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MPXI level may help to differentiate subtypes of AML. Paper-13844714.
In addition, Galanin reduced MPO and TNF-alpha values significantly. Paper-12147370.
In the third, CD19 or CD79a was more highly expressed than CD3e and MPO. Paper-10320668.
Interaction of ceruloplasmin, lactoferrin, and myeloperoxidase. Paper-13246481.
Furthermore, myeloperoxidase colocalized with human leukocyte elastase. Paper-2024331.
The blasts showed myeloperoxidase ( MPO) activity and CD13 antigen expression. Paper-1746369.
Cytoplasmic expression of myeloperoxidase, CD3, and CD22 could not be demonstrated. Paper-170788.
Thus, intracellular transport of MPO appears to be linked to that of serglycin. Paper-10011713.
MMPs and TIMP-1 were expressed predominantly by MPO-and CD68-positive cells. Paper-10431812.
MPO cytochemistry was also associated with immunologic detection of LF. Paper-4884486.
In transient co-transfection experiments HBP1 enhances MPO promoter activity. Paper-8953072.
MPO is expressed in macrophages-microglia in multiple sclerosis ( MS) lesions. Paper-8488800.
They were not directed against proteinase 3, myeloperoxidase, elastase or lactoferrin. Paper-7653160.
CP subjected to partial proteolysis was virtually unable to inhibit activity of MPO. Paper-13503432.
PMN were activated by IL-8 and secreted hydrogen peroxide and myeloperoxidase ( MPO). Paper-1816210.
MPO co-localized with majority of MMP-9 signal by immunohistochemistry. Paper-12016362.
These peptides are able to displace CP from its complexes with LF and MPO. Paper-13246481.
In contrast, myeloperoxidase binding to E. coli is strongly inhibited by BPI. Paper-6305239.
An allelic association implicates myeloperoxidase in the etiology of acute promyelocytic leukemia. Paper-1196821.
In these 24 sera the antigenic targets were BPI in 14, cathepsin G in 13, and MPO in 8. Paper-9898595.
Catalase, an antioxidant enzyme, partially inhibited the virucidal effect of myeloperoxidase. Paper-8035495.
MPO/H2O2- mediated cytotoxicity of CF sputum was measured in cell culture assays. Paper-1439330.
Myeloperoxidase was associated with max- CIMT, and oxAT correlated with max- CIMT and GNRI. Paper-13576694.
Interestingly, MPO inhibited IL-8 production in bronchial, but not alveolar epithelium. Paper-12715463.
Inactivation of transferrin iron binding capacity by the neutrophil myeloperoxidase system. Paper-6450958.
IL-17 staining and co-staining with CD3 and myeloperoxidase were performed on liver biopsy specimens. Paper-13600081.
The lactoperoxidase technique did not succeed in labeling MPO with an adequate specific activity. Paper-7134662.
Six sera reacted to BPI, five to LF, one to MPO, one to PR3, and one to CG by ELISA testing. Paper-11447305.
Both human and canine MPO could form a complex when mixed with CP from seven mammalian species. Paper-13246481.
Loss of activity and loss of the MPO spectrum were blocked by SOD but not by deferoxamine or catalase. Paper-932473.
Susceptibilities of lactoferrin and transferrin to myeloperoxidase-dependent loss of iron-binding capacity. Paper-5817500.
Genetic determination of TNF and myeloperoxidase production in dialyzed patients with diabetic nephropathy. Paper-10863537.
This process may allow transferrin to retain its iron binding function during MPO exposure in vivo. Paper-292886.
Chlorinated oxidants formed in the MPO system (in the absence of CPZ) induced TG peptide bond splitting. Paper-6838328.
In homogenates of MS cortex, cortical demyelination was associated with significantly elevated MPO activity. Paper-12709640.
The LDH5/ LDH1 coefficient positively correlated with uPA, IL-8, IL-10, sICAM, sVCAM, MPO and MMP-9. Paper-13540504.
Myeloperoxidase mediates neutrophil activation by association with CD11b/ CD18 integrins. Paper-11187971.
Role of myeloperoxidase in the killing of Naegleria fowleri by lymphokine-altered human neutrophils. Paper-5483654.
(3) What role does the mannose-6-phosphate receptor ( M6PR) system play in the delivery of MPO to the lysosome? Paper-7201412.
Lactoferrin co-purifies with myeloperoxidase and is recognised by anti-neutrophil cytoplasm antibodies. Paper-7652939.
Similarly, the MPO ab reactivity of patients with systemic vasculitis could not be inhibited by native TPO. Paper-1106512.
Included in this group are myeloperoxidase, eosinophil peroxidase, lactoperoxidase, and thyroid peroxidase. Paper-12783084.
Immunohistochemically, the cells stain positive for myeloperoxidase, CD45, and CD117 but negative for CD34. Paper-13530166.
GLN enhanced GSH synthesis and attenuated interleukin-8 release and myeloperoxidase activity in lung tissues. Paper-13746492.
Discordant expression of myeloid antigens and myeloperoxidase in a case of t(8;21) positive AML expressing CD7. Paper-1962368.
Increasing concentrations of externally added authentic MPO progressively down-regulated both PLD and PLC activity. Paper-1585323.
CONCLUSIONS: MPO genotype GG is associated with cirrhosis in patients with hereditary hemochromatosis. Paper-10793652.
Lactoferrin was found in ten of 13 fractions (L1 through L8, H1 to H2), whereas MPO was found in every fraction. Paper-5137339.
In granules labeled for uPA the corresponding overlap with MMP-9, MPO and NE was 24, 64, and 51%, respectively. Paper-8625706.
Association of major depressive disorder with serum myeloperoxidase and other markers of inflammation: a twin study. Paper-12975607.
While immunogold labeling of PDE4A was reduced after fMLP stimulation, staining of MPO-containing granules remained high. Paper-9925425.
Recombinant TNF alone failed to induce release of myeloperoxidase ( MPO) and lysozyme by neutrophils. Paper-7526024.
With flow cytometric immunophenotyping the blasts expressed CD13, CD33, CD117, myeloperoxidase and CD34. Paper-12400046.
Combined effect of MPO, GSTM1 and GSTT1 polymorphisms on chromosome aberrations and lung cancer risk. Paper-10073260.
MPO inhibits human mast cell tryptase in a time-dependent manner with an IC50 of 16 nM at 1 h. Paper-1874902.
Injection of purified human recombinant TNF (2 to 200 micrograms/kg i.v.) mimicked the effect of LPS on lung MPO activity. Paper-7923729.
Ultrastructural MPO was positive in one out of five cases and platelet peroxidase ( PPO) was negative in the four cases studied. Paper-1487090.
The data suggest oxidative inactivation of alpha 1-protease inhibitor by secreted myeloperoxidase and hydrogen peroxide. Paper-4487558.
Co-treatment with TNF- binding protein decreased both lung MPO and lung leak increases in rats given TNF intratracheally. Paper-892990.
Ligation of CR1 attenuates Fc receptor- mediated myeloperoxidase release and HOCl production by neutrophils. Paper-1386982.
CTS cells expressed CD7, CD13, CD33, CD34 and HLA-DR antigens, and showed ultrastructural myeloperoxidase activity. Paper-775316.
However, it did enhance the release of MPO and lysozyme by neutrophils stimulated with C5a and FMLP, but not with PMA. Paper-7526024.
Oxidation of alpha1- proteinase inhibitor by the myeloperoxidase-hydrogen peroxidase system promotes binding to immunoglobulin A. Paper-1774121.
MCP-1 protein ( ELISA) was elevated 21-fold and myeloperoxidase activity 95-fold in RV of PE2.0 compared with Veh or PE1. Paper-12153320.
Double labelling experiments of MMPs and TIMP-1 were performed with MPO and CD68, labelling neutrophils and macrophages. Paper-10431812.
TNF-alpha, TNF-beta, IL-6, IL-10, PECAM-1 and the MPO inflammatory gene polymorphisms in osteosarcoma. Paper-13223587.
In this study, we have investigated the genetic role of the myeloperoxidase ( MPO) gene encoding myeloperoxidase in MS. Paper-13328542.
Complement activation products, myeloperoxidase, lactoferrin, and thrombospondin were quantified in enzyme immunoassays. Paper-10377664.
Moreover, the OR for max- CIMT with positive PEW and high MPO was significantly increased in the four groups with combined MPO and PEW. Paper-13576694.
The MPO and SULT1A1 genotypes were examined with polymerase chain reaction and restriction fragment length polymorphism. Paper-13685161.
Plasma exudation of radiolabelled albumin, myeloperoxidase ( MPO), TNF-alpha, MCP-1, superoxide and hydrogen peroxide was measured. Paper-10097311.
The possible protein-protein interface is comprised of the area near active site of MPO and the loop linking domains 5 and 6 in CP. Paper-13503432.
Emerging evidence suggests that HDL can also be modified by MPO derived oxidants, resulting in an impairment of cholesterol efflux. Paper-10604208.
Cloning and expression of human HBP1, a high mobility group protein that enhances myeloperoxidase ( MPO) promoter activity. Paper-8953072.
Antibodies against SP and MP were produced using bovine milk lactoperoxidase ( LP) and human MP as the immunogens, respectively. Paper-7166380.
We previously showed that NGAL is sorted to azurophil granules and colocalizes with myeloperoxidase in undifferentiated HL-60 cells. Paper-930423.
The data suggest the presence of some unique components in PSK which directly stimulate the iodination of myeloperoxidase-positive cells. Paper-6697116.
All six patients with AITD had TPO antibodies in enzyme immunoassay (EIA) and four of them had simultaneously MPO antibodies in EIA. Paper-1106512.
Myeloperoxidase delays neutrophil apoptosis through CD11b/ CD18 integrins and prolongs inflammation. Paper-12908983.
We also measured nitro-tyrosinylation (NO(2)-Tyr) of LDL as an indicator of biological activity of CRP- mediated MPO release. Paper-13594910.
PMA induced exocytosis of lactoferrin, the specific granule marker, but not of myeloperoxidase, the azurophil granule marker. Paper-2962256.
BAL analysis showed a higher percentage of neutrophils and of myeloperoxidase ( MPO) in BAL fluid in Group 1 than in Group 2. Paper-7889762.
GCF glutathione peroxidase, lactoferrin, myeloperoxidase and IL-1beta were analyzed by enzyme-linked immunosorbent assays ( ELISA). Paper-10528054.
Endothelial cell damage mediated by the myeloperoxidase deficient cells was also inhibited by catalase but not superoxide dismutase. Paper-3873284.
These data suggest that MPO inhibits tryptase by interfering with the heparin stabilization of tryptase tetramer. Paper-1874902.
In the absence of added taurine the hypochlorite formed by MPO oxidized endogenous amines that also activated C5. Paper-839510.
Metabolically labeled SGD nucleated marrow cells produced normal amounts of myeloperoxidase, but there was no detectable synthesis of lactoferrin. Paper-6245392.
Five candidate genes were chosen: apolipoprotein E ( APOE), alpha 2-macroglobulin, cathepsin D, myeloperoxidase and nitric oxide synthase. Paper-9729782.
TNF-alpha-primed PMN were stimulated with a monoclonal antibody to myeloperoxidase ( MPO) and with PR3- and MPO-ANCA, respectively. Paper-9232838.
Thioglycollate-induced macrophages exposed to HRP, bovine lactoperoxidase, or human myeloperoxidase demonstrated enhanced secretion of TNF. Paper-6190075.
Thirty-five sera with binding greater than 20% in a myeloperoxidase ( MPO, Calbiochem) ELISA were tested in Western blot analyses. Paper-7652939.
We have shown by size-exclusion chromatography that MPO promotes the dissociation of active tryptase tetramer to inactive monomer. Paper-1874902.
Tyrosine modification is not required for myeloperoxidase- induced loss of apolipoprotein A-I functional activities. Paper-11070740.
CONCLUSIONS: These results suggest that the MPO -463G>A polymorphism does not significantly affect the susceptibility to lung cancer in Koreans. Paper-12167570.
Polymorphisms for GSTM1 and MPO were amplified by polymerase chain reaction and detected by electrophoresis after restriction digestion. Paper-10867921.
In addition, E-B cells expressed T/NK lineage and myeloid-associated genes including CD2, NOTCH1, CD99, PECAM1, TNFSF13B, and MPO. Paper-13422488.
The presence of 0.1 N Cl- or Br- shifted the pH optimum for MPO to about 5.4 but had little or no effect on TPO- or LPO-catalyzed iodination. Paper-7523342.
We show that MPO binding to isolated HDL depends on the lipidation state of apolipoprotein A-I (apo A-I), the major protein constituent of HDL. Paper-12275896.
The variant genotype of MPO was associated with decreased risk of lung cancer among Caucasians (random effects OR = 0.70, 95% CI = 0.47-1.04). Paper-11441029.
However, in double labeling experiments, blasts with myeloperoxidase coexpressed lymphoid and myeloid markers including cALLA and CD 19 antigen. Paper-5843608.
A cell-free extract of vitamin B12 binding protein was readily inactivated on exposure to purified myeloperoxidase, H2O2, and a halide. Paper-4884483.
Reagent or myeloperoxidase-generated hypochlorite affects discrete regions in lipid-free and lipid- associated human apolipoprotein A-I. Paper-2174848.
These data indicate extracellular destruction of functional B12 binding protein by the halide-dependent heme enzyme myeloperoxidase and H2O2. Paper-4884483.
COPD patients had significantly lower CD63 expression and released less MPO upon chemokine stimulation compared with the healthy individuals. Paper-12475445.
Concentrations of H2O2 were diminished by catalase and enhanced by sodium azide owing to inhibition of cellular catalase and myeloperoxidase. Paper-448387.
RESULTS: Carvedilol dose-dependently decreased superoxide generation and MPO release from intact neutrophils stimulated by FMLP. Paper-12365987.
Two components of neutrophilic granules, MPO and lactoferrin, were strongly elevated postoperatively, and the levels of both were correlated with IL-8. Paper-10860956.
The prevalence of ANCA specificities in serum samples from RA patients were as follows: anti- PR3, 6%; anti- MPO, 2%; anti- LF, 8%; anti-LZ, 4%. Paper-8702027.
The glutathione peroxidase ( GSH-Px), malondialdehyde ( MDA) and myeloperoxidase ( MPO) levels of the 2 groups were studied. Paper-12533198.
Similarly, horseradish peroxidase and myeloperoxidase also protected responsiveness from these inhibitors while boiled catalase was without effect. Paper-4759300.
Flow cytometry showed that p38- MAPK inhibition decreased the translocation of PR3 (by 93 +/- 2%) and of MPO (by 64 +/- 2%). Paper-8774777.
The monoclonal antibodies used included those to CD1a, CD4, CD8, CD40, CD40L, CD68, Fas, Fas ligand ( FasL) and myeloperoxidase. Paper-11335007.
The release of myeloperoxidase correlated to an enhanced local release of the neutrophil activating peptide interleukin-8 ( IL-8). Paper-7901118.
The concentrations of lactoferrin, polymorphonuclear neutrophil elastase ( PMN-E), myeloperoxidase, and lysozyme in WGLF were measured by ELISA. Paper-9387225.
BASDAI was positively correlated with VAS, ESR and CRP; but MPO was negatively correlated with thiol/albumin ratio, both in total and active AS patients. Paper-10615946.
Both MPO alleles were expressed in a subset of lesions in high-fat-fed LDLR(-/-) mice, notably at necrotic lesions with cholesterol clefts. Paper-12134437.
Myeloperoxidase plays critical roles in killing Klebsiella pneumoniae and inactivating neutrophil elastase: effects on host defense. Paper-10986726.
The reaction with myeloperoxidase required chloride and was inhibited by catalase and methionine, indicating the involvement of hypochlorite. Paper-7836984.
At pH 5.5 LP activity was inhibited by 85% and MP by 34% with 10 mM F-. TSP activity was also inhibited only at low pH (5.5) by approximately 25%. Paper-8186601.
Endothelin-1 and the neutrophil glycoproteins lactoferrin and myeloperoxidase were quantified throughout the operation and 3 hours postoperatively. Paper-1000079.
The serum concentrations of MPO were measured by enzyme-linked immunosorbent assay ( ELISA) and CRP were measured by turbidimetric immunoassay. Paper-12022175.
Studies on the enzymatic properties shows that CP behaves as a competitive inhibitor impeding the binding of aromatic substrates to the active centre of MPO. Paper-13503432.
The expression of CXCR2 but not CXCR1 on neutrophils and monocytes correlated negatively with the levels of interleukin-8 and myeloperoxidase. Paper-9989418.
Clinical data was monitored and ECP, MPO, bFGF, VEGF and albumin concentrations were analyzed by immunochemical methods in perfusates and in serum. Paper-12319008.
Here we show that peroxisome proliferator-activated receptor gamma (PPARgamma) agonists strongly regulate MPO gene expression through the AluRRE. Paper-10205399.
In the literature, the requirement of TNF priming has been attributed to an effect of TNF-alpha on the expression of PR3 or MPO on the cell surface. Paper-12340736.
Interaction of LF and MPO with CP-Sepharose is blocked at ionic strength above 0.3 M NaCl and at pH below 4.1 ( LF) and 3.9 ( MPO). Paper-13246481.
The aim of this study was to evaluate whether the -463GA MPO promoter polymorphism is linked to clinical severity of CF-associated pulmonary inflammation. Paper-12162053.
Rosiglitazone inhibits hypercholesterolaemia-induced myeloperoxidase upregulation--a novel mechanism for the cardioprotective effects of PPAR agonists. Paper-13575724.
In conclusion, MPO polymorphisms were associated with the extent of brain damage and the functional outcome rather than with the risk of developing a BI. Paper-9753548.
In all cases the leukemic cells expressed CD34 and reacted with at least one of the antibodies to early myeloid antigens, ie, CD13, CD33, or myeloperoxidase. Paper-7937322.
The bactericidal activity of the MPO-supplemented system is inhibited by catalase, benzoate, azide, DABCO, and histidine but not by SOD or mannitol. Paper-3288569.
Seventeen single nucleotide polymorphisms ( SNPs) were identified in NQO1, CYP2E1, and MPO genes, including 6 novel SNPs in CYP2E1 and MPO. Paper-9332803.
RESULT: Combination of emodin and baicalein significantly reduced pancreatic TNF-alpha, IL-6 and MPO, and also inhibited pancreatic SDF-1 expression. Paper-13709414.
This study assessed the impact of polymorphisms of the MPO (-463G/A) and the HO-1 promotors of Vienna (GT)n on the evolution of cirrhosis in patients with HHC. Paper-10793652.
CONCLUSIONS: CRP stimulates MPO release both in vitro and in vivo, providing further cogent data for the proinflammatory effect of CRP. Paper-13594910.
In addition, serum DAO activity, TNF-alpha, IL-1beta and IL-6 levels, tissue MDA, protein carbonyl and MPO activity were all increased significantly by I/R injury. Paper-13732409.
Posttreatment with erdosteine and NAC significantly reduced the increases in the local production of TNF-alpha and VEGF, and epithelial MPO activity. Paper-12312589.
RESULTS: The DSS+iron group showed a significant increase in inflammatory scores, MPO, TNF-alpha, IL-1, LPO and NF-kappaB activity compared to DSS or DSS+vitamin E. Paper-11367236.
Intralymphatic mononuclear histiocytes expressed CD68 ( PGM1), although some cases also had variable immunoexpression for myeloperoxidase, CD31, and podoplanin. Paper-13681706.
A sequential pattern of first LF release followed by MPO and beta-glu was demonstrated with each of the stimuli examined, with or without cytochalasin B pretreatment. Paper-3550847.
These results suggest that butyrate induces MPO rather than EPO in EoL-1 cells and that the formation of nitrotyrosine in butyrate- induced cells is dependent on MPO. Paper-10544615.
The TaqMan technique was used to detect polymorphisms of CYP1A1, CYP1A2, CYP1B1, ADH1B, EPHX1, EPHX2, NQO1, MPO, GSTP1 and UGT1A6 genes. Paper-13480350.
C-reactive protein stimulates myeloperoxidase release from polymorphonuclear cells and monocytes: implications for acute coronary syndromes. Paper-13594910.
On the other hand, the plasma levels of myeloperoxidase and elastase in complex with alpha 1- proteinase inhibitor increased comparably in both groups of patients. Paper-5703640.
The anti-IgE antibody also significantly suppressed the activities of MPO and chymase as well as the expression of TNF-alpha and COX-2 in the DSS-treated colon tissue. Paper-12251866.
Immunohistochemical stains for CD4, CD34, CD56, CD68, CD117, CD123, TdT, lysozyme and myeloperoxidase were performed on 12 with available tissue blocks. Paper-12688823.
Neutrophil migration was quantified by measuring myeloperoxidase, and surface expression of endothelial PECAM-1 was examined using cell-surface enzyme immunoassay. Paper-10419152.
We investigated the stability of LF and MPO mRNA and the effects of purified recombinant human TNF-alpha on LF and MPO levels in normal human bone marrow. Paper-6902890.
CML production by neutrophils was inhibited by the H2O2 scavenger catalase and the heme poison azide, implicating myeloperoxidase in the cell-mediated reaction. Paper-1926535.
In addition, myeloperoxidase inhibited interleukin-8 production by bronchial epithelial cells, indicating a negative feedback loop for neutrophil recruitment. Paper-12715463.
Anti- MPO mAb, C6 was administered to young MRL mice which had been primed with exogenous TNF alpha to induce neutrophil activation and expression of MPO. Paper-2116787.
As AML1 protein regulates the expression of the myeloperoxidase gene, the relationship between AML1 mutations and Mo phenotype in AML will have to be further explored. Paper-8533608.
RESULTS: CRP treatment significantly increased release of MPO (both mass and activity) from human PMNs as well as monocytes (P < 0.05) and caused NO(2)-Tyr of LDL. Paper-13594910.
The present study shows that autoantibodies (aAb) to the TMA/ TPO antigen cross-react with human leucocyte myeloperoxidase, bovine lactoperoxidase and horseradish peroxidase. Paper-6141717.
Stimulated neutrophils at sites of inflammation can inactivate SLPI by myeloperoxidase- mediated oxidation of the methionine residue in the active site of SLPI. Paper-7927505.
These findings indicate that the C5 activating agent was produced by stimulated PMN through MPO-generated hypochlorite, trapped as taurine chloramine. Paper-839510.
In the present study, MPO is shown to colocalize with amyloid beta ( Abeta) in senile plaques in cerebral cortex sections from Alzheimer's disease (AD) brain tissue. Paper-1757888.
Its consensus DNA binding site has been isolated, and sites in several promoters of myeloid-specific genes, such as CD34, lactoferrin, and myeloperoxidase, have been defined. Paper-501040.
Demyelination in MS is associated with increased activity of MPO, suggesting that this production of reactive oxygen species may contribute to axonal injury within plaques. Paper-12998795.
We sought to examine whether MPO and other markers of inflammation are associated with MDD and whether the association is confounded by genetic or other shared familial factors. Paper-12975607.
MATERIAL AND METHODS: Blood samples from 298 patients hospitalized with a myocardial infarction were subsequently tested for NT-proBNP, hsCRP, MMP-9, PAPP-A, MPO, sCD40L and FM. Paper-13057793.
Data on Pholasin luminescence were compared with results of superoxide anion radical generation detected by the cytochrome c test as well as with the release of elastase and MPO. Paper-9118666.
Myeloperoxidase inactivates TIMP-1 by oxidizing its N-terminal cysteine residue: an oxidative mechanism for regulating proteolysis during inflammation. Paper-12534131.
Myeloperoxidase ( MPO) may mediate neutrophil adherence to the endothelium through upregulation of CD11B expression--an effect downregulated by taurine. Paper-1530119.
When cytochemical detection of MPO was coupled with immunologic detection of LF, LF was observed in the population of MPO-negative granules, which were identified as specific. Paper-4884486.
The presence of each marrow-derived lineage, dysplasia and immunohistochemical results were evaluated ( CD34, CD117, myeloperoxidase, CD68, p53, TdT, CD42b and hemoglobin). Paper-11266254.
In humans with established cardiovascular disease, myeloperoxidase ( MPO) oxidizes HDL, and oxidation by MPO impairs apoA-I's ability to activate LCAT in vitro. Paper-12920463.
The intraneutrophilic concentrations of lactoferrin, myeloperoxidase, collagenase and chymotrypsin-like cationic proteins were measured sequentially during acute bacterial infection. Paper-3132399.
The ectodomain of TPO consists of a large N-terminal myeloperoxidase-like module followed by a complement control protein (CCP)-like module and an epidermal growth factor-like module. Paper-10167089.
Azide, an inhibitor of myeloperoxidase, and catalase which destroys H2O2, essential for MPO-catalyzed oxidations, prevented the generation of C5 activating potency and of chloramines. Paper-839510.
We introduced the NQO1 gene into the HL-60 cell line to create a high MPO-, high NQO1-expressing cell line, and tested its response in assays of benzene metabolite toxicity. Paper-1931528.
The absence of cANCA, anti- PR3, and anti- MPO shows that with appropriate assay conditions, ANCA testing assists in the differentiation between SLE and the ANCA-associated vasculitides. Paper-226303.
Three of the patients with anti- LF antibodies had vasculitis affecting areas additional to the pulmonary-renal involvement which characterised the patients with anti- MPO antibodies. Paper-7652939.
The ability of lipid-free apoA-I to facilitate ATP-binding cassette transporter A1 cholesterol transport was greatly reduced after chlorination by MPO. Paper-10766500.
The relationship between ApoE and MPO genes' polymorphism and the MS activity as well as the defect of remyelination (diffuse demyelination) and brain atrophy on MRI were analysed. Paper-10439177.
GSTM1 deletion was quite common in both controls (49.4%) and cases (50.3%) but was not associated with risk of lung cancer alone or in combination with the MPO polymorphism. Paper-9500840.
Polymorphisms in genes involved in oxidative stress-related mechanisms ( GSTA1, GSTM1, GSTT1, GSTP1, MPO, MnSOD, eNOS, CAT) were determined from blood samples by MALDI-TOF. Paper-12709952.
Arterial blood (10 mL) was collected for assay of leukocyte PLD activity, myeloperoxidase ( MPO) activity, and CD11b expression at 8 different time points in perioperative period. Paper-9146559.
DPI (a dual inhibitor of NADPH-oxidase and NOS), ABAH ( MPO inhibitor) and BAPTA-AM (calcium chelator) significantly reduced 80 mM KCl or NO mediated free radical generation. Paper-13732414.
Localization of the thyroid peroxidase autoantibody immunodominant region to a junctional region containing portions of the domains homologous to complement control protein and myeloperoxidase. Paper-9172980.
Among the patients, GSTM1 null was associated with a significant increase of CA and MPO AA was associated with a significant decrease of CA compared to their respective wild-type genotypes. Paper-10073260.
We investigated a functional biallelic (G/A) polymorphism in the promoter region (-463) of the MPO gene in 465 patients affected by MS, divided into 204 cognitively normal and 261 impaired. Paper-11383980.
MMP-8 levels correlated significantly with the small airway flow parameters (MEF50, MEF25) (p = 0.005 and p = 0.0004) and markers of neutrophil activation ( myeloperoxidase, lactoferrin). Paper-13447481.
Immunogold cytochemistry on LR White resin sections localised elastase and myeloperoxidase to the primary granules, lactoferrin to the secondary granules and lysozyme to both types of granule. Paper-6448649.
Maturation of cells into the myeloid lineage was evaluated by the expression of CD15, CD11b and CD16 and by the presence of primary ( myeloperoxidase) and secondary granules ( lactoferrin). Paper-10025538.
The blasts in this group were non-reactive for myeloperoxidase or non-specific esterase and expressed CD7, CD34 and CD36 with variable expression of CD61, CD13 and CD33. Paper-338557.
RESULTS: During untreated phase of LJP myeloperoxidase, lysozyme and lactoferrin concentrations were remarkably elevated in peripheral blood PMNs, also reflected in their high concentrations in GCF. Paper-784410.
Moreover, significant associations with multiple SNPs in the phase II genes ALDH2, COMT, EPHX1, SOD2, NAT1, NAT2, GSTM3, GSTP1, GSTT2 and MPO were also found. Paper-12774741.
There was weak risk reduction associated with GSTM1 null in heavy smokers (OR = 0.71; 95%CI 0.54-0.94; P = 0.02), but neither GSTM1 nor MPO genotypes affected the overall risk of NSCLC. Paper-10823008.
Following rhTNF-alpha (10(-9) M) pretreatment, the release of LTB4 by PMN stimulated with the P-fimbriate strain was synergistically augmented, while B12 BP and MPO release were additively increased. Paper-12368.
We investigated whether ALL outcome was related to polymorphisms in genes CYP2D6, MPO, EPHX1, NQO1, TS, XPD and XRCC1 in 95 consecutive ALL children by PCR or PCR-FRLP techniques. Paper-13752871.
In contrast, CPZ metabolites generated by the MPO system (in the absence of Cl-) induced polymerization of TG, as revealed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis ( SDS-PAGE). Paper-6838328.
In both cases, Ph+ myeloblasts showed positive stain for myeloperoxidase and naphthol ASD chloroacetate esterase, which fulfilled the FAB criteria of acute myelogenous leukemia (AML). Paper-94899.
We also demonstrate that LRG localizes to the same cytoplasmic compartment as myeloperoxidase and that G-CSF treatment of the 32Dcl3 myeloid cell line induces nuclear translocation of LRG. Paper-12761276.
C-reactive protein ( CRP), protein carbonyls (PC), malondialdehyde ( MDA), susceptible lipoperoxidation of plasma substrates (SLPS), and myeloperoxidase activity ( MPO) were measured. Paper-13800264.
The aim of this study is to summarize the available molecular epidemiologic studies of lung cancer and metabolic genes, such as NAD(P)H quinone reductase 1 ( NQO1) and myeloperoxidase ( MPO). Paper-11441029.
Cathepsin S values significantly correlated with LDH, alpha-1-AT, VEGF, sICAM, sVCAM, MPO, uPA, MMP-9/ TIMP-1, IL-8 and MCP-1, but not with CRP, IL-10 or cathepsin H. Paper-13743194.
Thus, if the M6PR is important in the intracellular transport of MPO, it is the phosphorylated mature MPO that is directed to the lysosomal compartment by this system.(ABSTRACT TRUNCATED AT 400 WORDS) Paper-7201412.
CD11b neutrophil expression, and myeloperoxidase and lactoferrin production, were found to be upregulated during CPB and then to decline to preoperative levels by the third postoperative hour. Paper-8708705.
RESULTS: In the affected limb of CAD+PAD patients, the transfemoral gradients of neutrophil MPOx content and IL-6 were higher (P < .01, for both) than in the healthy leg of CAD-only patients. Paper-13823030.
Collectively, these results reveal that binding of MPO to CD11b/ CD18 integrins stimulates PMN signaling pathways to induce PMN activation in a mechanism independent of MPO catalytic activity. Paper-11187971.
Structure of the murine lactotransferrin gene is similar to the structure of other transferrin- encoding genes and shares a putative regulatory region with the murine myeloperoxidase gene. Paper-7519202.
The results obtained suggest that TNF-alpha- stimulated PMN effectively cause the disruption of EC monolayers by an adherence-dependent mechanism which is mediated by the release of myeloperoxidase. Paper-6556539.
BACKGROUND: The percentage of myeloperoxidase (MPO)-positive blast cells is associated with prognosis in adult acute myeloid leukemia ( AML), but this association is unsubstantiated in pediatric AML. Paper-12692125.
Peroxisome proliferator-activated receptor gamma ligands regulate myeloperoxidase expression in macrophages by an estrogen-dependent mechanism involving the -463GA promoter polymorphism. Paper-10205399.
Of importance, our in vitro studies found that MPO mediated oxidative inactivation of NE, an enzyme that has been widely implicated in the pathogenesis of various tissue-destructive diseases. Paper-10986726.
In a multiple regression analysis, MPO, IL-1beta, IL-8 and CC-16 in BL and MPO in BAL contributed to the explanation of variations in DL(CO) to 41% and 22%. respectively, independent of smoking habits. Paper-8940781.
RESULTS: Children with diabetes had significantly higher plasma MPO levels (p=0.006), increased AIx@75 (p=0.02), IMT (p=0.005) and IMT standard deviation scores (IMT SDS) (p=0.02), compared to the control group. Paper-13714262.
Quantitation of myeloperoxidase ( MPO) activity by guaiacol peroxidation (GP) assay is profoundly affected by the peroxidase present in eosinophils ( EPO) that contaminate the granulocyte suspensions. Paper-4699440.
However, most enzymatic assays for MPO are susceptible to interference from other peroxidases (including eosinophil peroxidase, EPX) and hemoproteins (such as hemoglobin and myoglobin) present in the tissues. Paper-1987559.
Inclusion of 3-amino-1,2,4-triazole ( AMT) in the GP assay permits quantitation of MPO activity in mixed neutrophil-eosinophil suspension because of the differential inhibition of EPO and MPO by AMT. Paper-4699440.
The flavonoid fisetin significantly reduced lung myeloperoxidase-levels and gene-expression of inflammatory mediators such as IL-6, TNF-alpha, IL-1beta, MIP-1alpha and MIP-2. Paper-13717014.
Blood markers of inflammation included MPO, interleukin-6, white blood cell count, C-reactive protein, tumor necrosis factor (TNF)-alpha, the TNF-alpha soluble receptor II, and fibrinogen. Paper-12975607.
Extracellular myeloperoxidase ( MPO) is a macrophage modulator which stimulates release of the pro-inflammatory cytokine TNF alpha in addition to reactive oxygen species (ROS) generated by these cells. Paper-1530119.
Immunocytological methods enable cell typing, using labels such as CD3 for T-cells in reactive inflammation; CD20 for B-cells in retinal lymphoma; CD34 and myeloperoxidase for myeloid leukaemic cells. Paper-13037089.
By contrast other inflammatory markers, neutrophil myeloperoxidase levels, monocyte CD11b, base line C-reactive protein, and platelet CD62P expression did not differ between the two patient groups. Paper-9843216.
The exposure of alpha 1-protease inhibitor to the myeloperoxidase-hydrogen peroxide-halide system resulted in a nearly complete loss of its ability to bind and inactivate purified human neutrophil elastase. Paper-4487558.
Inflammation activates a variety of inflammatory cells, which induce and activate several oxidant-generating enzymes such as NADPH oxidase, inducible nitric oxide synthase, myeloperoxidase, and eosinophil peroxidase. Paper-9837576.
These observations document the ability of neutrophils to inactivate transferrin iron binding capacity via the secretion of myeloperoxidase, formation of H2O2, and subsequent myeloperoxidase-catalyzed iodination. Paper-6450958.
The observations presented led us to conclude that the administrations of IBA at subacute and subchronic exposure decreased AChE, BChE and ADA activities whereas increased MPO activity in various tissues of rats. Paper-13773243.
Bound proteinases have an increased resistance to inhibition by protein proteinase inhibitors, while bound MPO retains its ability to oxidatively inactivate alpha-1- proteinase inhibitor (alpha-1-PI). Paper-181141.
Using a hemolytic plaque assay to detect secretion of lactoferrin and myeloperoxidase ( MPO) from single adherent neutrophils, we showed that LT induced secretion from both primary and secondary granules. Paper-6839642.
Polymorphisms of the GSTM1, GSTP1, MPO, XRCC1, and NQO1 genes in Chinese patients with non-small cell lung cancers: relationship with aberrant promoter methylation of the CDKN2A and RARB genes. Paper-10751323.
We found that activated neutrophils lost cathepsin G activity by a pathway requiring myeloperoxidase, suggesting that oxidants generated by myeloperoxidase might regulate cathepsin G activity in vivo. Paper-11035949.
Coexpression of lymphoid antigens ( CD19, CD10, or CD2) and MPO was shown by the immunogold method in four out of 11 cases; in seven cases the blasts coexpressed myeloid antigens ( CD13, CD33) and MPO. Paper-7617387.
Associations between deletion genotypes of GSTM1 and GSTT1 and between single nucleotide polymorphisms ( SNPs) of GSTP1 Ile105Val and MPO G-463A were first tested by adjusted logistic regression. Paper-10823008.
BALF KL-6 also correlated with the BALF myeloperoxidase ( MPO) activity (r = 0.363, p=0.027), the BALF cell count ml-1 (r = 0.318, p=0.038), BAL ENA-78 (r=0.37, p=0.016) and BALF VEGF (r=0.35,p=0.024. Paper-12760105.
Bone marrow aspiration revealed massive proliferation of blasts that were positive for CD13, CD33, CD34, CD56 and myeloperoxidase, and negative for other T-cell, B-cell and monocytic markers. Paper-8778335.
The de novo MPO-negative acute leukemias, middle level of expression of MPO precursor protein, was found in the blasts of MPO-negative AML (AML, M0), which coexpressed CD13, CD33, CD34, and CD38. Paper-1493127.
The major findings were a relation between exposure to (1--> 3)- beta-D-glucan and an increased prevalence of atopy, a slightly increased amount of MPO, and a decrease in FEV1 over the number of years lived in the house. Paper-1471667.
Myeloperoxidase will catalyse the peroxidation of the chloride ion but salivary peroxidase will not; the product of this in neutral solution is the hypochlorite ion, which is also a reactive oxidizing agent. Paper-5364776.
There is a G-->A polymorphism located in the 5' untranslated region of the MPO gene that may be responsible for reduced transcriptional activity due to the decreased binding affinity for the SP1 transcription factor. Paper-9235085.
Under our experimental conditions, TNF-alpha (2 ng/ml) increased the binding of the antibody against PR3, whereas binding of the antibody against MPO could hardly be detected, not even after TNF-alpha treatment. Paper-12340736.
Infiltrates and microabscesses contained some intact granulocytes and many neutrophils releasing myeloperoxidase, elastase, lactoferrin, defensin, lysozyme, alpha 1-antitrypsin and alpha 1-antichymotrypsin. Paper-732778.
RESULTS: The MPO levels were significantly higher in case subjects than in control subjects and correlated with C-reactive protein ( CRP) (rho = 0.25; p < 0.001) and white blood cell count (rho = 0.33; p < 0.001). Paper-13304079.
The contact between CP and MPO probably entails conformational changes close to the p-phenylenediamine binding site in CP, which explains the observed activation by MPO of the substrate's oxidation. Paper-13503432.
In the apical-to-basolateral direction, epithelial exposure to IFN-gamma markedly upregulated transepithelial migration of PMN in a dose- and time-dependent fashion as measured by both electrical and myeloperoxidase assays. Paper-7582877.
In four combined MPO and oxAT groups classified according to median values, a multinomial logistic regression model showed that high MPO together with high oxAT was independently associated with increased max- CIMT. Paper-13576694.
In AITD patients antibody binding to TPO could not be inhibited by adding native MPO to the serum diluent, suggesting that the possible cross-reactive epitopes were exposed in the denaturated MPO molecule. Paper-1106512.
In conclusion, the present data indicate that TPO autoantibodies can interact with TPO molecules in which the amino-terminus is replaced with the homologous MPO prosequence region, not normally present in mature MPO. Paper-7631103.
The effects of genetic polymorphisms in the NQO1 (rs1800566), MPO (rs2333227), and XRCC1 (rs25487) genes on benzene-induced chromosome abnormalities were assessed in 108 benzene-exposed workers and 33 office workers. Paper-12705767.
Our findings indicate that the level of MPO gene expression influences the CF pathogenesis, presumably reflecting cellular damage by MPO-generated oxidants or other activity of MPO in airway inflammation. Paper-12162053.
Biochemical assays of 12 substances (hemoglobin, albumin, transferrin, alpha(1)-antitrypsin, fibronectin, IgA, IgG, IgM, lactoferrin, myeloperoxidase and neutrophil elastase) were conducted at a commercial laboratory. Paper-11067885.
Results. The increases of TM, vW, sVCAM-1, CRP, SOD and Mpx correlated with the CAD status in the order CO < SAP < ACS, whereas NO and sL-selectin were inversely correlated (p < 0.05, resp.). The other markers remained unchanged. Paper-12250371.
In addition, the cells generated by SCF + TPO were stained with monoclonal antibodies against myeloperoxidase, elastase, lactoferrin, and CD11b, but they had negligible levels of alkaline phosphatase (ALP) and CD35. Paper-1795489.
A questionnaire was used to determine relevant demographic and lifestyle characteristics, and polymorphisms in following genotypes were determined GSTM1, GSTM3, GSTP1, GSTT1, GPX1, MPO, NQO1 and NAT2. Paper-11178082.
HL-60 leukemia cells were transfected with GMPR2 and the expression of CD14 and myeloperoxidase ( MPO) in HL-60 cells with and without 12- o-tetra-decanoyl-phorbol-13-acetate (TPA) induction was monitored by FACS analysis. Paper-9695502.
All sera positive for ANCA on IIF were analyzed for reactivity against antigenic targets other than MPO [bactericidal/permeability-increasing protein ( BPI), cathepsin G, lysozyme, elastase, PR3, and lactoferrin]. Paper-9898595.
Leder's chloroacetate esterase stain; immunostaining for myeloperoxidase, CD34, CD43, CD68, and lysozyme; and ultrastructural finding of cytoplasmic lysosomal granules and Auer bodies all aided in confirming the diagnosis. Paper-1438384.
RESULTS: With a median follow-up of 4.3 years, patients with AML blasts negative for CD9, CD11b, CD13, CD34, and CD41, or positive for CD15, CD33, CD38, CD64, and MPO had superior overall survival. Paper-10020494.
However, adhesion to myeloperoxidase was inhibited by monoclonal antibodies to alpha M ( CD11b) or to beta2 ( CD18) integrin subunits, but not by antibodies to alpha L (CD11a), alpha M ( CD11c), or to other integrins. Paper-1079765.
Measurement of myeloperoxidase indicated that RA SF PMN had degranulated and secreted their myeloperoxidase prior to isolation, 26.5 +/- 11.7% being found extracellularly compared to less than 2.9% in RA and normal blood PMN. Paper-6803252.
We have examined the effect of the myeloperoxidase-hydrogen peroxide-halide system and of activated human neutrophils on the ability of serum alpha 1-protease inhibitor (alpha 1-PI) to bind and inhibit porcine pancreatic elastase. Paper-3923724.
In pneumonia patients, the pulmonary neutrophils released significantly more lactoferrin, MPO and ROS compared to blood neutrophils (basal lactoferrin secretion of pulmonary neutrophils: 1.19+/-1.55 pg/PMN; p<0,01). Paper-1830669.
In this investigation, we studied 120 AR patients and 90 matched controls to elucidate the association between polymorphisms in some metabolizing genes ( GSTM1, GSTT1, CYP2E1, mEH, PON1, and MPO) and susceptibility to AR. Paper-9196437.
METHODS: The expression of CD63 and CD66b on PMN and the release of MPO and LF were investigated in 10 chronic HD patients, during both heparin (HDhep) and trisodium citrate anticoagulation (HDcit), in a randomized order. Paper-8478996.
The TPO extracellular region comprises a large myeloperoxidase-like domain, linked to the plasma membrane by two smaller domains with homology to complement control protein (CCP) and epidermal growth factor ( EGF), respectively. Paper-9172980.
No reduction was seen in neutrophil numbers in the bronchoalveolar lavage fluid, myeloperoxidase activity, or expression of neutrophil chemoattractants CXCL1 and CXCL2, reflecting the specificity of the response. Paper-13480823.
OBJECTIVE: Apolipoprotein A-I (apoAI) acts as an ABCA1-dependent acceptor of cellular phospholipids and cholesterol during the biogenesis of HDL, but this activity is susceptible to oxidative inactivation by myeloperoxidase. Paper-13051770.
Statins inhibit oxidant enzymes activity such as that of reduced nicotinamide adenine dinucleotide phosphate (NAD[P]H) oxidase and myeloperoxidase and up-regulate the activity of antioxidant enzymes such as catalase and paraoxonase. Paper-10532998.
Salivary peroxidase activities were significantly low both in the whole and in the parotid saliva samples of the JP patients, and leukocyte-derived myeloperoxidase was present in significantly low amounts in whole saliva of these patients. Paper-6796072.
Interestingly, none of the ANCA-positive patients had antibodies to myeloperoxidase or to alpha granules which are usually found in the sera of patients with ANCA-associated vasculitis, and only one had antibodies to lactoferrin. Paper-970716.
Abnormal expression patterns have been observed for proteins related to angiogenesis (e.g., vascular endothelial growth factor, angiopoietin-2, matrix metalloproteinase-9), and inflammation (e.g., interleukin-6 [ IL-6] and myeloperoxidase). Paper-13500335.
Expression of CD3, CD10, CD15, CD20, CD34, CD61, CD68, CD79a, CD99, CD117, CD138, myeloperoxidase, haemoglobin A1, glycophorin and terminal deoxynucleotidyl transferase was immunohistochemically analysed. Paper-12400967.
We assessed the presence of selected sequences from promoters of platelet-derived growth factor A ( PDGF-A), c-myc, myeloperoxidase ( MPO), CD11b, p53, WT1, CCR5, ING1, and NM23-H1 genes in the cross-linked complexes. Paper-11802234.
Interactions of these autoantibodies with MPO target antigen, Fcgamma receptors and Beta2 integrins at the neutrophil surface, can set in train a sequence of intracellular signal transduction events that culminate with functional responses. Paper-10604217.
Preincubation with pertussis toxin inhibited rGM- CSF- induced secretion of both lactoferrin and MPO. rTNF-induced MPO secretion was also blocked by pertussis toxin, whereas lactoferrin secretion was only slightly affected. Paper-6266970.
The use of immunogold double-labeling of CD67 and lactoferrin ( LF; as marker for specific granules) or CD67 and myeloperoxidase ( MPO; as marker for azurophilic granules) showed that CD67 occurred only in the specific granules. Paper-6922886.
Potential cross-reactivity between thyroid peroxidase ( TPO) and myeloperoxidase ( MPO) molecules was evaluated by analysing the binding of 199 TPO antibody- and MPO antibody-positive sera to TPO and MPO molecules. Paper-1106512.
Granulocyte-mediated reactions such as opsonization, chemotaxis, and release of granulocyte myeloperoxidase and lactoferrin were studied in properdin-deficient and normal human serum incubated with serogroup A and W-135 meningococci. Paper-7016644.
Studies of the potential role of polymorphisms in the genes encoding the glutathione S-transferases, cytochrome P450 3A4, NAD(P)H:quinone oxidoreductase and myeloperoxidase in the etiology of treatment-related complications are reviewed. Paper-9584478.
Bronchial lavage fluids showed higher levels of protein and myeloperoxidase in the I/R than in the sham-treated group (P < .01). eNOS expression was down-regulated and iNOS expression up-regulated in I/R lung tissues (n = 3). Paper-12233035.
Tyrosine 192 in apolipoprotein A-I is the major site of nitration and chlorination by myeloperoxidase, but only chlorination markedly impairs ABCA1-dependent cholesterol transport. Paper-10766500.
TNF-alpha-primed neutrophils were stimulated with monoclonal antibodies (MAb) to human myeloperoxidase ( MPO) and proteinase 3 ( PR3), and with preparations of human ANCA (three patients with PR3-ANCA and two patients with MPO-ANCA). Paper-8774777.
Stimulated PMN from patients with hereditary MPO deficiency had decreased viricidal activity unless MPO was added, and the viricidal activity of MPO-supplemented, MPO-deficient PMN was inhibited by catalase, implicating endogenous H2O2. Paper-7523108.
Antibodies against myeloperoxidase, proteinase-3, and other specific granule proteins (elastase, lactoferrin, cathepsin G, lysozyme, and bactericidal permeability-increasing protein) were measured by an enzyme-linked immunosorbent assay. Paper-13705478.
Tissue inflammatory injury progressed over hours in the post-resuscitation phase. pGz-CPR group had significantly lower myeloperoxidase ( MPO) activity and plasma creatine phosphokinase (CPK) and cardiac troponin I, TNF-alpha, and IL-6 than TH-CPR. Paper-12207896.
Administration of rolipram after LPS and before zymosan treatment obliterated the increase in pulmonary vascular permeability, but its effect on sequestration of neutrophils in pulmonary microvessels, as measured by MPO, was less marked. Paper-1354207.
The results obtained thus suggest that CYP1A1 induces iNOS expression leading to the generation of endogenous nitric oxide (NO) that could be responsible for the augmentation of myeloperoxidase-mediated benzo(a)pyrene-induced injury in PMNs. Paper-11832676.
The finding that MPO is a potent inhibitor of tryptase lends further support to the hypothesis that neutrophil proteins, such as MPO and lactoferrin, may play a regulatory role as endogenous suppressers of tryptase enzyme activity. Paper-1874902.
Pancreatic tissue for histopathologic scores and myeloperoxidase, glutathione reductase, glutathione peroxidase, and catalase activites were collected, and blood for serum amylase, urea, creatinine, and inleukin-6 measurements was withdrawn. Paper-13509337.
Several additional immunohistochemical staining showed that the cells were positive for CD13, CD34, CD117, and HLA DR, but negative for myeloperoxidase, CD42b, glycophorin, B cell marker, T cell marker, cytokeratin and desmin. Paper-13649236.
This contrasted with lactoferrin and NGAL, which were synthesized almost exclusively in the group containing myelocytes and metamyelocytes, and with MPO, which was mainly synthesized in the group containing myeloblasts and promyelocytes. Paper-157785.
ANCAs directed against either myeloperoxidase ( MPO) or proteinase 3 ( PR3) can activate cytokine-primed neutrophils by binding cell surface- expressed MPO or PR3, with the concurrent engagement of Fcgamma receptors (FcgammaR). Paper-8855251.
Genetic variations in catalase (CAT) (C-262T), myeloperoxidase ( MPO) (G-463A), endothelial nitric oxide synthase (NOS3) (G894T) and heme oxygenase-1 ( HO-1) [(GT)(n) dinucleotide length polymorphism] were not associated with breast cancer risk. Paper-13745098.
Median serum levels of HNL (200.5 microg x L(-1)), MPO (595 microg x L(-1)) and lactoferrin (1,356.5 microg x L(-1)) were significantly increased in patients with CF compared to control subjects (57.7, 178 and 478 microg x L(-1), respectively; p<0.0001). Paper-2052591.
The SSP levels of MPO and IL-8, and the degree of plasma protein leakage in the COPD-HI group, were retrospectively compared with and found significantly higher than those of noninfected COPD patients, suggesting a more marked inflammatory response in COPD-HI. Paper-8385211.
Our objective was to investigate the correlation between lipoprotein-associated phospholipase A2 (PLA2-LDL), myeloperoxidase ( MPO), and paraoxonase ( PON), enzymes implicated in the evolution of endothelial dysfunction associated with type 2 diabetes. Paper-10566204.
The total content of histamine, ECP, EPX, and MPO were 10-70-fold higher in all unfiltered erythrocyte products compared to donor plasma concentrations, while PAI-1 content was 15-20-fold higher only in plasma-reduced whole-blood and whole-blood. Paper-1046828.
Particularly, genetic polymorphisms in NAD(P)H-quinone oxidoreductase ( NQO1), cytochrome P450 (CYP)1A1, myeloperoxidase ( MPO), glutathione-S-transferase (GST)P1, GSTT1, and GSTM1, and have been suspected to affect lung cancer risk. Paper-13339475.
Glucosamine treatment during resuscitation significantly attenuated the T-H-induced increase in cardiac levels of TNF-alpha and IL-6 mRNA, IkappaB-alpha phosphorylation, NF-kappaB, NF-kappaB DNA binding activity, ICAM-1, and MPO activity. Paper-13589972.
We conclude that (a) an immunohistochemical panel including CD20, CD43, CD68, and MPO can successfully identify the vast majority (96%) of EMT in paraffin sections, and (b) there is an association between morphology and phenotype in these lesions. Paper-7665972.
The release of lactoferrin and HNL, but not of myeloperoxidase ( MPO), was slightly enhanced after preincubation of isolated normal neutrophils with G-CSF in vitro, but no obvious release of these proteins was observed with G-CSF alone. Paper-568924.
Immunostains for myeloperoxidase, lysozyme, neutrophil elastase, LCA, CD79a, CD20, CD43, CD45RO, CD3, CD30, CD15, CD68, MAC387, VS38C, MIC2, and the Leder stain for naphthol-ASD-chloroacetate esterase were performed on all cases. Paper-1888048.
We determined whether episodes of a high CRP value were paralleled by simultaneous increases in mediators of inflammatory injury or molecules associated with endothelial cell adhesion or growth and whether CRP levels correlated with those of VEGF and MPO. Paper-12366540.
DEX transiently increased the concentration of surfactant protein-A in epithelial lining fluid but had no effect on surface activity of the sedimentable surfactant complex or on concentrations of phosphatidylcholine, IL-1 beta, lactoferrin, or myeloperoxidase. Paper-8162414.
MAIN OUTCOME MEASURES: Self-reported respiratory symptoms; plasma prostaglandin E2, myeloperoxidase, Interleukin (IL)-6, IL-8, IL-10 and IL-1 receptor antagonist ( IL-1ra) concentrations; and salivary myeloperoxidase and IL-6 concentrations. Paper-13080381.
CONCLUSION. -: An immunohistochemical panel including CD43, lysozyme, myeloperoxidase ( MPO), CD68 (or CD163), CD117, CD3 and CD20 can successfully identify the vast majority of MS variants in formalin-fixed paraffin-embedded tissue sections. Paper-13440526.
In addition, it significantly inhibited oxidative damage of purified genomic DNA and suppressed activity of myeloperoxidase ( MPO), a generator of potent oxidant ( hypochlorous acid), in tumor necrosis factor-alpha ( TNF-alpha) stimulated human myeloid cells. Paper-13889363.
Although the precursor synthesized by cells expressing the Y173C mutation (MPOY173C) was glycosylated, associated with the molecular chaperones calreticulin and calnexin, and acquired heme, it was neither proteolytically processed to mature MPO subunits nor secreted. Paper-1474228.
Differential cell counts and eosinophilic cationic protein ( ECP) were determined in blood and sputum, and myeloperoxidase ( MPO), tumour necrosis factor-alpha ( TNF-alpha), and interleukin (IL)-8 and IL-10 were determined in sputum supernatants. Paper-9136130.
In the current studies, we used tandem mass spectrometry to identify the major sites of tyrosine oxidation when lipid-free apolipoprotein A-I (apoA-I), the major protein of HDL, was exposed to MPO or peroxynitrite ( ONOO(-)). Paper-10766500.
After pretreatment of PMN with 5 micrograms of cytochalasin b per ml, slime predominantly induced release of specific granule contents (33.8% lactoferrin release by 250 micrograms of slime per ml versus 10% myeloperoxidase release by 250 micrograms of slime per ml). Paper-5164643.
The most valuable markers to differentiate between myeloperoxidase-negative AML subtypes M0 and ALLs were CD13, CD33, and CD117, typical of M0, and intracytoplasmic CD79a, intracytoplasmic CD3, CD10, and CD2, typical of B cell- or T cell-lineage ALL. Paper-9197964.
Higher concentrations of CB or Lat B, or stabilization of F-actin with jasplakinolide ( JP), inhibited primary granule exocytosis measured as myeloperoxidase release but did not affect secondary granule exocytosis determined by lactoferrin release. Paper-13093282.
Changes in mediators of inflammation, such as eosinophilic cationic protein ( ECP), myeloperoxidase ( MPO), interleukin-8 ( IL-8), IL-1beta, tumor necrosis factor alpha (TNFalpha) and C-reactive protein ( CRP) in the airways and/or blood, have also been found. Paper-9079990.
Attempts to characterize this quasi-lipoxygenase activity revealed that calcium potentiated the quasi-lipoxygenase activities of hemoproteins (hemoglobin, myoglobin, myeloperoxidase, catalase, cytochrome c) and hemin at the physiological pH of 7. Paper-1730977.
Immunohistochemical staining was performed to measure expression of CD3, CD4, CD8, tryptase, eosinophil cationic protein, myeloperoxidase, basophil granular protein, IL-4, IL-5, IL-8, CCR3 and CXCR3, ICAM-1, VCAM and ELAM. Paper-11048024.
Cortical demyelination in MS is associated with increased activity of MPO, which is expressed by a CD68-positive subset of activated microglia, suggesting that microglial production of reactive oxygen species is likely to be involved in cortical demyelination. Paper-12709640.
These results indicate that ligation of CR1 on neutrophils by C3b fixed to IgG may alter signal transduction events linking ligation of neutrophil Fc receptors to cellular events required for release of myeloperoxidase and generation of HOCl. Paper-1386982.
Lactoferrin was found to be released spontaneously from a fraction of neutrophils while MPO was released only after phagocytosis, reflecting different mechanisms for degranulation of MPO-containing azurophil and lactoferrin-containing specific granules. Paper-4558956.
PMN adhered to fibrinogen in the presence of rTNF alpha could be further stimulated with cytochalasin B and N-formyl-methionyl-leucyl-phenylalanine ( FMLP) to release azurophilic granule markers as measured by increasing MPO activity and A alpha(1-21) production over time. Paper-7008329.
AGEPC-induced PMN exocytosis of azurophilic ( myeloperoxidase and beta-glucuronidase) and specific ( lactoferrin and lysozyme) lysosomal granules was rapid ( T 1/2 = 20 sec), dependent on the presence of cytochalasin B, but was not associated with release of cytoplasmic LDH. Paper-3813536.
Concentrations of 20 microM auranofin and 200 microM GST resulted, respectively, in a 61.5% and 19.3% reduction of release of lysozyme, 61.7% and 27.1% reduction of beta-glucuronidase, 84.8% and 33.7%s reduction of myeloperoxidase, and 50.0% and 25.0% reduction of lactoferrin. Paper-3997396.
Catalase, cytochrome C, histidine, and methionine inhibited the PMA-induced 51Cr-release by human neutrophils, whereas superoxide dismutase, myeloperoxidase inhibitors, and some hydroxyl radical scavengers or singlet oxygen quenchers had no effect. Paper-3524159.
During hemodialysis of heparinized blood without having a patient in the circuit, the serum concentrations of lactoferrin, myeloperoxidase ( MPO) and eosinophil cationic protein ( ECP) steadily increased, indicating neutrophil and eosinophil degranulation. Paper-4170119.
TNF alpha caused a time-dependent secretion of the granule markers gelatinase and lactoferrin but no liberation of myeloperoxidase and minimal production of A alpha(1-21), a specific cleavage product of fibrinogen generated by elastase, as markers for the azurophilic granule. Paper-7008329.
With this approach, several absorption peaks corresponding to myeloperoxidase and eosinophil peroxidase, which overlap with peaks of cytochrome b, were obliterated from reduced-minus-oxidized spectra, whereas the peaks of cytochrome b were not and could be readily quantitated. Paper-5220235.
In the sputum sol phase of 9 patients with symptomatic asthma the levels of IL-8 were lower than in 9 patients with COPD (asthma: 6.4 ng/ml; COPD: 16.3 ng/ml; p < 0.02) and significantly correlated with those of neutrophilic myeloperoxidase ( MPO; r = 0.85; p < 0.005). Paper-477441.
Thus, we conclude that neutrophils in synovial fluid from patients with rheumatoid arthritis have been activated in vivo to secrete myeloperoxidase and propose that the products of this enzyme system can contribute to the tissue damage associated with this disease. Paper-5817490.
It is expected that utilisation of molecular studies including immunoglobulin and T-cell receptor gene rearrangement and m-RNA expression for myeloperoxidase will provide a better insight into the level of differentiation for the presently unclassifiable cases of CML-blast crisis. Paper-454943.
The negative correlation of CXCR2 expression with interleukin-8 and myeloperoxidase indicates that myeloid cells were stimulated by CXC chemokines with Glu-Leu-Arg (ELR) motif and thereby contributed to tissue damage, leading to impairment of cardiovascular and respiratory function. Paper-9989418.
Liver tissue was removed to study the activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase ( GSH-Px), myeloperoxidase ( MPO), xanthine oxidase ( XO), adenosine deaminase ( ADA), and the levels of malondialdehyde and nitric oxide (NO). Paper-12132825.
The effect of carvedilol was studied on stimulated superoxide generation, MPO release and iNOS expression in phagocytes by using receptor operating stimuli [N-formyl-Met-Leu-Phe ( FMLP), lipopolysaccharide (LPS) and specific inhibitors (wortmannin, propranolol). Paper-12365987.
ANCA positivity was searched for by indirect immunofluorescence (IIF) and enzyme linked immunosorbent assay ( ELISA) using a neutrophil extract, and antigen specificity was determined by proteinase 3 ( PR3), lactoferrin ( LF) and myeloperoxidase ( MPO) ELISA. Paper-8204414.
Analysis of the DNA methylation status at key sites within these genes showed a pattern of differentiation- and expression-associated demethylation of the LZM gene, which was also enhanced by G-CSF, and constitutive and unaltered demethylation at key regions of the CD34 and MPO genes. Paper-475933.
Taken in their entirety, the data suggest a dichotomy of function for myeloperoxidase; that is, enzymatically active MPO functions primarily in cell killing through the 'cytotoxic triad' and iMPO functions as an immunoregulatory molecule through the induction of numerous cytokines. Paper-8875160.
At the same time, FG alone, unlike recombinant GH alone, led to significant increases in anastomotic bursting pressures, tensile strength, and tissue HP content, along with decreases in anastomotic MPO and NF-kappaB activity and later plasma levels of TNF-a and IL-6. Paper-13618579.
We therefore suggest that in some patients with RA, MPO-ANCA necrotizing glomerulonephritis (GN) may occur as a kidney-limited form of rheumatoid vasculitis, and that RA should be added to the list of diseases potentially associated with necrotizing GN with anti- MPO antibodies. Paper-1759541.
Bronchoalveolar lavage was performed on 45 subjects (FASSc n = 20; CFA n = 15; normals n = 10); cell counts and levels of neutrophil-derived enzymes, myeloperoxidase, elastase (total elastase and elastase/ alpha 1 antitrypsin complexes), collagenase and lactoferrin were measured. Paper-743791.
Degranulation responses, as measured by the extracellular release of the granule enzymes myeloperoxidase or lysozyme, were amplified by approximately 50-100% for both MSUM or CPPD crystal-induced neutrophil activation when cells were pretreated with TNF-alpha at 2000 pM or GM-CSF at 75 pM. Paper-1036232.
A significant augmentation was observed in the nitrite content, activities of superoxide dismutase, MPO and GST and the expressions of iNOS and CYP1A1, however, catalase activity was attenuated in PMNs of benzo(a)pyrene treated rats as compared with their respective controls. Paper-11832676.
All sera were tested by enzyme-linked immunosorbent assay ( ELISA) for the presence of antibodies to proteinase 3, myeloperoxidase ( MPO), elastase, lactoferrin ( LF), and cathepsin G ( CG), and by Western blotting for antibodies to neutrophil proteins. Paper-7551829.
Eleven of 35 sera exhibited binding in Western blot studies with the MPO preparation used in the ELISA: five sera bound at the size of MPO, but five sera reacted with a 78 kD species (p78) co-purifying with MPO, and one serum blotted both MPO and p78. Paper-8207467.
In particular, the degree of correlation was high in the following genes critical in the diagnostic setting: CD4, CD8, CD13 ( ANPEP), CD33, CD23 ( FCER2), CD64 ( FCGR1A), CD117 (KIT), CD34, MPO, CD20 ( MS4A1), CD7 (range of r, 0.589-0.807). Paper-12315911.
Thirteen single nucleotide polymorphisms ( SNPs) from 10 oxidative stress genes ( AKR1A1, AKR1C1, CYBA, GPX, MPO, NOS2A, NOS3, OGG1, PPARG and SOD2) were genotyped in 1172 NHL cases and 982 population-based controls from a USA multicenter case-control study. Paper-12180974.
We find that phorbol ester (PE) treatment of K562 cells greatly stimulates promoters ( T cell receptor beta, myeloperoxidase, macrophage colony-stimulating factor receptor, and granulocyte macrophage colony-stimulating factor receptor) containing AML1 transcription factor binding sites. Paper-10647715.
The binding involves three cell types, neutrophils, eosinophils, and monocytes and at least two reaction mechanisms, one involving the peroxidase of neutrophils and monocytes ( myeloperoxidase [ MPO]) and possibly the eosinophil peroxidase, and the second involving catalase. Paper-2700685.
Proteins binding to CS were identified by mass spectrometry as MPO, lactoferrin, cathepsin G, and azurocidin/cationic antimicrobial protein of molecular weight 37 kDa, suggesting that serglycin may be a general transport vehicle for the cationic granular proteins of neutrophils. Paper-10011713.
In permeabilized cells, anti-VAMP-7, but not anti-VAMP-8, antibody impaired the secretion of all mediators examined (in eosinophils, eosinophil peroxidase and eosinophil-derived neurotoxin; in neutrophils, myeloperoxidase, lactoferrin and matrix metalloprotease-9) in a dose-dependent manner. Paper-11845010.
The concentration ofmalondialdehye (MDA), protein carbonyl content, conjugated dienes, mucosal (SH) sulphydryls, uric acid, tumor necrosis factor-alpha ( TNF-alpha), and activities of myeloperoxidase ( MPO), xanthine oxidase ( XO) and antioxidative enzymes were determined in the gastric mucosa. Paper-11529908.
Plaque expression of MPO, AGEs, RAGE, NF-kappaB, COX-2, mPGES-1, matrix metalloproteinase (MMP)-2 and MMP-9, lipid and oxidized LDL (oxLDL) content, procollagen 1, and interstitial collagen was analyzed by immunohistochemistry and Western blot; zymography was used to detect MMP activity. Paper-12320257.
In parallel, we observed a similar time-dependent decrease of gelatinase B (a marker of specific and gelatinase B-containing granules) but not myeloperoxidase (a marker of azurophil granules) in the granule fraction, and release of lactoferrin (a marker of specific granules) in the extracellular medium. Paper-13049272.
Monocytes were cultured in the absence or presence of various PKC activators for up to 2 weeks, and examined for the number of adherent cells, expression of myeloperoxidase enzymes, CD14 antigens, mannose/ N-acetylglucosamine ( Man/ GlcNAc) receptors, and the production of TNF-alpha. Paper-110071.
In multivariable-adjusted models there were significant overall between-smoking group differences (defined as p<0.0045 to account for multiple testing) for every inflammatory marker tested, except for serum CD40 ligand ( CD40L), myeloperoxidase ( MPO) and tumor necrosis factor receptor-2 ( TNFR2). Paper-12768166.
However, when neutrophils were loaded with increasing concentrations of quin-2 to buffer any local, not detectable, changes in the concentration of cytoplasmic Ca2+, both rTNF- and rGM- CSF- induced secretion of lactoferrin and MPO were almost totally abolished at a relatively low quin-2 concentration. Paper-6266970.
The samples collected on the first day contained high-abundant plasma proteins, such as albumin and immunoglobulins, glandular serous cell proteins (lysozyme, lactoferrin, and polymeric immunoglobulin receptor), epithelial keratins, and inflammatory cell proteins ( myeloperoxidase, IL-16, and IL-17E). Paper-10422502.
PURPOSE: Because radiotherapy exerts cytotoxic effects via generation of massive oxidative stress, we hypothesized that catalase, manganese superoxide dismutase, myeloperoxidase ( MPO), and endothelial nitric oxide synthase ( eNOS) genotypes might result in greater risk of radiotoxicity. Paper-12344994.
The genes in which SNPs were analyzed include CCR2, CCR5, COX1, COX2, CRP, CSF1, CSF2, IFNG, IL1A, IL1B, IL2, IL4, IL6, IL8, IL10, IL13, IL18, LTA, MPO, NOS2A, NOS3, PPARD, PPARG, PPARGC1 and TNF. Paper-12476405.
A 30% release of myeloperoxidase ( MPO) and lactoferrin ( LF) from the primary and specific granules, respectively, was detected by enzyme-linked immunosorbent assay in adhered neutrophils stimulated with 0.1 microM N-formyl-methionyl-leucyl-phenylalanine ( FMLP) or 20 microM A-23187. Paper-7727719.
Signaling through TLR2 promoted the fungicidal activity of PMNs through oxidative pathways involving extracellular release of gelatinases and proinflammatory cytokines while TLR4 favored the oxidative pathways through the participation of azurophil, myeloperoxidase-positive, granules and IL-10. Paper-10624010.
RESULTS: Myeloperoxidase ( MPO), N-acetyl -beta-D- glucosaminidase (NAGase), tumor necrosis factor-alpha ( TNF-alpha), interleukin-8 ( IL-8) in mammary tissues and CD4(+)/CD8(+) in peripheral blood were increased and serum MPO and IL-2 in mammary tissues were decreased 12h after LPS infusion. Paper-13596919.
The main purpose of the present study was to evaluate myeloperoxidase ( MPO) positive cell infiltration, COX-2 and HIF-1alpha protein expression in colorectal carcinogenesis, especially in its early phases, using immunohistochemistry and immunofluorescence confocal microscopy techniques. Paper-13760507.
In a multivariate model that included other biochemical markers, troponin T (HR 1.99; P=0.023), C-reactive protein (1.25; P=0.044), vascular endothelial growth factor (HR 1.87; P=0.041), soluble CD40 ligand (HR 2.78; P<0.001), and MPO (HR 2.11; P=0.008) were all independent predictors of the patient's 6-month outcome. Paper-9995694.
In this study, the relationship between the expression of PMN degranulation markers ( CD63 and CD66b) and the release of degranulation products [ myeloperoxidase ( MPO) and lactoferrin ( LF)] was investigated during clinical HD in order to evaluate cell surface markers as a useful index of PMN degranulation. Paper-8478996.
Immunohistochemical studies of jejunal biopsy specimens from another group of patients with celiac disease demonstrated a prominent extracellular deposit of ECP in the lamina propria of the atrophic intestinal mucosa, whereas the release of neutrophil constituents ( cathepsin G, MPO) was scarce. Paper-6245034.
Using an in vitro expansion and differentiation system for human CD34+ cord blood (CB) progenitor cells, we analyzed the induction and expression kinetics of the granulomonocyte associated lysosomal proteins myeloperoxidase ( MPO), lysozyme (LZ), lactoferrin ( LF), and macrosialin ( CD68). Paper-424903.
The authors assessed the sputum concentration of the neutrophil chemoattractants interleukin-8 ( IL-8) and leukotriene (LT)B4, myeloperoxidase ( MPO) as a marker of neutrophil influx, neutrophil elastase activity and its natural inhibitors, alpha1AT and secretory leukoprotease inhibitor ( SLPI). Paper-8353197.
Brain edema was formed by cold injury using metal sterile rods with a diameter of 4 mm that were previously cooled at -80 degrees C. Twenty-four hours after the injury, animals were decapitated and brain tissues were investigated for brain edema, tissue MPO and caspase-3 levels, and ultrastructure. Paper-12769177.
The cationic proteins were extracted with 0.2 mol/L sodium acetate, pH 4.0 from the granules in the PMN and subjected to both non-denaturing and denaturing acid urea polyacrylamide gel electrophoresis (AUPAGE) for identification of myeloperoxidase ( MPO), lysozyme, protease activity and lactoferrin. Paper-1130802.
Myeloperoxidase ( MPO), which displays considerable amino acid sequence homology with thyroid peroxidase ( TPO) and lactoperoxidase ( LPO), was tested for its ability to catalyze iodination of thyroglobulin and coupling of two diiodotyrosyl residues within thyroglobulin to form thyroxine. Paper-7523342.
TRL-01 had the same immunophenotype as the original leukemia cells: positive for CD13, CD33, CD11a, CD18, CD29, CD49d, CD49e, CD54, CD62L, and CD117, and negative for CD3, CD4, CD8, CD19, CD34, CD41a, CD41b, CD135, and myeloperoxidase. Paper-12076113.
Six polymorphisms in five different genes were analysed: myeloperoxidase ( MPO) -129G/A and -463G/A, toll-like receptor 4 ( TLR4) Asp299Gly, interleukin-6 ( IL6) -174G/C, surfactant protein D ( SFTPD) Met11Thr and regulated upon normal T-cell expressed and secreted ( CCL5) -403G/A. Paper-13575239.
Tumor cells expressed vimentin, S-100 protein, CD68, and MAC387, but were negative for LCA, CD1a, CD3, CD15, CD20, CD21, CD23, CD30, CD35, carcino-embryonic antigen, HMB45, cytokeratin AE1/3, EMA, myeloperoxidase, lysozyme, smooth-muscle actin, and desmin. Paper-11189532.
We conclude that although determination of the serum-levels of lactoferrin, lysozyme and myeloperoxidase in certain cases may be valuable as a supplement to the morphological examination of acute myeloid leukemia, it is evident that none of the three determinations can be used alone to distinguish between the FAB groups. Paper-5510256.
The present study comprised 20 complex heart operations, 10 with heparin-coated circuits (group HC) and 10 controls (group C), with evaluation of changes in terminal complement complex, the granulocyte enzymes myeloperoxidase and lactoferrin, and the cytokines interleukin-6 ( IL-6) and interleukin-8 ( IL-8). Paper-713898.
METHODS: Biopsy specimens were obtained from 42 KFD cases for microscopic examination after the sections were stained with haematoxylin and eosin, and the immunohistochemical features were analyzed by monoclonal antibodies ( CD20, CD8, CD45RO, CD57, CD68) and polyclonal antibody ( myeloperoxidase, MPO). Paper-9957945.
Therefore, we analyzed both immune (total IgA, IgG, IgM, anti-Streptococcus mutans IgA, IgG, and IgM antibodies) and nonimmune (lysozyme, lactoferrin, salivary peroxidase, myeloperoxidase, hypothiocyanite, thiocyanate, and agglutinins) factors in whole saliva of 15 patients with common variable immunodeficiency. Paper-7980005.
The extent of the contribution of polymorphisms in other genes involved in the metabolism of benzene and related compounds-such as the P450 2E1 ( CYP2E1), myeloperoxidase ( MPO), glutathione-S-transferase ( GSTM1, GSTT1), microsomal epoxide hydrolase ( EPHX1), and other genes-should also be considered. Paper-9396613.
Inhibition of CPPD crystal-induced activation of the neutrophil inflammatory response as measured by chemiluminescence, superoxide anion generation and degranulation as determined by myeloperoxidase and lysozyme release was observed in the presence of the specific p38 MAP kinase inhibitor SB203580 (5 microM). Paper-10322326.
OBJECTIVE: To evaluate the performance of 11 commercial enzyme-linked immunosorbent assay ( ELISA) kits for the detection of antineutrophil cytoplasmic antibodies (ANCA) directed against proteinase 3 ( PR3) and myeloperoxidase ( MPO) in patients with Wegener's granulomatosis ( WG) and microscopic polyangiitis (MPA). Paper-9185689.
Multiple enzymes are expressed in vascular cells that are involved in the elimination and production of reactive oxygen species, including the superoxide dismutases, catalase, thioredoxin reductase, glutathione peroxidase, NAD(P)H oxidase, xanthine oxidase, myeloperoxidase, and endothelial nitric oxide synthase. Paper-11372484.
Double labeling of the cells with myeloperoxidase and lymphoid markers demonstrated that individual blasts in all the five T+ AML tested were simultaneously expressing myeloperoxidase activity and CD7; however, most blasts in the three B+ AML studied expressed either myeloperoxidase activity or CD10, but not both. Paper-7770568.
RESULTS: Pre- or posttreatment with C-PC (30 or 50 mg/kg, IP) significantly attenuated carrageenan-induced inflammatory nociception and the induction of iNOS and COX-2 at the late phase, (4 h) accompanied by an inhibition of the formation of TNF-alpha, prostaglandin E(2), nitrate and myeloperoxidase activity. Paper-13673932.
In this model, Escherichia coli endotoxin ( LPS, 0.1 microgram/kg) combined with platelet-activating factor (1 pmol/kg/min over 60 min, n = 10) caused microvascular lung injury characterized by elevation of myeloperoxidase activity, deposition of C3 and C5b-9 on the endothelium of pulmonary vessels, and pulmonary edema. Paper-7526407.
After blood stasis in varicose veins, the leukocyte markers lactoferrin, myeloperoxidase, and interleukin-8 were not modified, whereas L-selectin shed from leukocytes increased (P<0.05), and a major increase in pro-MMP-9, which is released from tertiary granules during polymorphonuclear activation, was observed (P=0.0001). Paper-9523724.
PGP expression was positively correlated to the presence of myeloperoxidase activity in less than 3% of blasts (p = 0.025), and CD34 antigen expression (p = 0.04), whereas CD33 antigen expression had borderline significance (p = 0.07), demonstrating that PGP expression predominated in blasts with an immature phenotype. Paper-8223021.
MMP-8 is activated by hypochlorous acid produced by myeloperoxidase from hydrogen peroxide and chloride ion and by the hydroxyl radical produced in Haber Weiss reaction fed by superoxide produced by, eg, NADPH (reduced nicotinamide adenine dinucleotide) oxidase and xanthine oxidase. Paper-7201027.
To investigate interactions between the endothelium and leukocytes in patients with sepsis, we measured soluble adhesion molecules (sE-selectin and sICAM-1), von Willebrand factor antigen ( vWf:Ag), myeloperoxidase ( MPO), and lactoferrin ( Lacto-f) as plasma markers of endothelial and neutrophil activation. Paper-1361419.
The proportion of genotypes of cytochrome P450 2E1 ( CYP2E1), glutathione-S-transferase mu-1 ( GSTM1), glutathione-S-transferase theta-1 ( GSTT1), myeloperoxidase ( MPO), and NAD(P)H, quinone oxidoreductase 1 ( NQO1) were compared between workers with WBC <4 x 10(9)/L and those with WBC >/=4 x 10(9)/L. Paper-12324340.
EPO also caused a substantial reduction of (i) the rise in myeloperoxidase activity ( mucosa), (ii) the expression in the tissue of TNF-alpha, TGFbeta and VEGF (iii) the increase in staining ( immunohistochemistry) for nitrotyrosine and for PAR, as well as (iv) the NF-kappaB activation caused by CG in the peritoneum. Paper-13604333.
Introduction of purified eosinophil peroxidase ( EPO) into the phagosome by binding the enzyme to the surface of the zymosan particles changed the hypermetabolic characteristics of superoxide production in MPO-deficient cells to more closely resemble normal cells, but had no effect on superoxide generation by the normal monocytes. Paper-4410842.
METHODS AND RESULTS: Conditioned media from luminal, intermediate, and abluminal layers of 29 human ILTs were analysed for neutrophil markers [elastase/alpha1-antitrypsin and MMP9/ NGAL complexes, myeloperoxidase ( MPO), and alpha-defensin peptides], RANTES, platelet factor 4 ( PF4), and interleukin-8 ( IL-8). Paper-13771808.
Since it has been shown that alterations in innate immune pathways contribute to the risk for serious infections, we analyzed well-characterized variants in innate immune genes ( TNF, IL6, IL8, MPO, CHIT, FCGR2A, TLR2, and TLR4) to determine their possible contribution to infectious complications during therapy for pediatric AML. Paper-10992823.
In the nasal irrigation we investigated the following inflammatory cells and soluble mediators: eosinophils, neutrophils, granulocyte-macrophage colony-stimulating factor, interleukin-4, interleukin-6, interleukin-8, ECP, EPX, MPO, leukotriene C4, leukotriene B4, prostaglandin E2, tryptase and fibrinogen. Paper-1316766.
Various agonists, pathological conditions, and therapeutic interventions lead to modulated expression and function of oxidant and antioxidant enzymes, including NAD(P)H oxidase, endothelial nitric oxide synthase, xanthine oxidase, myeloperoxidase, superoxide dismutases, catalase, thioredoxin reductase, and glutathione peroxidase. Paper-10928342.
Adduct formation in stimulated neutrophils was inhibited 80% by the myeloperoxidase inhibitor sodium azide (1 mM) but was not affected by proadifen (100 microM), indomethacin (100 microM), or eicosatetraynoic acid (100 microM), inhibitors of cytochrome P450, prostaglandin synthetase, and lipoxygenase, respectively. Paper-1769963.
To clarify the role of myeloperoxidase ( MPO) in multiple sclerosis ( MS), we measured serum MPO levels in 86 Japanese patients with relapsing remitting MS, 47 with opticospinal MS (OSMS) and 39 with conventional MS ( CMS), and 85 healthy subjects by sandwich enzyme immunoassays and analyzed relationships with clinical features. Paper-12210041.
Plaques from the simvastatin group had less (P<0.0001) immunoreactivity for MPO, AGEs, RAGE, p65, COX-2, mPGES-1, MMP-2, and MMP-9, lipids and oxLDL; reduced (P<0.0001) gelatinolytic activity; increased (P<0.0001) procollagen 1 and collagen content; and fewer (P<0.0001) macrophages, T-lymphocytes, and HLA-DR+ cells. Paper-12320257.
Biochemical and metabolic parameters, circulating adiponectin, resistin, ICAM-1, VCAM-1, E-selectin, P-selectin, PAI-1, myeloperoxidase ( MPO), and matrix metalloproteinase-9 ( MMP-9) concentrations were assessed in 10 women with type 2 DM before and after rosiglitazone treatment and in a control group of healthy women. Paper-13443046.
We studied the presence of proteinase 3 ( PR3), myeloperoxidase ( MPO) and elastase ( HLE) on the plasma membrane of neutrophils in patients with biopsy-proven Wegener's disease ( WG), pANCA-positive vasculitis, control patients (SLE, rheumatoid arthritis, ankylosing spondylitis), sepsis patients and healthy donors. Paper-7850725.
The possible role of DNA methylation changes during several commitment steps of immature myeloid precursor cells toward functional, terminally differentiated phagocyte cells has previously been examined in the human myeloperoxidase ( MPO) and macrophage colony- stimulating factor/ c-fms genes using normal and transformed myeloid precursor cells. Paper-992496.
Two recent studies [Britigan, Rosen, Thompson, Chai & Cohen (1986) J. Biol. Chem. 261, 17026-17032; Winterbourn (1987) J. Clin. Invest. 78, 545-550] both reported that neutrophil degranulation could potentially inhibit the formation of .OH, but differed in their conclusions as to the responsible factor, myeloperoxidase ( MPO) or lactoferrin ( LF). Paper-1987.
The GSTM1 homozygous null type and GSTT1 homozygous null type were no differences in the patients and controls (chi2 = 0.01, P = 0.92 versus chi(2) = 0.31, P = 0.57), and no significant differences in the polymorphisms of the MPO and MnSOD genotypes were found between the patients and controls (chi2 = 2.00, P = 0.37 versus chi2 = 0.07, P = 0.96). Paper-11292930.
Immunohistochemistry can help diagnose and distinguish four variants: granulocytic myeloperoxidase ( MPO+, CD 68+ [KP1+/-, PGM1-] lysozyme+, CD 34+/-), monoblastic (MPO-, CD 68+, [KP1+, PGM1+] lysozyme+, CD 34-), myelomonoblastic (MPO-, CD 68+, [KP1+, PGM1+] lysozyme+, CD 34-), or megakaryoblastic (positivity for factor VIII, CD 61, CD 31). Paper-10108224.
There are no changes in the phorbol myristate acetate receptor number or affinity, glucose transport, NADPH levels, cytochrome b559 content, catalase (EC 1.11.1.6) GSH, GSH peroxidase (EC 1.11.1.9), GSH reductase (EC 1.6.4.2) or myeloperoxidase, consistent with the suppressed ROI secretory capacity and antiprotozoal activity of these cells. Paper-5440438.
Because MPO participates in the eradication of Mycobacterium tuberculosis in the in vitro model and the extracellular enzyme may activate cells to cytokine synthesis, we investigated the changes in the enzyme concentration in serum of patients with active pulmonary tuberculosis (TB) and correlations between MPO and TNF-alpha, IFN-gamma, and IL-12. Paper-10868900.
Candidates included genes that control the transcription of metabolizing genes [ aryl hydrocarbon receptor ( AHR), AHRR and aryl hydrocarbon nuclear translocator ( ARNT)] and genes that activate/detoxify AA or PAH ( AKR1C3, CYP1A1, CYP1A2, CYP1B1, CYP3A4, EPHX1, EPHX2, NQO1, MPO, UGT1A4, SULT1A1 and SULT1A2). Paper-12955278.
Superoxide dismutase (SOD, 10 U/ml) prevented 1) the effects of TNF on the hemodynamic responses to U-46619 and ACh and 2) the TNF- induced decrease in NO2-. The effects of TNF on lung MPO and effluent O2- were prevented using cyclophosphamide intraperitoneally (100 mg/kg 5 days before, and 50 mg/kg 1 day before, treatment with TNF or control). Paper-7875202.
These synonyms are used for gene MPO (myeloperoxidase): Myeloperoxidase.
These accession numbers are used for gene MPO: X04876 (NCBI_GENBANK__AC), Q14862 (UNIPROT__AC), BC130476 (NCBI_GENBANK__AC), A1L4B8 (UNIPROT__AC).
MPO is a homologue of MPO (myeloperoxidase) from Pan troglodytes.
MPO is a homologue of MPO (myeloperoxidase) from Gallus gallus.
MPO is a homologue of MPO (myeloperoxidase) from Canis lupus familiaris.
MPO is a homologue of Mpo (myeloperoxidase) from Mus musculus.
MPO is a homologue of Mpo (myeloperoxidase) from Rattus norvegicus.
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iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.