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

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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cell line, HAFTL-1, derived by in vitro transformation of fetal liver cells with v-Ha-ras, was found to have molecular and phenotypic characteristics of pro-B cells recently committed to the Ly-1+ B cell differentiation pathway. Stimulation of these cells with LPS resulted in their differentiation within either the B or myelomonocytic lineages. Thus, lines derived from LPS-stimulated HAFTL-1 cells were shown to be clonally related, as evidenced by common v-ras integrations, but to exhibit characteristics of pre-B cells (ThB expression, continuing DJ heavy chain rearrangements) or mature macrophages (expression of Mac-1 and Mac-2, lysozyme and nonspecific esterase production, phagocytosis) while maintaining their Ly-1+ phenotype. These results suggest that events resulting in the irrevocable commitment to a single lineage occur late in differentiation, at least within the pathway yielding Ly-1+ B cells and a proposed subpopulation of Ly-1+ monocytes and macrophages. Final commitment to these lineages is carefully orchestrated, as evidenced by restricted expression of Ly-5 isoforms and production of IgH transcripts.
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PMID:Relationships between B cell and myeloid differentiation. Studies with a B lymphocyte progenitor line, HAFTL-1. 329 35

Soft-agar colonies of mouse splenic macrophages were examined for surface and functional characteristics that might prove useful in studying the origin(s) of macrophage diversity. Flow cytoflurometric analysis revealed that essentially all cells in all of the colonies bore the Mac-1 and Mac-3 antigens. The colonies did not differ appreciably in their phagocytic activity or in their secretion of lysozyme, but did show different patterns of Mac-2 antigen expression. In most colonies, the cells expressed low levels of the antigen, and in the remainder they expressed a high or an intermediate level of Mac-2. The colonies also differed in their ability to present keyhole limpet hemocyanin (KLH) to an antigen-specific H-2-restricted T-cell hybridoma. About 6% of the colonies gave rise to subcultures with antigen-presenting activity. This presentation was always associated with subcultures containing a high proportion of Ia-bearing macrophages, but not all cultures with similarly high proportions of Ia-bearing cells presented KLH to the hybridoma. Indeed, the induction of Ia on all cells in all cultures increased the proportion of KLH-presenting subcultures only about twofold. The results show that not all splenic macrophages have the ability to process KLH and present it to a T-cell hybridoma. This suggests the presence of functionally specialized subpopulations of macrophages, possibly derived from distinct progenitors, in the spleens of mice.
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PMID:Origins of macrophage diversity: functional and phenotypic analysis of cloned populations of mouse splenic macrophages. 347 67

An accessory cell line, designated line A, was generated from bone marrow stem cells which differentiated in vitro in response to colony-stimulating factor (CSF) in substratum cultures. The cells were found to constitutively secrete large amounts of CSF, the activity of which was neutralized by anti-CSF-1 antibodies. Cells of line A and its supernatants potentiate the suboptimal response of thymocytes to PHA, manifesting an interleukin-1 (IL-1)-like activity. Culture fluids of this line also reconstitute the response to T cell mitogens of spleen cells depleted of adherent accessory cells. It was also found that cells of line A bear low levels of surface Ia, and they efficiently present soluble antigen to proliferating memory T cells. Constitutive prostaglandin secretion, which sometimes masks antigen-presenting capacity, was also demonstrated. Cells of line A are poorly phagocytic, do not secrete lysozyme, and lack Fc and complement receptors. However, they manifest strong cytoplasmic nonspecific esterase staining and an ectoenzyme profile resembling that of elicited inflammatory macrophages. In addition, the cell surface antigen Mac-2 was demonstrated, while stainings with anti-Mac-1 and anti-Mac-3 were negative. Thus, line A may represent a unique subpopulation of immunoregulatory accessory cells, the features of which are discussed.
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PMID:Establishment and characterization of a novel bone-marrow-derived macrophage-like accessory cell line. 348 60

Twenty cases of histiocytic sarcoma in 15 female and five male (384 to 722 days of age) hybrid F1 (C57BL/6 x BALB/c) or F2 (F1 x F1) mice were studied for expression of mononuclear phagocyte and other antigens. Histiocytic sarcomas were found most often in liver, uterus, spleen, and lung. Tissues fixed in Bouin's fluid provided preservation of antigen immunoreactivity, using avidin biotin peroxidase complex immunohistochemistry, with monoclonal and polyclonal antibodies. The mononuclear phagocyte antigens, lysozyme and Mac-2 (a galactose-specific lectin that binds IgE), were found in 60-70% of the cases. The receptor for the macrophage colony-stimulating factor (CSF-1), c-fms, was expressed in 2/20 (10%) of the cases. Mouse immunoglobulins were not found in histiocytic sarcoma cells. In uterine histiocytic sarcomas, previously reported as Schwannomas because of their histologic appearance, S-100 protein was not expressed by tumor cells, although they usually expressed Mac-2 and lysozyme. Hyaline droplets were found in the renal tubules of only 2/19 cases. Our studies provide evidence that murine histiocytic sarcoma expresses antigens (Mac-2, lysozyme, c-fms) found in cells of the mononuclear phagocyte series, in contrast to the B-cell origin of many human histiocytic tumors.
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PMID:Expression of mononuclear phagocyte antigens in histiocytic sarcoma of mice. 811 50

Proteins modified by advanced glycation endproducts (AGE) bind to cell surface receptors and other AGE binding proteins. AGE-binding receptors are: scavenger receptors types I and II, the receptor for advanced glycation endproducts (RAGE), oligosaccharyl transferase-48 (OST-48, AGE-R1), 80K-H phosphoprotein (AGE-R2) and galectin-3 (AGE-R3). AGE receptors are found in monocytes, macrophages, endothelial cells, pericytes, podocytes, astrocytes and microglia. AGE-modified proteins also bind to lysozyme and lactoferrin. A critical review of the evidence for receptors binding AGE-modified protein binding in vivo is presented. Scavenger receptors have only been shown to bind proteins modified by AGE to a much higher extent than found in vivo. 80K-H phosphoprotein is involved in FGFR3 signal transduction to MAP kinase, and may be involved in AGE-receptor signal transduction. Whether all of these proteins bind AGE-modified proteins in vivo is not yet clear. Cell activation in response to AGE-modified proteins is associated with increased expression of extracellular matrix proteins, vascular adhesion molecules, cytokines and growth factors. Depending on the cell type and concurrent signaling, this is associated with chemotaxis, angiogenesis, oxidative stress, cell proliferation or programmed cell death (PCD). Receptor recognition factors for agonism at the AGE receptor have been little studied but to date hydroimidazolones appear to be the most likely candidates. Pharmacologic inhibition of AGE receptor-mediated cell activation with specific antagonists may provide the basis for therapeutic intervention in diseases where AGE accumulation is a suspected etiological factor vascular complications of diabetes, macrovascular disease, renal insufficiency and Alzheimer's disease.
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PMID:Cell activation by glycated proteins. AGE receptors, receptor recognition factors and functional classification of AGEs. 984 83

Immunohistochemistry is an indispensable tool in human pathology enabling immunophenotypic characterization of tumor cells. Immunohistochemical analyses of mouse models of human hematopoietic neoplasias have become an important aspect for comparison of murine entities with their human counterparts. The aim of this study was to establish a diagnostic antibody panel for analysis of murine lymphomas/leukemias, useful in formalin-fixed/paraffin-embedded tissue. Overall, 48 antibodies (4 rabbit monoclonal, 12 rabbit polyclonal, 2 goat polyclonal, 11 rat, and 19 mouse monoclonal), which were either mouse-specific (14) or cross-reactive with murine tissue (34) were tested for staining quality and diagnostic value in 468 murine hematopoietic neoplasms. Specific staining was achieved with 29 antibodies, of which 18 were human antibodies cross-reactive with murine tissue. Only 23 (B220, BCL-2, BCL-6, CD117, CD138 (2x), CD3 (2x), CD43, CD45, CD5, CD79 alpha cy, cyclin D1, Ki-67 (2x), Mac-3, Mac-2, lysozyme, mast cell tryptase, MPO, Pax-5, TdT, and TER-119) were regarded as valuable for diagnostic evaluation. Immunohistochemistry was also established in an automated immunostainer for high throughput analysis. The antibody panel developed is useful for the classification of murine lymphomas and leukemias analyzed, and a valuable tool for human and veterinary pathologists involved in the diagnostic interpretation of murine models of hematopoietic neoplasias.
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PMID:A comprehensive antibody panel for immunohistochemical analysis of formalin-fixed, paraffin-embedded hematopoietic neoplasms of mice: analysis of mouse specific and human antibodies cross-reactive with murine tissue. 1745 84

Under mechanical ventilation with high-inspired oxygen concentration, diffuse alveolar damage was found to take place in some patients. To clarify the molecular pathophysiology of this condition, we investigated the time course of gene expression changes induced by hyperoxia exposure in mouse lung using real-time quantitative polymerase chain reaction (qPCR). Our results normalized by glyceraldehyde 3-phosphate dehydrogenase showed that mRNA levels of cysteine rich protein 61 (CYR61) and connective tissue growth factor (CTGF) were significantly upregulated, while those of surfactant-associated protein C (SFTPC), cytochrome P450, 2F2 (CYP2F2), Claudin 1, (CLDN1), membrane-associated zonula occludens protein-1 (ZO-1), lysozyme (LYZS), and P lysozyme structural (LZP-S) were significantly downregulated. Increasing level of mRNAs, each encoding CYR61 and CTGF, suggests a serious risk of fibrosing alveolitis. Decrease in levels of mRNAs for SFTPC, CYP2F2, CLDN1, ZO-1, LYZS, and LZP-S suggests alveolar dysfunction and disruption of the immune system. Moreover, we confirmed apoptotic conditions, such as significant upregulations of mRNA levels in Myc and Galectin-3. Hyperoxic condition probably yielded reactive oxygen species (ROS), which resulted in a malignant cycle of ROS production by Myc overexpression.
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PMID:Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase. 1830 9

In order to identify genes associated with primary chemotherapy-resistance, gene expression profiles (GEP) in tumour tissue from 37 patients with de novo diffuse large B-cell lymphoma (DLBCL), stage II-IV, either in continuous complete remission (n = 24) or with progressive disease during primary treatment (n = 13), were examined using spotted 55K oligonucleotide arrays. Immunohistochemistry was used for confirmation at the protein level. The top 86 genes that best discriminated between the two cohorts were chosen for further analysis. Only seven of 86 genes were overexpressed in the refractory cohort, e.g. RABGGTB and POLE, both potential targets for drug intervention. Seventy-nine of 86 genes were overexpressed in the cured cohort and mainly coded for proteins expressed in the tumour microenvironment, many of them involved in proteolytic activity and remodelling of extra cellular matrix. Furthermore, major histocompatibility complex class I molecules, CD3D and ICAM1 were overexpressed, indicating an enhanced immunological reaction. Immunohistochemistry confirmed the GEP results. The frequency of tumour infiltrating lymphocytes, macrophages, and reactive cells expressing ICAM-1, lysozyme, cathepsin D, urokinase plasminogen activator receptor, signal transducer and activator of transcription 1, and galectin-3 was higher in the cured cohort. These findings indicate that a reactive microenvironment has an impact on the outcome of chemotherapy in DLBCL.
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PMID:Genes associated with the tumour microenvironment are differentially expressed in cured versus primary chemotherapy-refractory diffuse large B-cell lymphoma. 1841 22

We have found diffuse alveolar damage (DAD) has taken place in some patients under mechanical ventilation with high-inspired oxygen concentrations. To clarify the molecular pathophysiology of this, the time course of gene expression changes induced by hyperoxia exposure in mouse lungs was examined using real-time quantitative polymerase chain reaction (real-time qPCR). Our raw data and those normalized with glyceraldehyde 3-phosphate dehydrogenase (GAPDH) showed that: (1) there is a decrease in levels of mRNAs for surfactant-associated protein C (SFTPC), cytochrome P450, 2F2 (CYP2F2), Claudin 1 (CLDN1), membrane-associated zonula occludens protein-1 (ZO-1), lysozyme (LYZS), and this suggests alveolar dysfunction and a disruption of the immune system, (2) we confirmed apoptotic conditions, such as significant up-regulations of mRNA levels in Myc and Galectin-3, and (3) hyperoxic conditions probably yielded reactive oxygen species (ROS), which resulted in a malignant cycle of ROS production by Myc overexpression [Shimada I, Matsui K, Brinkmann B, Hohoff C, Hiraga K, Tabuchi Y, et al. Novel transcript profiling of diffuse alveolar damage induced by hyperoxia exposure in mice: normalization by glyceraldehyde 3-phosphate dehydrogenase. Int J Legal Med 2008;122:373-83]. In this experiment, GAPDH was up-regulated when hyperoxia exposure was continued. Therefore, we reexamined our data and found that: (1) mRNA levels of other housekeeping genes, including beta(2)-microglobulin (beta2M), ribosomal protein: large P2 (RPLP2), and importin 8 (IPO8) altered to a lesser extent, (2) mRNA levels of beta2M and IPO8 were down-regulated when hyperoxia exposure was continued, and (3) our previous work was validated by normalization with these three housekeeping genes.
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PMID:Time course of housekeeping gene expression changes in diffuse alveolar damage induced by hyperoxia exposure in mice. 1927 28

Galectins are beta-galactoside-binding lectins involved in several biological processes and galectin-3 (Gal-3) is related to modulation of immune and inflammatory responses. This study aimed to evaluate the role of Gal-3 in the life span and biological functions of murine neutrophils during in vitro infection by virulent Toxoplasma gondii RH strain. Inflammatory peritoneal neutrophils (Nphi) from C57BL/6 wild-type (WT) and Gal-3 knockout (KO) mice were cultured in the presence or absence of parasites and analyzed for phosphatidylserine (PS) exposure and cell death using Annexin-V and propidium iodide staining, and cell viability by MTT assay. Cell toxicities determined by lactate dehydrogenase (LDH), degranulation by lysozyme release, and cytokine production were measured in Nphi culture supernatants. Phorbol myristate acetate (PMA)- or zymosan-dependent reactive oxygen species (ROS) were measured in Nphi cultures. Our results demonstrated that Gal-3 is involved in the increase of the viable Nphi number and the decrease of PS exposure and cell death following T. gondii infection. We also observed that Gal-3 downmodulates T. gondii-induced Nphi toxicity as well as Nphi degranulation regardless of infection. Furthermore, Gal-3 expression by Nphi was associated with increased levels of IL-10 in the beginning and decreased levels of TNF-alpha later on, regardless of parasite infection, as well as with decreased levels of IL-6 and increased IL-12 levels, following early parasite infection. Our results also showed that Gal-3 suppresses PMA- but not zymosan-induced ROS generation in Nphi following T. gondii infection. In conclusion, Gal-3 plays an important modulatory role by interfering in Nphi life span and activation during early T. gondii infection.
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PMID:Galectin-3 plays a modulatory role in the life span and activation of murine neutrophils during early Toxoplasma gondii infection. 1972 Apr 28


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