Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anti-Fc gamma R IgM monoclonal antibodies (mAbs) isolated from lipopolysaccharide-stimulated spleen cells from tightskin (TSK) mice were found to be polyspecific, reacting with a wide variety of molecules, including double-stranded DNA, topoisomerase, RNA polymerase, and different collagen types. Approximately 60% of the polyspecific IgM mAbs have anti-Fc gamma R specificity. These anti-Fc gamma R mAbs induce the release of hydrolases from both azurophil and specific granules of human neutrophils. 25-45% of the total cellular content (determined in Nonidet P-40 lysates) of neutrophil elastase, 10-25% of beta-glucuronidase, and 30-50% of alkaline phosphatase was released after incubation with the mAbs. The degranulation process was accompanied by dramatic morphological changes shown by scanning and transmission electron microscopy. The release of hydrolytic enzymes stimulated by the IgM anti-Fc gamma R mAbs was inhibited by preincubation of neutrophils with Fab fragments of either anti-human Fc gamma RII (IV.3) or anti-human Fc gamma RIII (3G8) mAbs. The binding of the anti-Fc gamma R TSK mAbs to human neutrophils was inhibited by Fab fragments of mAb 3G8. However, we found that the TSK anti-Fc gamma R mAbs do not bind to human Fc gamma RII expressed in either CHO cells or the P388D1 mouse macrophage cell line. Since the enzyme release could be inhibited by Fab fragments of mAb IV.3, we suggest that the signal transduction may require Fc gamma RII activation subsequent to crosslinking of the glycan phosphatidyl inositol-anchored Fc gamma RIII-1. These data demonstrate for the first time that polyspecific autoantibodies with Fc gamma R specificity can trigger neutrophil enzyme release via human Fc gamma RIII-1 in vitro and indicate a possible role for such autoantibodies in autoimmune inflammatory processes.
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PMID:IgM anti-Fc gamma R autoantibodies trigger neutrophil degranulation. 182 27

Tannins of natural or synthetic origin are well-known adjuvants in topical anti-inflammatory therapy of skin diseases. In this study, the influence of synthetic tannin on neutrophil accumulation, enzyme release, and on the proinflammatory activity of neutrophil-derived enzymes was investigated. The results show that synthetic tannin (Tamol) specifically inhibits the neutrophil serine protease human leukocyte elastase (HLE) in an irreversible manner with a half-maximal inhibitory concentration (IC50) of 0.3 microgram/ml. Exogenous protein partially abolished the tannin-dependent HLE inhibition (IC50 of Tamol at 1% protein-concentration:1.0 microgram/ml). Synthetic tannin did not influence the activities of other neutrophil enzymes like Cathepsin G, beta-glucuronidase, and myeloperoxidase. The specificity of Tamol for HLE was further substantiated by the lack of inhibition of other serine proteases. Additionally, Tamol had no effect on f-met-leu-phe-induced neutrophil chemotaxis and did not alter enzyme degranulation of neutrophils in response to f-met-leu-phe and opsonized zymosan. We conclude from our results that the anti-inflammatory properties of synthetic tannin may at least in part be due to inactivation of the proinflammatory protease HLE.
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PMID:Selective inactivation of human neutrophil elastase by synthetic tannin. 187 53

The contribution of neutrophil-derived elastase and cathepsin G to joint pathology has been examined in immune arthritis in the mouse. Neutrophils from beige mice are genetically deficient in lysosomal elastase and cathepsin G, but have normal levels of the acid hydrolases, beta-glucuronidase, and N-acetyl-beta-glucosaminidase. The development of antigen-induced arthritis in normal mice has been compared with that in beige mice. The pattern of synovitis (both leukocyte accumulation and plasma leakage) were indistinguishable in normal and beige mice. Cartilage proteoglycan depletion was quantified by measuring the decrease in safranin O staining intensity, and this, too, was unaltered in mice lacking elastase and cathepsin G. These results suggest that neutrophil elastase and cathepsin G do not contribute to these aspects of joint pathology in antigen-induced arthritis in the mouse.
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PMID:Pathogenesis of antigen-induced arthritis in mice deficient in neutrophil elastase and cathepsin G. 224 Jan 59

Plasma polymorphonuclear leukocyte elastase (PMNE) activity is known to increase during cardiopulmonary bypass (CPB), and is considered to mediate pulmonary tissue damage causing postoperative respiratory failure. We made a clinical study in order to clarify the effects of ulinastatin (Miraclid), a proteolytic enzyme inhibitor, on plasma PMNE activity and respiratory function. Twenty adult patients undergoing coronary artery bypass grafting were divided into 2 groups; 10 to group U and 10 to group C. The patients in group U received 500 U/kg body weight of ulinastatin intravenously before and after CPB, and the patients in group C not receiving the dose served as controls. Arterial blood samples were obtained before the operation, 1 hour after CPB, 3 hours, 1 day and 4 days after the operation. The leukocyte count was significantly lower in group U 1 hour after CPB and 3 hours after the operation compared to group C (p less than 0.01). The plasma PMNE activity rose rapidly after starting CPB and the peak level appeared 1 hour after CPB; 1165 +/- 560 micrograms/l in group U and 1981 +/- 562 micrograms/l in group C (p less than 0.02). There was a significant correlation between the leukocyte reduction and the rate of increase of beta-glucuronidase activity were diminished in group U compared to preoperative values (p less than 0.05). The recovery of the oxygenation index (PaO2/F1O2), which was used for evaluation of the respiratory function, was worse in group C (p less than 0.01). These results suggest that the administration of ulinastatin in patients undergoing CPB is useful for the prevention of the deleterious effects of PMNE on the lung.
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PMID:[Effects of ulinastatin on plasma polymorphonuclear leukocyte elastase activity and respiratory function in patients undergoing cardiopulmonary bypass]. 237 94

Although ozone (O3) has been shown to induce inflammation in the lungs of animals, very little is known about its inflammatory effects on humans. In this study, 11 healthy nonsmoking men, 18 to 35 yr of age (mean, 25.4 +/- 3.5), were exposed once to 0.4 ppm O3 and once to filtered air for 2 h with intermittent exercise. Eighteen hours later, bronchoalveolar lavage (BAL) was performed and the cells and fluid were analyzed for various indicators of inflammation. There was an 8.2-fold increase in the percentage of polymorphonuclear leukocytes (PMN) in the total cell population, and a small but significant decrease in the percentage of macrophages after exposure to O3. Immunoreactive neutrophil elastase often associated with inflammation and lung damage increased by 3.8-fold in the fluid while its activity increased 20.6-fold in the lavaged cells. A 2-fold increase in the levels of protein, albumin, and IgG suggested increased vascular permeability of the lung. Several biochemical markers that could act as chemotactic or regulatory factors in an inflammatory response were examined in the BAL fluid (BALF). The level of complement fragment C3 alpha was increased by 1.7-fold. The chemotactic leukotriene B4 was unchanged while prostaglandin E2 increased 2-fold. In contrast, three enzyme systems of phagocytes with potentially damaging effects on tissues and microbes, namely, NADPH-oxidase and the lysosomal enzymes acid phosphatase and beta-glucuronidase, were increased neither in the lavaged fluid nor cells. In addition, the amounts of fibrogenic-related molecules were assessed in BALF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ozone-induced inflammation in the lower airways of human subjects. 291 89

Lysosomal neutral proteases, once released, are considered to play an important role in the rheumatoid inflammatory process. The effect of two gold compounds on human polymorphonuclear lysosomal enzymes was studied during reverse endocytosis. Phagocytosis was assessed using dual-labeled liposomes. Auranofin, a new antirheumatic gold compound, reduces human polymorphonuclear leukocyte phagocytoses and lysosomal elastase and beta-glucuronidase release at a therapeutically achievable concentration (5 microM). Sodium aurothiomalate was ineffective at this concentration.
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PMID:Effect of two gold compounds on human polymorphonuclear leukocyte lysosomal function and phagocytosis. 392 Jan 44

Macrophages carry receptors on their surface for acetylated low density lipoprotein (ac-LDL). Receptor-mediated endocytosis of ac-LDL is followed by intracellular cholesterol accumulation. We investigated whether occupation of these binding sites evokes the release of hydrolytic enzymes from mouse peritoneal macrophages cultured for up to 48 h. ac-LDL at concentrations ranging from 25-250 micrograms protein/ml was noted to promote in a dose-dependent fashion secretion of the neutral proteinase elastase (EC 3.4.21.37) and the lysosomal acid hydrolases N-acetyl-beta-glucosaminidase (EC 3.2.1.30), beta-glucuronidase (EC 3.2.1.31), beta-galactosidase (EC 3.2.1.23), alpha-mannosidase (EC 3.2.1.24) and cathepsin D (EC 3.4.23.5). This stimulatory effect was non-cytotoxic. LDL modified by treatment with malondialdehyde was also capable of augmenting enzyme liberation into culture supernates. These findings may have implications for some aspects of the atherosclerotic process.
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PMID:Chemically modified low density lipoproteins as inducers of enzyme release from macrophages. 400 64

The possibility of minimizing organ damage following cardiopulmonary bypass (CPB) was examined. In the control group, n = 21, upon completion of CPB, elevation of the lysosomal enzyme beta-glucuronidase, which is a sensitive indicator of cellular damage, was affected by the concentration of granulocyte elastase (r = 0.59) or the endothelial-derived constricting factor, endothelin, (r = 0.8). Renal damage, which was detected by an increase in renal tubular enzymes (N-acetyl-beta-D-glucosaminidase and gamma-glutamyltranspeptidase) in urine, was also affected by endothelin (r = 0.79, r = 0.56), elastase (r = 0.6, r = 0.71), and by free hemoglobin levels (r = 0.76, r = 0.82). Next, the efficacy of pharmacological intervention for the prevention of renal damage was evaluated. During CPB, the administration of an elastase inhibitor (ulinastatin, 3 x 10(5) IU), n = 8, or a calcium antagonist (nicaldipine HCl, elastase release inhibitor; 5 gamma/kg per min), n = 8, significantly reduced the elevation of beta-glucuronidase and renal tubular enzymes (p < 0.05). Although the ulinastatin and nicardipine groups demonstrated low values of elastase in the Intensive Care Unit (ICU), only the values of the nicardipine group reached statistical significance (p < 0.05). A reduction in endothelin levels compared to the control group was observed in the nicardipine group. However, preventive and counteractive effects of nicardipine against vasoconstriction caused by endothelin were also considered to play an important role in the prevention of renal damage. The addition of haptoglobin (4,000 IU) to the priming solution of the CPB also reduced levels of renal tubular enzymes (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacological intervention for renal protection during cardiopulmonary bypass. 830

We have studied the effects of prostaglandin E1 (PGE1) on the release of lysosomal enzymes such as beta-glucuronidase in leukocyte (beta-GL) and granulocyte elastase (GEL) in 52 patients for major abdominal surgery. All patients were divided into two groups; the PG group (24 patients) and the control group (28 patients). The patients of the PG group received PGE1 continuously at the rate of 0.03 to 0.1 micrograms.kg-1.min-1 during surgery. Plasma levels of GEL and beta-GL, which are known to be the indicators of tissue destruction, were measured during and after surgery. The GEL/granulocyte ratio in the PG group was significantly smaller than that of the control group during surgery. The rate of change of beta-GL was significantly depressed in the PG group compared to that of the control group. These findings suggest that the administration of PGE1 during major abdominal surgery inhibits the release of lysosomal enzymes, and this prevents tissue injury during and after surgery.
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PMID:[The effects of prostaglandin E1 on the release of beta-glucuronidase in leukocyte and granulocyte elastase in patients for major abdominal surgery]. 851 50

Several neutrophil-derived enzymes that are present in the gingival crevicular fluid have been evaluated for use as risk markers for periodontal disease progression. However, very little information is available about the presence of these enzymes in peri-implant tissues. The purpose of this cross-sectional study was to compare levels of enzymes in gingival crevicular fluid between natural teeth and endosseous dental implants and between well-integrated and failing implants. Scores of plaque and gingivitis were recorded for 68 integrated implants, five failing implants, and 34 natural teeth in 12 completely edentulous and 18 partially edentulous subjects. Samples of gingival crevicular fluid were obtained from these sites using filter paper strips and were assayed for levels of neutral protease, neutrophil elastase, myeloperoxidase, and beta-glucuronidase. Neutral protease levels were higher (P = .066) at moderately to severely inflamed implant sites (Gingival Index of 2, 3) compared to mildly or noninflamed sites (Gingival Index of = 0, 1). Despite the small number (n = 5) of failing implants evaluated in this study, levels of neutrophil elastase, myeloperoxidase, and beta-glucuronidase were significantly higher (P < or = .001) around failing implants compared to successful implants. Neutral protease levels were also elevated around failing implants, but the difference was not statistically significant. Results of this study indicate that neutrophil elastase, myeloperoxidase, and beta-glucuronidase levels in GCF appear to be good candidates for study as risk markers of implant failure.
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PMID:Crevicular fluid enzymes from endosseous dental implants and natural teeth. 875 53


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