. We evaluated the effects of the PKC inhibitors staurosporine and calphostin C on human Caco-2 intestinal epithelial proliferation, motility, and differentiation. Motility was quantitated by monolayer expansion and the brush border enzymes dipeptidyl dipeptidase (DPDD) and alkaline phosphatase (AP) by synthetic substrate digestion. Staurosporine (0.03-1.0 ng/ml) and calphostin C (10(-12) M-10(-4) M) dose-dependently inhibited monolayer expansion and AP but stimulated DPDD. Proliferation was also inhibited but the effects of each inhibitor on motility, AP, and DPDD were preserved after mitomycin C proliferative blockade, suggesting that these effects were proliferation-independent. PKC inhibitors independently inhibit motility, AP and proliferation in human intestinal Caco-2 epithelial cells, but selectively stimulate the small intestinal differentiation marker DPDD. PKC may regulate small intestinal epithelial differentiation.
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PMID:Modulation of human CACO-2 intestinal epithelial cell phenotype by protein kinase C inhibitors. 972 28

Peptide YY (PYY) is produced by colonic mucosal endocrine cells and modulates gastrointestinal endocrine activity through specific Y-receptors. The direct effects of PYY on intestinal mucosal growth and differentiation remain uncharacterized. The abundance of PYY in colonic mucosa suggests that PYY acts locally to maintain colonocytic differentiation. We tested this hypothesis in human Caco-2 intestinal epithelial cells, which express alkaline phosphatase (AP) and dipeptidyl dipeptidase (DP), brush-border enzymes differentially concentrated in large and small intestinal mucosa, respectively. The effects of PYY on enzyme specific activity were compared with those of pancreatic polypeptide, neuropeptide-Y, vasoactive intestinal peptide, pentagastrin, bombesin, and selective Y1- and Y2-receptor agonists. Brush-border enzyme activity was assessed by AP and DP specific activity in cell lysates quantitated spectrophotometrically following synthetic substrate digestion. PYY, neuropeptide-Y, pancreatic polypeptide, and vasoactive intestinal peptide (10(-7) mol/L) stimulated AP activity. PYY brought about the greatest increase (38.0%+/-11.0%, n=48). Only PYY decreased DP specific activity (7.9%+/-2.2%, n=48). The Y2-agonist but not the Y1-agonist mimicked these PYY effects (increasing AP 28.3%+/-3.5% and decreasing DP 10.4%+/-3.6%). These data suggest that PYY promotes differentiation toward a colonocytic phenotype in Caco-2 intestinal epithelial cells and that this effect may be mediated through the Y2-receptor subtype.
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PMID:Peptide YY selectively stimulates expression of the colonocytic phenotype. 983 92

A 69-year-old Japanese woman was referred to our hospital because of abnormal skull X-ray findings. Serum total alkaline phosphatase, bone-specific alkaline phosphatase 3, osteocalcin and propeptide carboxyterminal of type I procollagen (PICP) levels were markedly elevated. Urinary excretion of hydroxyproline was also increased, suggesting that both bone formation and resorption were accelerated. Radiography of the skull showed "cotton wool" appearance. T1-enhanced MRI revealed that the skull-cap and diploe were swelled up. In 99mTc-MDP bone scintigraphy, all areas of the skull and a part of the right hemipelvis showed high uptake of the radioisotope. Based on the findings we made diagnosis of Paget's disease of bone which is a rare bone disorder in Japanese. Three-month oral administration of etidronate disodium resulted in normalization of serum PICP levels and urinary hydroxyproline excretion, whereas alkaline phosphatase levels were only partially lowered. Levels of the markers of bone turnover remained normal during a follow-up period of 3 months after the discontinuation of the treatment.
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PMID:A patient with Paget's disease of bone treated with etidronate disodium. 991 22

In this study, we evaluated the efficacy of bone marrow immunoscintigraphy (BMIS) for the detection of skeletal metastases in 23 patients with histologically confirmed breast cancer. All patients underwent whole-body BMIS 3-6 h after the intravenous injection of 0.20-0.33 mg of the intact anti-NCA 95 MAb BW 250/183 labelled with 259-555 MBq 99Tcm and a whole-body 99Tcm-MDP bone scan. In four patients, BMIS SPET of the lumbar spine was also performed. Serum alkaline phosphatase was determined in all patients and the level of human anti-mouse antibody (HAMA) in 16. Final diagnosis was confirmed by radiology and 2 years follow-up. Compared with the 99Tcm-MDP bone scan, BMIS demonstrated better specificity (88% vs 75%) and a better positive predictive value (92% vs 85%). There were no significant differences between BMIS and the bone scan in the detection of skeletal metastases (P > 0.05). In one patient with normal planar BMIS of the lumbar spine, SPET disclosed a metastatic lesion in the bone marrow. The correlation coefficient between BMIS and bone scan and between BMIS and serum alkaline phosphatase was r = 0.688 and r = 0.483 respectively. One patient developed a minor HAMA response after BMIS. Patients with diffuse increased activity of the skull on the bone scan had a significantly higher skull to whole body ratio on BMIS (P < 0.01). Thus BMIS can improve the specificity and positive predictive value of bone scanning in the detection of skeletal metastases, with a low HAMA response. Diffuse increased activity of the skull on bone scans could be explained by bone marrow extension. SPET scanning of the spine may improve the sensitivity of BMIS.
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PMID:Bone marrow immunoscintigraphy for the detection of skeletal metastases in patients with breast cancer. 1008 62

Short chain fatty acids such as sodium butyrate are concentrated in the colonic lumen and may protect against colon carcinogenesis by maintaining colonocytic differentiation, but the mechanisms by which they act are not fully understood. It has recently been suggested that short chain fatty acids modulate cellular tyrosine kinase activity in addition to altering chromatin structure via regulation of histone acetylation and DNA methylation. Therefore, the authors evaluated the influence of tyrosine kinase inhibition on the effects of 10 mM butyrate on human Caco-2 intestinal epithelial differentiation, using alkaline phosphatase and dipeptidyl dipeptidase specific activity as markers of differentiation, and two tyrosine kinase inhibitors, of different mechanisms of action and different effects on Caco-2 brush border enzyme specific activity, to block tyrosine kinase activity. As expected, butyrate stimulated both alkaline phosphatase and dipeptidyl dipeptidase specific activity. The tyrosine kinase inhibitors prevented, and indeed one inhibitor reversed the effects of butyrate on alkaline phosphatase specific activity. However, tyrosine kinase inhibition did not prevent butyrate stimulation of dipeptidyl dipeptidase specific activity. Different pathways are likely to regulate the effects of butyrate on expression of these two brush border enzymes. Butyrate stimulation of alkaline phosphatase, but not dipeptidyl dipeptidase, may involve tyrosine phosphorylation signaling.
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PMID:Tyrosine kinase inhibitors reverse butyrate stimulation of human Caco-2 intestinal epithelial cell alkaline phosphatase but not butyrate promotion of dipeptidyl dipeptidase. 1019 53

One of the classic histologic forms of renal osteodystrophy is osteitis fibrosa, and its distinguishing characteristic is bone marrow (BM) fibrosis, caused by the activation of marrow parenchymal cells. A bone biopsy must be performed in order to establish the diagnosis of renal osteodystrophy. The clinical use of bone biopsy is restricted, however, due to the invasiveness of the procedure. In recent studies, bone scans have provided information useful for the differential diagnosis between osteomalacia and osteitis fibrosa. However, bone scans can not provide information on the bone marrow status. Bone marrow immunoscintigraphy (BMIS) using Tc-99m anti-granulocyte antibody (AGA), a highly sensitive test for the detection of bone marrow abnormalities which is also a noninvasive method, has rarely been reported in chronic renal failure (CRF). BMIS can provide information in patients with myelofibrosis. The purpose of this study was to evaluate the usefulness of BMIS in CRF patients with special regards to biochemical parameters. Nineteen CRF patients (13 men, 6 women; mean age: 48 +/- 11 years) in whom bone scintigraphy using Tc-99m MDP (methylene diphosphonate) showed the so-called superscan pattern were included in the study. Their primary renal diseases were chronic glomerulonephritis (n = 14), diabetes (n = 4), and polycystic kidney disease (n = 1). Modes of therapies were continuous ambulatory peritoneal dialysis (CAPD) (n = 13; mean duration: 9.5 months), HD (n = 5; mean duration: 7.8 months), and conservative treatment (n = 1). BMIS using Tc-99m labeled anti-granulocyte monoclonal mouse antibody BW250/183 was performed, and the results were compared with the biochemical parameters of the patients. According to the presence of BM expansion, which may represent marrow fibrosis, the 19 patients were divided into two groups: Group I (n = 7) with BM expansion and Group II (n = 12) with normal marrow distribution. The biochemical parameters and bone markers of Group I were compared with those of Group II. There was no significant difference in biochemical parameters (blood hemoglobin, serum ferritin, erythropoietin, BUN, creatinine) between the two groups. There were no significants difference in serum calcium, phosphorus, tartate-resistant acid phosphatase (TRAP), and intact parathyroid hormone (iPTH) between the two groups. Serum alkaline phosphatase (ALP) and osteocalcin were significantly (P < 0.05) higher in Group I than in Group II. These results suggest that patients with bone marrow expansion in BMIS have increased levels of ALP and osteocalcin, indicating an increased osteoblastic activity. BMIS may be useful for the detection of bone marrow expansion due to marrow fibrosis in renal osteodystrophy, and for the evaluation of the extent of bone marrow fibrosis.
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PMID:Bone marrow immunoscintigraphy (BMIS): a new and important tool for the assessment of marrow fibrosis in renal osteodystrophy? 1064 20

Short chain fatty acids may protect colonic mucosa against neoplastic transformation by modulating colonocyte phenotype, DNA synthesis, and c-myc levels. To test this hypothesis, nonmalignant and malignant human colonocytes were isolated from surgical specimens and treated with 10 mM acetate, propionate, or butyrate. Markers of cellular phenotype, DNA synthesis, and c-myc protein levels were assayed by alkaline phosphatase and dipeptidyl dipeptidase IV activities, [3H]thymidine labeling, and western blotting, respectively. Butyrate, in particular, exerted discordant effects on alkaline phosphatase (P < 0.05), and c-myc levels (P < 0.05, N > or = 6) in nonmalignant and malignant human colonocytes. DPDD was unaffected by any of the short chain fatty acids tested. [3H]Thymidine labeling was differentially stimulated by short chain fatty acids in both cell types and greater DNA synthesis rates were observed in malignant colonocytes (P < 0.005, N = 16). These data suggest that in vitro, butyrate, in particular, may differentially modulate phenotype, DNA synthesis, and c-myc in nonmalignant and malignant human colonocytes.
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PMID:Short chain fatty acids differentially modulate cellular phenotype and c-myc protein levels in primary human nonmalignant and malignant colonocytes. 1127 Aug

Edwardsiella tarda is responsible for hemorrhagic septicemia (edwardsiellosis) in fish and also causes diseases in higher vertebrates such as birds, reptiles, and mammals, including humans. Interactions of E. tarda with blue gourami phagocytes were studied by light microscopy as well as by adherence, intracellular replication, and superoxide anion assays. Both nonopsonized virulent (PPD130/91 and AL9379) and avirulent (PPD125/87 and PPD76/87) bacteria could adhere to and survive and replicate within phagocytes, while only opsonized virulent strains replicated within the phagocytes. Furthermore, only avirulent E. tarda elicited a higher rate of production of reactive oxygen intermediates (ROIs) by phagocytes, indicating that they were unable to avoid and/or resist reactive oxygen radical-based killing by the fish phagocytes. TnphoA transposon mutagenesis was used to construct a library of 200 alkaline phosphatase (PhoA+) fusion mutants from a total of 182,000 transconjugants derived from E. tarda PPD130/91. Five of these mutants induced more ROI production in phagocytes than the wild-type strain. Two mutants had lower replication ability inside phagocytes and moderately higher 50% lethal dose values than the wild-type strain. Sequence analysis revealed that three of these mutants had insertions at sequences having homology to PhoS, dipeptidase, and a surface polymer ligase of lipid A core proteins of other pathogens. These three independent mutations might have changed the cell surface characteristics of the bacteria, which in turn induced phagocytes to produce increased ROIs. Sequences from two other mutants had no homology to known genes, indicating that they may be novel genes for antiphagocytic killing. The present study showed that there are differences in the interactions of virulent and avirulent E. tarda organisms with fish phagocytes and PhoA+ fusion mutants that could be used successfully to identify virulence genes. The information elucidated here would help in the development of suitable strategies to combat the disease caused by E. tarda.
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PMID:Opsonized virulent Edwardsiella tarda strains are able to adhere to and survive and replicate within fish phagocytes but fail to stimulate reactive oxygen intermediates. 1150 Apr 45

There are evidences that some drugs used for the human diseases can modify the biodistribution of radiopharmaceuticals. The N-methyl meglumine antimoniate, commercially known as glucantime (Rhodia, Brazil), is the elected drug for the treatment of all the clinical forms of leishmaniasis. As therapeutic drugs can present important toxic effects, we studied the effects of the glucantime on the kinetic of biodistribution of radiopharmaceuticals. To study the glucantime effect on the biodistribution of technetium-99m-methylenediphosphonic acid (99mTc-MDP), glucantime IM (80 mg/kg/day) was administered into male Wistar rats (3 months old age) in single dose during 7 days. 99mTc-MDP was injected 1 hr after the last dose. The animals (n = 24) were divided into two groups: treated (n = 12) and control (n = 12) and they were rapidly sacrificed, respectively, in 3 periods (5, 30 and 120 min) after administration of the 99mTc-MDP. The organs were isolated (brain, heart, thyroid, lungs, kidneys, testis, stomach, intestines, pancreas, spleen, liver, muscle, bone and bladder) and the percentages of radioactivity (%ATI) in each organ were calculated. The results were analyzed by the Wilcoxon test (p < 0.05). The analysis of the results has shown a significant increase of the %ATI after 5 min administration of the 99mTc-MDP in spleen, kidneys, testis, heart, liver and a reduction of %ATI in bladder. Thirty minutes after administration of the 99mTc-MDP, the analysis ofthe results reveals a significant reduction of the %ATI in femur, kidneys, thin bowel, lungs, heart, liver and an increase in abdominal muscle and stout bowel. One hundred-twenty min after administration of the 99mTc-MDP, the analysis of the results shows a significant reduction of the %ATI in spleen, thyroid, blood, femur, kidneys, liver and an increase in bladder, pancreas and lungs. Biochemical dosages were also performed before (control group, n = 12) and after (treated group, n = 12) treatment with glucantime. There was a significant (p < 0.05) decrease to the biochemical levels after the treatment with glucantime in following dosages: blood urea nitrogen, creatinine, alkaline phosphatase, lactic dehydrogenase, aspartate amino transferase, total creatine kinase, total protein, globulin and albumin. These results were compared with the control group, without glucantime, and statistical analyses were performed (t-student test, p < 0.05). These results could be associated with the biological effects and/or metabolization of the studied drug.
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PMID:Effects of the glucantime on the kinetic of biodistribution of radiopharmaceuticals in Wistar rats. 1261 72

Low protein content in the ration of rat pups during transfer from mixed to definitive nutrition (days 21-30 of life) has a negative impact on digestive function of the small intestine and trophic and barrier functions of the large intestine, liver, and kidneys and increases (sucrase, glycyl-L-leucin dipeptidase) or decreases (alkaline phosphatase, aminopeptidase M, glycyl-L-leucine dipeptidase) enzyme activities in these organs in 6-month-old rats. Protein deficiency during the early ontogeny modulates functioning of the enzyme systems in digestive and non-digestive organs in adult life, which can lead to the development of not only gastrointestinal, but other visceral diseases.
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PMID:Relationship between protein deficiency in the ration of rats during early ontogeny and function of enzyme systems of digestive and non-digestive organs in adult life. 1551 9


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