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Y Honma

Publications and source records attributed to Y Honma.

At least 343 records · Page 19Linked to original sources

Cellular retinoid-binding proteins in cultured human and mouse myeloid leukemia cells.

Retinoic acid and retinol induced functional and morphological differentiation of human promyelocytic leukemia cells (HL-60) into mature granulocytes, but did not induce functional or morphological differentiation of mouse myeloid leukemia cells (M1). Cellular retinoic acid-binding protein, but not retinol-binding protein, was detected on HL-60 cells. Neither binding protein could be detected on M1 cells. These results suggest that retinoic acid-binding protein may be necessary for induction by retinoids of functional and morphological differentiation of myeloid leukemia cells.

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Scanning and transmission electron microscope studies of the supraependymal neurons in the third ventricular wall of the Arctic lamprey, Lampetra japonica.

Scanning electron microscopy of the third ventricular wall of the arctic lamprey, Lampetra japonica, revealed the occurrence of supraependymal neurons in several regions of the ventricular surface. These neurons--as varicose fibers of various calibers--traversed among the cilia, microvilli, and bulbous protrusions of the ependymal surface. Occasionally synapse-like contact were found between these nerve fibers and the intraventricular processes of the cerebrospinal fluid (CSF)-contacting subependymal neurons in the hypothalamus. A possible function of the supraependymal neurons is discussed in relation to the hypothalamic neuroendocrine system.

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Ectopic presence of saccus vasculosus tissue in the neurohypophysis of three species of plectognath fishes (Tetraodontiformes, Teleostei).

The extraregional occurrence of saccus vasculosus tissue was observed in the neurohypophysis of several specimens of three species of plectognath fishes, Fugu niphobles. Fugu poecilonotus and Canthidermis rotundatus. The ectopic tissue occurred as a compact multitubular structure in the posterior portion of the pars nervosa, either being buried in it or attaching to its dorsal margin. Scanning electron microscopy revealed that ectopic crown cells of F. niphobles were distributed further in the ependymal layer of the infundibulum. A possible route of these crown cells to the neurohypophysis was discussed with special reference to the close anatomical relationship between the neurohypophysis and the saccus vasculosus in the embryonic stage.

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Production of differentiation-inhibiting factor in cultured mouse myeloid leukemia cells treated with retinoic acid.

Mouse myeloid leukemia cells (M1) could be induced to differentiate into mature macrophages and granulocytes with dexamethasone or proteinaceous inducer. Retinoic acid inhibited functional and morphological differentiation of M1 cells, but the pyridyl analog of retinoic acid had no effect. M1 cells could be induced to produce a factor(s) inhibiting their own differentiation to macrophage- and granulocyte-like cells by retinoic acid but not by its pyridyl analog. This factor(s) inhibited induction by inducers of phagocytic activity, locomotive activity, lysozyme activity, and morphological changes in M1 cells. The production of the inhibitory factor(s) by M1 cells incubated with retinoic acid was inhibited by a low concentrations (5--10 ng/ml) of actinomycin D. The inhibitory factor seemed to be a protein(s), since it was susceptible to heat treatment and proteases. The effect of retinoic acid in inducing production of the inhibitory factor(s) by M1 cells seemed to be reversible, since it was low on washing the cells with fresh medium. Therefore, induction of this inhibitory factor may be involved in the mechanism of inhibition of functional and morphological differentiation of M1 cells by retinoic acid.

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Induction of differentiation of cultured human and mouse myeloid leukemia cells by alkyl-lysophospholipids.

Alkyl-lysophospholipids are synthetic analogs of naturally occurring lysophospholipids. The effects of these compounds on cell proliferation and differentiation of cultured human (HL-60) and mouse (M1) myeloid leukemia cells were studied. Both cell lines were induced to differentiate into morphologically and functionally mature granulocytes and macrophages by incubation with a wide variety of these compounds. Some alkyl-lysophospholipids induced differentiation (judged morphologically and by the appearance of abilities to reduce nitro blue tetrazolium, to phagocytize latex particles, and to induce lysozyme activity) of both the cells lines at concentrations of 1 microgram/ml. However, these compounds did not affect colony formation of normal mouse bone marrow cells even at a higher concentration, 20 microgram/ml. These results suggest that alkyl-lysophospholipids induce cell differentiation of myeloid leukemia cells without affecting proliferation and differentiation of normal bone marrow cells. Thus, these compounds could be useful in therapy of myeloid leukemia.

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Inhibition of differentiation of mouse myeloid leukemia cells by phenolic antioxidants and alpha-tocopherol.

Mouse myeloid leukemia cells (Ml) could be induced to differentiate into mature macrophages and granulocytes by treatment with dexamethasone or a protein induced in ascitic fluid from tumor-bearing rats. The effects of antioxidants (butyrated hydroxyanisole, butyrated hydroxytoluene, alpha-tocopherol, propyl gallate, disulfiram, cysteamine, ascorbate, selenite and glutathione) on differentiation of the cells were examined. Butyrated hydroxyanisole, butyrated hydroxytoluene and alpha-tocopherol significantly inhibited the differentiation of the cells induced by dexamethasone or a protein inducer. Other antioxidants had little or no inhibitory activity. Among the antioxidants tested, butyrated hydroxyanisole was the most potent inhibitor. The inhibition by butyrated hydroxyanisole was the most potent inhibitor. The inhibition by butyrated hydroxyanisole was not due to cytotoxicity and was reversible. The butyrated hydroxyanisole-mediated inhibition was counteracted by prostaglandin E1 or E2 but not F1 alpha. Moreover, butyrated hydroxyanisole inhibited the production of prostaglandin E2 by M1 cells treated with dexamethasone. These results suggest that the inhibition by butyrated hydroxyanisole of differentiation of M1 cells may be due to the inhibition of synthesis of prostaglandin E2.

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The tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate inhibits or enhances induction of differentiation of mouse myeloid leukemia cells depending on the type of serum in the medium.

The tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) inhibited the induction of both functional and morphological differentiation of mouse myeloid leukemia cells (Ml) cultured in medium containing 10% calf serum, but enhanced these inductions in medium containing 10% fetal calf serum and several inducers. These results suggest that some factor(s) in sera modifies the differentiation-inducing action of TPA on leukemia Ml cells.

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Effects of histone fractions on induction of differentiation of cultured mouse myeloid leukemia cells.

Mouse myeloid leukemic cells (M1) could be induced to differentiate into macrophage-like and granulocyte-like cells by a lysine-rich, histone H1 fraction (10 to 100 microgram/ml). The differentiated M1 cells expressed phagocytic and lysozyme activity and were macrophage-like and granulocyte-like cells. The differentiation-inducing activity of histone H1 was found in histone H1 fractions isolated from calf thymus, rat liver, and mouse leukemia M1 cells. Histone H2A and H2B fractions did not induce differentiation of M1 cells at concentrations of 10 to 100 microgram/ml but did induce differentiation at a high concentration (200 microgram/ml). The histone H3 fraction, poly-L-lysine and poly-L-arginine, inhibited induction of differentiation of M1 cells.

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Selection and characterization of pulmonary colonizing cells from cultured mouse mammary carcinoma cells.

Pulmonary colonizing cells were selected by an in vivo-in vitro selection method from cultured mouse mammary carcinoma FM3A cells. When 10(6) parent cells (P-O) were injected iv into syngeneic C3H/He mice, no tumor nodules were reduced. However, when the selected variant cells (P-15) were injected iv, tumor nodules formed predominantly in the lungs within 2 weeks. Mice inoculated iv with 10(6) P-15 cells began to die on day 22, but mice inoculated with P-O cells survived for more than 6 months. When injected sc into C3H/He mice, P-O cells were as tumorigenic as P-15 cells to the syngeneic mice. There was no significant difference between P-O and P-15 cells in their proliferation in vitro or in the inducibility of alkaline phosphatase activity. During successive selection of colonizing variants, the proportion of adherent cells increased. Adherent P-15 cells had a higher colonizing potential than nonadherent P-15 cells. The correlation of the adhesive property of the cells and their colonizing potential is discussed.

Alkaline Phosphatase↗

Regulation of prostaglandin synthesis during differentiation of cultured mouse myeloid leukemia cells.

Mouse myeloid leukemia cells (Ml) were induced to differentiate into mature macrophages and granulocytes by various inducers. The differentiated Ml cells synthesized and released prosetaglandins, whereas untreated Ml cells did not. When the cells wee prelabelled with [14C]arachidonate, the major prostaglandins released into the culture media were found to be prostaglandin E2, D2, and F2 alpha in an early stage of differentiation, but the mature cells produced predominantly prostaglandin E2. The synthesis and release of prostaglandins were completely inhibited by indomethacin. Dexamethasone, a potent inducer of differentiation of Ml cells, did not induce production of prostaglandins in resistant Ml cells that could not differentiate even with a high concentration of dexamethasone. These results suggest that production of prostaglandins in Ml cells is closely associated with differentiation of the cells. Homogenates of dexamethasone-treated Ml cells converted arachidonate to prostaglandins, but this conversion was scarcely observed with homogenates of untreated Ml cells. Dexamethasone and the other inducers stimulated the release of arachidonate from phospholipids. Therefore, induction of prostaglandin synthesis during differentiation of Ml cells may result from induction of prostaglandin synthetase activity and stimulation of the release of arachidonate from cellular lipids. Lysozyme activity, which is a typical biochemical marker of macrophages, was induced in Ml cells by prostaglandin E2 or D2 alone, as well as by inducers of differentiation of the cells, but it was not induced by arachidonate or prostaglandin F2 alpha. These results suggest that prostaglandin synthesis is important in differentiation of myeloid leukemia cells.

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Induction of differentiation of human promyelocytic leukemia cells (HL-60) by arginase.

Human promyelocytic leukemia cells (HL-60) were found to be induced by dimethylsulfoxide and several other compounds to phagocytize, reduce NBT dye, and change into forms that were morphologically similar to granulocytes and macrophages. Arginase also induced these differentiation-associated properties of the cells. The induction of differentiation by arginase was significantly inhibited by addition of excess arginine, but not by lysine or leucine; therefore, the effect of arginase may be due to arginase-mediated arginine depletion.

Arginase↗

Expression of a cell surface glycoprotein (p180) related to cell-substratum adhesion during differentiation of mouse myeloid leukemia cells.

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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