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)

The interaction of granulocyte-colony stimulating factor (G-CSF) and retinoic acid (RA) in proliferation and differentiation of acute promyelocytic leukemia (APL) cells was examined. G-CSF stimulated proliferation of APL cells at concentrations of 0.1 to 50 ng/ml in a dose dependent manner. More than 10(-8) M RA induced granulocytic differentiation of APL cells. Although G-CSF induced lysozyme activities in APL cells, it alone did not induce terminal differentiation of APL cells. G-CSF significantly enhanced the RA-induced granulocytic differentiation of APL cells in vitro. Enhancement by G-CSF was not due to the prolongation of survival of RA-induced differentiated cells, but the differentiation-inducing effects of G-CSF might be evident only in the presence of RA. Since G-CSF has a potential to induce the granulocytic differentiation of myeloid leukemia cells, G-CSF in combination with RA may be applicable in differentiation induction therapy for some types of myeloid leukemia.
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PMID:Granulocyte-colony stimulating factor and retinoic acid cooperatively induce granulocyte differentiation of acute promyelocytic leukemia cells in vitro. 248 63

The effect of transforming growth factor-beta (TGF-beta) on induction of differentiation of mouse myeloid leukemia M1 cells was investigated. TGF-beta 1 induced adherence of M1 cells to plastic dishes and inhibited their proliferation. However, it did not induce differentiation-associated properties, such as phagocytic activity, lysozyme activity or morphological maturation. TGF-beta 1 also caused dose-dependent inhibition of dexamethasone-induced differentiation of M1 cells. The inhibitory activity of TGF-beta 1 was 20 times that of TGF-beta 2 on M1 cells. These results suggest that TGF-beta 1 inhibits proliferation and dexamethasone-induced differentiation of M1 cells by interacting with receptors that can distinguish between TGF-beta 1 and TGF-beta 2. TGF-beta 1 had a much lower inhibitory effect on the growth of a variant M1 cell clone, which was resistant to differentiation inducers, and it did not induce adherence of the resistant M1 cells.
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PMID:Inhibitory action of transforming growth factor-beta on induction of differentiation of myeloid leukemia cells. 249 57

Granulocyte-colony stimulating factor (G-CSF) induces differentiation of M1 murine myeloid leukemia cells into mature granulocytes/macrophages and also causes accumulation of the cells in the G1 phase of the cell cycle. We examined, therefore, whether synchronization of M1 cells in the G1 phase could affect G-CSF-induced differentiation as quantitated by expression of Fc fragment receptors (FcR) and lysozyme activity. Cells were arrested in early G1 by density inhibition in the absence of serum and in late G1 by addition of aphidicolin. Cells synchronized in early G1, when stimulated with G-CSF, showed enhanced expression of FcR and lysozyme activity. Eighty percent of the cells expressed FcR 18 hr after addition of G-CSF while, in exponentially growing cells, this percentage was reached 72 hr after addition of G-CSF. Cells synchronized in late G1 did not show enhanced expression of differentiation markers. These results imply that with respect to G-CSF-induced differentiation, the G1 phase can be separated into an early permissive and a later nonpermissive stage.
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PMID:Colony stimulating factor-induced differentiation of murine M1 myeloid leukemia cells is permissive in early G1 phase. 308 80

Serum lysozyme activity was measured in samples from 65 children with acute lymphatic and myelogenous leukemia, solid tumors and malignant lymphoma in comparison with 45 healthy children. All children with acute lymphatic leukemia (ALL) had significantly reduced levels of lysozyme before starting therapy compared with a control group (p less than 0,01). Children with ALL in complete remission had lysozyme levels comparable to normal children, while children with ALL in relapse showed pathological low levels again. Children with acute myelogenous leukemia (AML), solid tumors and malignant lymphomas had higher lysozyme concentration before therapy than healthy children. Determination of lysozyme activity in children with acute leukemia and malignant tumors is of value for diagnosis and to control the effect of therapy.
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PMID:[Serum lysozyme level in children with acute leukemia and malignant diseases]. 385 10

Mouse monocytic Mm-A cells are a highly leukemogenic variant line of the monocytic and non-leukemogenic cell line Mm-1, which developed spontaneously from mouse myeloid leukemia M1 cells. Studies were made on whether Mm-A cells could be induced to differentiate further by agents that were effective for inducing differentiation of the parent M1 cells and other leukemic cells. Of the agents tested, butyrate, conditioned medium from concanavalin A-stimulated spleen cells, lipopolysaccharide (LPS) and N6,O2-dibutyryl adenosine 3'5'-cyclic-monophosphate (dbcAMP) significantly stimulated the lysozyme activity of Mm-A cells, which is one of the most characteristic biochemical markers of monocytes and macrophages. Butyrate was the most effective agent for increasing lysozyme production by Mm-A cells; culture with 0.5mM butyrate for 3 days increased lysozyme production by Mm-A cells about 50-fold. Inducers of M1 cell differentiation such as dexamethasone, 1 alpha,25-dihydroxyvitamin D3, arginase, and proteinous inducer did not increase the lysozyme activity. Butyrate also induced NBT reduction and stimulated other differentiation-associated functions, such as expressions of Fc receptors on the cell surface, immune phagocytosis and production of inducer for M1 cell differentiation. Its effect in stimulating differentiation of Mm-A cells was synergistic with that of dbcAMP or LPS. Incubation with butyrate inhibited the proliferation of Mm-A cells, about 0.3mM butyrate causing 50% inhibition. These results indicate that monocytic, leukemogenic Mm-A cells can be induced to differentiate further by butyrate and that the inducers of differentiation of Mm-A cells are markedly different from those of the parent myeloblastic M1 cells.
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PMID:Induction of differentiation of cultured mouse monocytic leukemia cells (Mm-A) by inducers different from those of parent myeloblastic leukemia cells (M1). 393 26

Mouse myeloid leukemia M1 cells were induced to differentiate in vitro into macrophages and granulocytes by various inducers including ascitic fluid. Differentiated M1 cells induced with ascitic fluid expressed a differentiation-associated cell surface glycoprotein with a molecular weight of 180,000 (p180), which can be labeled by lactoperoxidase-catalyzed radioiodination or metabolic labeling with L-[14C]fucose. p180 was also induced by treatment with conditioned medium of hamster embryo cells, dexamethasone, dibutyryl cyclic adenosine 3':5'-monophosphate, and prostaglandin E1. Ascitic fluid, conditioned medium of hamster embryo cells, and dexamethasone induced all the differentiation-associated properties tested, whereas dibutyryl cyclic adenosine 3':5'-monophosphate and prostaglandin E1 induced lysozyme activity and adhesiveness to the substratum but not phagocytosis, locomotive activity, Fc receptors, or morphological changes. The adherent cells induced by dibutyryl cyclic adenosine 3':5'-monophosphate produced a large amount of p180, while the floating cells produced very little, but no difference was detected in the lysozyme activities of the two cell types. These results suggest that p180 is associated with cell-substratum adhesion of differentiated M1 cells.
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PMID:Expression of a cell surface glycoprotein (p180) related to cell-substratum adhesion during differentiation of mouse myeloid leukemia cells. 625 64

Phorbol esters, including 12-O-tetradecanoylphorbol 13-acetate (TPA), induce terminal macrophagelike differentiation of cells from human acute myelogenous leukemia lines. We report that myelogenous leukemia cells obtained from patients undergo macrophagelike differentiation after exposure to TPA. The myeloid leukemic cell cultured with TPA became adherent to charged surfaces with long filamentous pseudopodia; developed positive staining for alpha-napthyl acetate esterase, increased lysozyme secretion, reduced nitroblue tetrazolium, and acquired the ability to phagocytose candida. Cells from patients with lymphocytic leukemia did not become macrophagelike when cultured with TPA.
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PMID:Phorbol diester-induced macrophage differentiation of leukemic blasts from patients with human myelogenous leukemia. 625 22

The GDM-1 permanent cell line was established from the peripheral blood of a patient with a Philadelphia chromosome negative myeloproliferative disorder, after transformation to acute myelomonoblastic leukemia. The GDM-1 cells exhibited the same characteristics as those isolated from the peripheral blood of the patient prior to death: cells contained non-specific esterase sensitive to fluoride, myeloperoxidase, lysozyme (muramidase), and exhibited both Fc and complement (C3) receptors but lacked B- and T-cell surface markers including T-associated antigens. E-rosetting capacity, surface and intracytoplasmic immunoglobulins and EBV determined nuclear antigen (EBNA). The GDM-1 cells bore the 1a receptor and the myeloid leukemia antigen (M-1). The karyotype of the cultured leukemic cells showed the same specific chromosomal abnormalities present in the monoblasts obtained from the peripheral blood prior to death, indicating that the cell line was derived from the original leukemic cells.
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PMID:Establishment and characterization of a new permanent cell line (GDM-1) from a patient with myelomonoblastic leukemia. 629 52

1 alpha, 25-Dihydroxyvitamin D3 [1,25-(OH)2D3] was shown to induce a high phagocytic capability in the macrophage-like murine tumor cell line P388D1. Induction of phagocytic capability by 1,25-(OH)2D3 was dose-dependent in the range of 0.2 to 5.0 ng/ml, required the continuous presence of the secosteroid in culture, and was reversible. 25-Hydroxyvitamin D3 was an effective inducer only at about 500 ng/ml, while 24R,25-dihydroxyvitamin D3 was ineffective. The induction of the high phagocytic capability was neither accompanied by increased synthesis of lysozyme nor closely associated with an inhibitory effect on cellular proliferation. P388D1 cells bound (without ingestion) nonopsonized sheep erythrocytes (sheep RBC), and the binding increased in 1,25-(OH)2D3-treated cells. Fc-receptor-mediated binding of immunoglobulin G-coated sheep RBC was not modulated in 1,25-(OH)2D3-treated cells, but the cells acquired an Fc-receptor-mediated phagocytic capability that was expressed only when preformed P388D1-sheep RBC rosettes were further exposed to immunoglobulin G. Several differentiation agents of myeloid leukemia cells (including dexamethasone) were not effective in inducing the high-phagocytic phenotype, while retinoic acid was very effective. Different myeloid or macrophage-like tumors (WEHI-265, J774.2, PU-5, and WEHI-3) were variable in their response to 1,25-(OH)2D3.
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PMID:Induction of a high phagocytic capability in P388D1, a macrophage-like tumor cell line, by 1 alpha, 25-dihydroxyvitamin D3. 654 2

The murine macrophage-like cell line (Mm-1), which is nonleukemogenic to syngeneic SL mice, was originally derived from spontaneously differentiated cells of a clonal line of mouse myeloid leukemia cells (M1). In the present experiment, variant cell lines with a high (Mm-A), moderate (Mm-P), and little or no (Mm-S1 and Mm-S2) leukemogenic potential were obtained from the Mm-1 cells. The mean survival times of syngeneic SL mice inoculated i.p. with 5 X 10(6) Mm-A and Mm-P cells were 17 and 33 days, respectively, whereas almost all the mice inoculated with Mm-S1 or Mm-S2 cells survived for more than 90 days. These variant cell lines did not lose their macrophage-like characteristics in vitro. These variant cell lines phagocytized latex beads and sensitized sheep erythrocytes, produced lysozyme, and adhered to culture dishes. The four variant cell lines showed no significant difference in proliferation rates in vitro in liquid medium containing 10% calf serum, but Mm-A cells could grow both in soft agar medium in the absence of ascitic fluid containing colony-stimulating factor (CSF) and in liquid medium containing 1% serum, whereas Mm-P cells could grow in the liquid medium but not in soft agar medium without ascitic fluid, and Mm-S1 and Mm-S2 cells could not grow in either medium. The ratio of the nuclear area to the cell area (NCR) of Mm-A cells was a high (51%) but those of Mm-S1 and Mm-S2 cells were low (40-41%), and that of Mm-P cells was intermediate (44%). The leukemogenicity of Mm-1 cell lines was roughly correlated with their NCR. The possibility that interactions between Mm-1 variant cells and host immune cells might be involved in the mechanisms of their different leukemogenicities was not supported by results on the in vitro susceptibilities of Mm-1 variant cells to the cytostatic actions by normal macrophages and spleen cells and on leukemogenicities of the Mm-1 variant cells in athymic nude mice. A possible method of control of the leukemogenicity of Mm-1 variant cells is discussed.
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PMID:Selection of mouse macrophage-like sublines that differ in leukemogenic potential and characterization. 658 65


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