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:3.2.1.31 (beta-glucuronidase)
7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prolonged exposure to formaldehyde induces in the rabbit lung reactional and dystrophic changes involving the intrapulmonary bronchi, the bronchioli and the lung tissue. These changes are represented by bronchial cell hyperplasia with hypermucigenesis, extrusion of bronchial cells, bronchiolar hypermucigenesis, parcellary squamous metaplasia or necrobiosis of epithelia, thickening of bronchial and bronchiolar walls by subepithelial cell accumulations, destruction of musculo-elastic structures with stenosis or ectasia; the vascular reactions are hyperhaemic and proliferative with an obstructive and fibrous tendency; the parenchymal lesions are atelectasias, intralobular emphysema, and cellular thickening of alveolar walls and interlobular areas. The acid phosphatase, Tween-60-esterase, naphthol-AS-D-acetate-esterase, proline-oxidase and hydroxyproline-2-epimerase activities are increasing, while the leucyl-aminopeptidase and beta-glucuronidase ones are decreasing. The qualitative observations are completed and sustained by quanitative studies of mucous cell kinetics, of cell accumulations and differentiations.
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PMID:Experimental chronic obstructive lung disease. I. Bronchopulmonary changes induced in rabbits by prolonged exposure to formaldehyde. 15 Dec 23

Differences in morphogenetic and metabolic activities of the arterial smooth muscle cells (s.m.c.) of the young rat's aorta and femoral artery were studied by histochemical, radiochemical and quantitative radioautographic methods. 3H-proline was found to be incorporated into the medial myocyte of both vessels and released into the extracellular connective tissue matrix during the first 6 hours. The intracellular and extracellular phases of this process were similar to those of other scleroprotein-synthesizing cells. The 3H-proline incorporation, the metachromasia (GAG) and the activities of acetyl-cholinesterase, beta-glucuronidase, aryl-sulfatase and 5'-nucleotidase were more intense in the aortic media. On the other hand, some oxido-reductases linked with cellular respiration, glycogenolysis and energy production as well as the myosin-ATPase and MAO activities are more intense in the femoral artery. These differences suggest the morpho-functional diversity of the arterial s.m.c.: greater morphogenetic activity of the aortic myocyte; earlier and higher contractile differentiation of the femoral one.
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PMID:Segmental differences in morphogenetic activity of arterial smooth muscle cells. Histochemical and radioautographic studies. 15 89

Amino-acid analyses on the acid hydrolysates of an angiofibroma and skin established that the former tissue contained less collagen than skin based on the reduced content of hydroxyproline, glycine, proline and alanine in the tumour. From lysosomal enzyme measurements it became evident that the specific activities of the hexosaminidases, beta-glucuronidase and beta-galactosidase were elevated. Analyses of the alcohol insoluble fraction following pronase digestion revealed that the tumour contained more acidic glycosaminoglycan (AG) than skin as assessed by uronic acid and hexosamine measurements. More outstanding, however, was the seven-fold increase in the total carbohydrate in the AG fraction of the tumour. The overall composition of this fraction was very similar to comparable material from foetal skin except that the tumour fraction contained increased sulphate concentration.
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PMID:Chemical analysis of an angiofibroma from a patient with tuberous sclerosis. 20 95

We have produced various proline-containing peptides as translational fusions with beta-glucuronidase (beta Glu) in Escherichia coli. When these linkers were introduced in the 5'-end of the beta Glu-encoding gene, the production of the enzyme was increased substantially in vivo. The peptides carrying repetitive Gly-Pro sequences could also stimulate the growth of the transformants in media with inhibitory concentrations of NaCl. Furthermore, the freezing tolerance could be improved.
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PMID:The oligopeptide (Gly-Pro)2-Ala-(Gly-Pro)2 increases the internal proline level and improves NaCl tolerance when produced in Escherichia coli. 175 72

In the present communication we report that fibroblasts, isolated from human gingiva obtained from 13 different patients, secreted soluble product(s) which can promote bone resorption in vitro. Fibroblasts were isolated from explants of human gingiva, subcultured, grown to confluent monolayers, subsequently cultured in growth arrest media for 0-72 h and conditioned media harvested. Bone resorption was assessed in cultured mouse calvarial bone by quantifying the mobilization of minerals and the release of lysosomal enzymes. Human fibroblast-conditioned media (HFCM) dose-dependently stimulated the release of 45Ca from prelabelled bones and the mobilization of stable calcium and inorganic phosphate from unlabelled bones. In addition, HFCM increased the release of beta-glucuronidase and beta-N-acetylglucosaminidase from the calvaria. No effect of HFCM on the release of 45Ca from dead bones could be seen. HFCM caused a dose-dependent increased degradation of bone matrix proteins, as assessed by the release of 3H from [3H]proline-labelled calvaria. The stimulation of 45Ca release could already be seen after 3-12 h of treatment. Treatment of the bones with HFCM for 12 h was sufficient to obtain a prolonged stimulation of 45Ca release. Bones cultured in the presence of HFCM showed an increased number of osteoclasts. Calcitonin, but not indomethacin, inhibited 45Ca release stimulated by HFCM. Ultrafiltration of HFCM did not cause any loss of the 45Ca release response. The amount of bone-resorbing activity produced by the gingival cells was proportional to the number of cells. In addition, HFCM stimulated the proliferation of human fibroblasts and osteoblast-enriched mouse calvarial bone cells. It is concluded that human gingival fibroblasts secrete one or several factors that can stimulate osteoclastic bone resorption in vitro by a prostaglandin-independent pathway.
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PMID:Stimulation of bone resorption and cell proliferation in vitro by human gingival fibroblasts from patients with periodontal disease. 222 7

The relation between the level of cyclic AMP and bone resorption was studied in a bone organ culture system, using calvaria from newborn mice. Two methylxanthines, iso-butyl-methylxanthine and theophylline and two non-xanthine inhibitors of cyclic AMP phosphodiesterase, Ro 20-1724 and rolipram, stimulated the release of [45Ca] and [3H] from bones prelabelled in vivo with [45Ca]- and [3H]proline, respectively. The release occurred after a delay of more than 24 hr. In 120-hr cultures, theophylline, IBMX, rolipram and Ro 20-1724, all stimulated the release of stable calcium, inorganic phosphate and the lysosomal enzymes, beta-glucuronidase and beta-N-acetylglucosaminidase from mouse calvarial bones. In addition, all four phosphodiesterase inhibitors decreased the amount of hydroxyproline in the bones at the end of the culture period. The release of minerals and the decrease of hydroxyproline was abolished by indomethacin. In short-term cultures (24 hr), rolipram and Ro 20-1724 did not reduce PTH-stimulated mineral mobilization, whereas the two methylxanthines, and dibutyryl cyclic AMP and 8-bromo cyclic AMP, did cause a reduction of PTH-stimulated mineral release during the first 24 hr. All four phosphodiesterase inhibitors increased the accumulation of cyclic AMP in the calvaria and inhibited cyclic AMP hydrolysis in extracts of calvarial bone. There was a correlation between the magnitude of the initial rise in cyclic AMP and the delayed stimulation of bone resorption. However, much lower concentrations of the PDE inhibitors were sufficient to produce a delayed increase in bone resorption than to block phosphodiesterase and significantly raise cyclic AMP levels. It is suggested that the elevation of cyclic AMP in a subset of bone cells results in an acute reduction of bone mobilization and the cAMP elevation in another subset to a delayed rise in bone resorption.
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PMID:Comparative study of the effects of cyclic nucleotide phosphodiesterase inhibitors on bone resorption and cyclic AMP formation in vitro. 243 92

The effect of prostaglandin E2 (PGE2) on the kinetic of bone resorption in vitro was assessed by following the release of minerals and degradation of matrix in cultured mouse calvarial bones. PGE2 (1 and 3 mumol/liter) caused an initial inhibition of the release of 45Ca, stable calcium, and inorganic phosphate from unstimulated calvarial bones. The effect was transient and after 24 and 48 hours the release of 45Ca, stable calcium, and inorganic phosphate from PGE2-treated bones was enhanced. 0.3 mumol/liter of PGE2 stimulated the release of 45Ca after 24 hours, but at this concentration no initial inhibition was observed. The initial inhibitory effect of PGE2 (1 mumol/liter) could be further increased by three structurally different inhibitors of cyclic AMP breakdown. PGE2 (1 mumol/liter) caused not only an initial inhibition of mineral release but also an initial inhibition of matrix degradation, as assessed by the release of 3H from [3H]-proline labeled bones. In addition, PGE2 (3 mumol/liter), in the presence of the phosphodiesterase inhibitor isobutylmethylxanthine, caused a rapid (6 hours) inhibition of the release of the lysosomal enzymes beta-glucuronidase and beta-N-acetyl-glucosaminidase, without affecting the release of the cytosolic enzyme lactate dehydrogenase. Similar specific initial inhibition of lysosomal enzyme release was also seen in the presence of calcitonin and dibutyryl cyclic AMP, but not in the presence of parathyroid hormone (PTH). Neither PGE2 nor the phosphodiesterase inhibitors rolipram and Ro 20.1724, could inhibit the initial stages of PTH-induced 45Ca release. Nor did PGE2 inhibit the stimulation of radioactive calcium mobilization induced by 1 alpha (OH)-vitamin D3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostaglandin E2 causes a transient inhibition of mineral mobilization, matrix degradation, and lysosomal enzyme release from mouse calvarial bones in vitro. 244 May 32

A gene encoding a novel cell wall hydroxyproline-rich glycoprotein (HRGPnt3) was isolated from a genomic library of tobacco. The deduced protein (620 amino acids, Mr, 65,406) contains an amino-terminal hydrophobic signal peptide, is highly basic, and is rich in proline, although characteristic Ser-Pro4 repeats are found only beyond residue 204. At the carboxyl terminus, there is a 34-amino-acid unit repeated three times. Arginine is the predominant basic amino acid rather than lysine, as in other HRGPs. A second gene homologous to HRGPnt3 was revealed by Southern blot hybridization of tobacco genomic DNA. Northern blot hybridization identified a 1.9-kb transcript present at low levels in roots. To determine the underlying spatial pattern of expression, the HRGPnt3 promoter and the first 27 nucleotides of the open reading frame were fused to the beta-glucuronidase (GUS) reporter gene and transformed back into tobacco. Histochemical localization of GUS activity showed that the HRGPnt3 promoter was transiently induced in the pericycle and endodermis, specifically in the discrete, small subset of cells involved in the initiation of lateral roots. This pattern of expression, in cells destined to form the tip of the emerging lateral root, indicates that the encoded cell wall protein has a specialized structural function, possibly in the mechanical penetration of the cortex and epidermis of the main root, and that the HRGPnt3 promoter responds to an early morphogenetic signal for lateral root induction.
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PMID:Specific expression of a novel cell wall hydroxyproline-rich glycoprotein gene in lateral root initiation. 261 9

We have utilized the adenylate cyclase stimulator, cholera toxin, as a tool to test the role of cyclic AMP as a mediator of the effects on bone resorption by the calcium-regulating hormones, parathyroid hormone (PTH) and calcitonin. The effects on bone resorption were studied in an organ culture system using calvarial bones from newborn mice. Cyclic AMP response was assayed in calvarial bone explants and isolated osteoblasts from neonatal mouse calvaria. Cholera toxin caused a dose-dependent cAMP response in calvarial bones, seen at and above approx. 1-3 ng/ml and calculated half-maximal stimulation (EC50) at 18 ng/ml. The stimulatory effect of cholera toxin could be potentiated by the phosphodiesterase inhibitor isobutylmethylxanthine (IBMX, 0.2 mmol/l). Cyclic AMP accumulation in the bones was maximal after 4-6 h, and thereafter declined. However, activation of the adenylate cyclase was irreversible and the total amount (bone + medium) of cAMP produced, in the presence of IBMX (0.2 mmol/l), increased with time, for at least 48 h. In osteoblast-like cells cholera toxin (1 microgram/ml) stimulated the cellular levels of cAMP with a peak after 60-120 min, which could be potentiated with IBMX. The total cAMP accumulation indicated an irreversible response. In short-term bone organ cultures (at most, 24 h) cholera toxin, at and above 3 ng/ml, inhibited the stimulatory effect of PTH (10 nmol/l) on 45Ca release from prelabelled calvarial bones. The inhibitory effect of cholera toxin (0.1 microgram/ml) on 45Ca release was significant after 6 h and the calculated IC50 value at 24 h was 11.2 ng/ml. Cholera toxin (0.1 microgram/ml) also inhibited PTH-stimulated (10 nmol/l) release of Ca2+, inorganic phosphate (Pi), beta-glucuronidase, beta-N-acetylglucosaminidase and degradation of organic matrix (release of 3H from [3H]proline-labelled bones) in 24 h cultures. 45Ca release from bones stimulated by prostaglandin E2 (1 mumol/l) and 1 alpha-hydroxyvitamin D3 (0.1 mumol/l) was also inhibited by cholera toxin (0.3 microgram/ml) in 24-h cultures. The inhibitory effect of cholera toxin on bone resorption was transient, and in long-term cultures (120 h) cholera toxin caused a dose-dependent, delayed stimulation of mineral mobilization (Ca2+, 45Ca, Pi), degradation of matrix and release of the lysosomal enzymes beta-glucuronidase and beta-N-acetylglucosaminidase.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of cholera toxin on cyclic AMP accumulation and bone resorption in cultured mouse calvaria. 282 May 4

The effects of 3-amino-1-hydroxy-propylidene-1,1-bisphosphonate (AHPrBP), 1-hydroxyethylidene-1,1-bisphosphonate (HEBP), dichloromethylenebisphosphonate (Cl2MBP) and azacycloheptylidene-2,2-bisphosphonate (AHBP) on bone were examined in organ culture using newborn mice calvaria. AHPrBP, HEBP and Cl2MBP caused a dose-dependent inhibition of PTH-stimulated (10 nmol/l) release of 45Ca from the calvaria, at and above a concentration of 3 mumol/l, whereas AHBP only caused a slight inhibition, at and above 100 mumol/l. AHPrBP inhibited PTH-stimulated release of 3H from bones prelabelled with [3H]-proline. AHPrBP (30 mumol/l) diminished the stimulatory effect of 1 alpha(OH)vitamin D3 (10 nmol/l), prostaglandin E2 (0.1 mumol/l) and renal tumor conditioned media on 45Ca release. AHPrBP and Cl2MBP, at and above 3 mumol/l, decreased PTH-stimulated mobilization of Ca2+ and Pi and in parallel the release of beta-glucuronidase without affecting the release of lactate dehydrogenase. The inhibitory effect of AHPrBP (30 mumol/l) on PTH-induced 45Ca release was irreversible. The inhibition by AHPrBP (30 mumol/l) on spontaneous and PTH-stimulated release of 45Ca can be seen first after 24 h of culture. Similarly the inhibitory effect by HEBP (30 mumol/l) and Cl2MBP (30 mumol/l) was delayed and could be observed after 36 and 24 h of culture, respectively. PTH-stimulated release of Ca2+, Pi, beta-glucuronidase and beta-N-acetylglucosaminidase was reduced by AHPrBP first after 24 h of culture. AHPrBP, HEBP and Cl2MBP, at concentrations which are inhibitory on bone resorption, do not affect protein synthesis and mitotic activities in mouse calvaria. These data show that AHPrBP, HEBP and Cl2MBP inhibit bone resorption in vitro and in parallel decrease lysosomal enzyme release by a mechanism, which is not related to cytotoxicity. In addition, the delayed inhibitory effect on bone resorption and lysosomal enzyme release by all the compounds suggest that bisphosphonates inhibit bone resorption indirectly and not by a direct effect on existing osteoclasts. The delayed inhibition by bisphosphonates on bone resorption may be due to decreased recruitment of new osteoclasts as a consequence of an inhibitory action on mononuclear osteoclast precursor cells.
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PMID:Effects of four bisphosphonates on bone resorption, lysosomal enzyme release, protein synthesis and mitotic activities in mouse calvarial bones in vitro. 295 2


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