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Biomedical subjects

M Tomida

Publications and source records attributed to M Tomida.

At least 55 records · Page 3Linked to original sources
PubMed1989

Antigenic determinants of the cytoplasmic domain of band 3 from bovine erythrocyte membrane.

Rabbit antibodies were prepared against the cytoplasmic 38K-Da fragment of bovine band 3 and the immunological cross-reactivity with human, murine, rat, and chicken band 3 was examined. The antibodies cross-reacted with human and rodent band 3, indicating that there is an antigenic determinant(s) common to primate and nonprimate species. However, the antibodies did not recognize chicken band 3. Antigenic sites on the 38K-Da fragment were determined via amino acid sequence and immunoblotting analyses of proteolytic peptides of the fragment. Positions of antigenic determinants which were assumed to be common to primate and nonprimate species were mapped to the areas of residues 127-160 and of residues 259-304 in the primary structure of human band 3. Another epitope(s), which is absent in human band 3, existed in a region having a bovine-specific amino acid sequence. In addition, comparison of sequence data from different species showed that a proposed hinge region and a tryptophan-rich region on the cytoplasmic domain of band 3 [P. S. Low et al. (1984) J. Biol. Chem. 259, 13,070-13,076; R. R. Kopito and H. F. Lodish (1985) Nature (London) 316, 234-238] are also conserved in the bovine case.

Amino Acid Sequence↗
PubMed1989

Contrasting effect of IFN-gamma and IFN-alpha/beta on differentiation of some clones of mouse myeloid leukemic cells.

Mouse myeloid leukemic M1 cells are induced to differentiate into macrophage-like cells by a differentiation-inducing factor (D-factor) and various agents. IFN-gamma alone did not induce differentiation of clone T22-3 of M1 cells but inhibited their differentiation by D-factor. That is, IFN-gamma at 4 U/ml inhibited 50% of phagocytic activity of T22-3 cells induced by 7 x 10(-11) M D-factor. In addition, it inhibited the induction of lysozyme activity and morphological differentiation of these cells by D-factor. IFN-gamma also inhibited dexamethasone-induced differentiation of T22-3 cells. Previously interferon-alpha/beta was shown not to induce differentiation of M1 cells itself, but to enhance induction of their differentiation by D-factor. The present study showed that IFN-alpha/beta and IFN-gamma had opposite effects on induction of differentiation of T22-3 cells by D-factor. The effect of IFN-gamma on the differentiation of M1 cells varied with the clone of M1 cells used: IFN-gamma inhibited D-factor-induced differentiation of cells of clones T22-3 and S2, but induced differentiation of cells of clones B24 and S1.

Animals↗
PubMed1989

Genomic cloning and heterologous expression of human differentiation-stimulating factor.

Differentiation-stimulating factor (D-factor) purified from mouse Ehrlich ascites cells was sequenced partially and found to be almost identical to leukemia inhibitory factor (LIF) from mouse Krebs II ascites cells. In comparison to LIF, D-factor had an additional amino-terminal serine residue. Using synthetic oligonucleotide probes designed from the murine D-factor sequence, we cloned the human gene encoding D-factor. A partial D-factor cDNA was cloned from COS-1 cells transfected with the human D-factor gene under the control of a heterologous promoter. We used this cDNA to construct a vector for direct expression of the protein in Escherichia coli. A mammalian cell expression vector was constructed using the signal sequence of interferon-alpha A linked to the D-factor cDNA. Both forms of recombinant human D-factor were active on the murine myeloid leukemia cell line M1 in a dose- and time-dependent manner for the inhibition of [3H]thymidine incorporation, and also induced phagocytosis, Fc receptor expression, and prostaglandin E2 synthesis by M1 cells.

Amino Acid Sequence↗
PubMed1989

Combined effects of differentiation-inducing factor and other cytokines on induction of differentiation of mouse myeloid leukemic cells.

Mouse myeloid leukemic M1 cells are induced to differentiate into macrophage-like cells by differentiation-inducing factors (D-factors) and granulocyte colony-stimulating factor. We examined the effects of recombinant human tumor necrosis factor (rTNF), lymphotoxin (rLT) and interleukin 1 (rIL-1) on the induction of differentiation of M1 cells, compared with the effects of D-factor purified from the conditioned medium of mouse Ehrlich ascites tumor cells and recombinant human granulocyte colony-stimulating factor (rG-CSF). rIL-1 induced phagocytic activity, a typical marker of cell differentiation, in at most 30% of M1 cells at concentrations ranging from 10(-10) M to 10(-7) M. The differentiation-inducing activity of rIL-1 was similar to that of rG-CSF and less than that of D-factor. rTNF induced phagocytic activity in 14% of M1 cells only at a high concentration (10(-7) M). rLT did not induce differentiation of the cells even at 10(-7) M. rTNF stimulated induction of differentiation of M1 cells by D-factor, rG-CSF or rIL-1 by two or three fold. The combination of any two of the cytokines D-factor, rG-CSF and rIL-1 induced differentiation of M1 cells more efficiently than any of these cytokines alone. Moreover, the combination of three cytokines rG-CSF, rIL-1 and rTNF, all of which are known to be produced by macrophages, was more effective than the combination of any two of these cytokines in induction of differentiation of M1 cells.

Animals↗
PubMed1988

Effect of stilbenedisulfonate binding on the state of association of the membrane-spanning domain of band 3 from bovine erythrocyte membrane.

The membrane-spanning domain of bovine band 3, the anion transport protein of erythrocyte membrane, was purified in the presence of nonaethyleneglycol lauryl ether (C12E9) and the effect of a covalent attachment of 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS), a potent transport inhibitor, on the state of association of the domain isolated (the 58 kDa fragment) was studied via gel filtration, gel electrophoresis and sedimentation velocity experiments. It was indicated that the DIDS-unlabeled fragment in C12E9 solution forms heterogeneous aggregates which are larger in size than the dimer. This contrasted with the behavior that bovine band 3 is present as dimers or tetramers in the same medium (Nakashima and Makino (1980) J. Biochem. 88, 933-947). When DIDS was covalently attached, the fragment was present as a single molecular species which was indicated to be a dimer by molecular weight determination. The secondary structure of the fragment was not affected by DIDS. The change in the state of association caused by the DIDS-binding was also found in the presence of sucrose monolaurate (SE12), which was a more potent detergent for extraction of the 58 kDa fragment from membranes than C12E9. However, the complex with SE12 was extremely unstable.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1987

Mathematical model of Klebsiella pneumoniae resistance to amikacin and gentamicin.

1. The resistance of Klebsiella pneumoniae to amikacin and gentamicin was studied by a mathematical model to predict the rate of sensitivity decrease. The results accurately matched experimental data, showing that the model is a reliable predicting tool. 2. The observations were carried out over six years and included 2677 cultures that were positive for K. pneumoniae. At the beginning of the observation period, 85.7% of the cultures were sensitive to amikacin and 40.8% were sensitive to gentamicin. Sensitivity to amikacin showed a surprisingly rapid decrease; at the end of the experimental period, amikacin and gentamicin sensitivities were 33.3% and 27.8%, respectively. 3. We conclude that patterns of resistance of other bacteria could be investigated using this method.

Amikacin↗
PubMed1986

Induction by recombinant human granulocyte colony-stimulating factor of differentiation of mouse myeloid leukemic M1 cells.

The effect of recombinant human granulocyte colony-stimulating factor (G-CSF) on induction of differentiation of mouse myeloid leukemic M1 cells was examined. Purified G-CSF caused dose-dependent induction of phagocytic activity and lysozyme activity in M1 cells. Its half-maximally effective concentration was 10 ng/ml. On treatment of M1 cells with G-CSF (100 ng/ml) for 4 days, 30-50% of the cells differentiated morphologically into macrophage cells; 30-40% of the cells were blast cells and 20-30% of the cells were forms intermediate between blastic cells and mature macrophages.

Animals↗
PubMed1986

Specific binding of a factor inducing differentiation to mouse myeloid leukemic M1 cells.

A factor inducing differentiation of mouse myeloid leukemic M1 cells into macrophages (differentiation-inducing factor, D-factor), which was purified to homogeneity from conditioned medium of mouse Ehrlich ascites tumor cells, could be iodinated without detectable loss of biological activity. The binding of 125I-D-factor to M1 cells was specific; the binding was inhibited competitively by D-factor derived from Ehrlich cells and mouse fibroblast L929 cells, but not by other growth factors or D-factor derived from differentiated M1 cells. The latter differs from D-factor of Ehrlich cells and L929 cells in antigenicity and molecular weight. At 21 degrees C, the binding was saturated at 370 pM 125I-D-factor. M1 cells showed a high affinity for 125I-D-factor (dissociation constant, 1.0 X 10(-10) M) and expressed a small number of binding sites (170 per cell). Specific binding of 125I-D-factor was observed only to several clones derived from M1 cells, including those sensitive and resistant to induction of differentiation by D-factor.

Animals↗
PubMed1986

Differentiation-inducing factor purified from conditioned medium of mitogen-treated spleen cell cultures stimulates bone resorption.

Spleen cells treated with mitogens produce a potent bone-resorbing factor called osteoclast-activating factor (OAF). To examine the relationship between the bone-resorbing factor and other protein factors produced by spleen cells, the colony-stimulating factor (CSF), the differentiation-inducing factor (DIF), the macrophage fusion factor (MFF), and the macrophage growth factor (MGF) were purified from 2.68 liters of conditioned medium of mouse spleen cell cultures treated with concanavalin A. Purification was performed successively by DEAE-cellulose, Blue Sepharose, and Sephadex G-150 column chromatography and high-pressure liquid chromatography (HPLC). The DIF was successfully separated from CSF and MGF on HPLC. CSF coincided with MGF on HPLC, but MFF disappeared before application to HPLC. Only the DIF exhibited bone-resorbing activity, whereas CSF and MGF did not. The DIFs purified from L929 cells and Ehrlich ascites tumors similarly exhibited bone-resorbing activity. The DIFs purified from spleen cells and Ehrlich ascites tumor cells exhibited neither interleukin 1 (IL-1) activity nor tumor necrosis factor (TNF) activity, though the unfractionated conditioned medium from spleen cells did exhibit them. In the light of recent reports that IL-1 beta and TNF also stimulate bone resorption, the term OAF should refer to a generic activity rather than a single factor.

Animals↗
PubMed1984

Characterization of a factor inducing differentiation of mouse myeloid leukemic cells purified from conditioned medium of mouse Ehrlich ascites tumor cells.

A factor inducing differentiation of mouse myeloid leukemic cells (MI) into macrophages was purified to apparent homogeneity from 168 1 of CM of Ehrlich ascites tumor cells. The purified factor was half-maximally active at 2 X 10(-11) M. The factor was analyzed by radioiodination, SDS-polyacrylamide gel electrophoresis and autoradiography. Its Mr was 40 000-50 000. On reduction, the factor lost activity, but showed no subunit structure. Treatment of the factor with endo-beta-N-acetylglucosaminidase F, but not endo-beta-N-acetylglucosaminidase H, gave rise to a molecule of Mr 20 000-28 000. The activity of the factor from Ehrlich cells was completely neutralized by antiserum to the factor of Mr 50 000-70 000 from mouse fibroblast L929 cells.

Animals↗
PubMed1984

Purification of a factor inducing differentiation of mouse myeloid leukemic M1 cells from conditioned medium of mouse fibroblast L929 cells.

A procedure is described for purification of a factor (D-factor)-inducing differentiation of mouse myeloid leukemic cells (M1) into macrophages from serum-free mouse L929 cell-conditioned medium. The procedure included ammonium sulfate precipitation, DEAE-cellulose, Sephadex G-200 and phenyl-Sepharose column chromatographies, reverse-phase high-performance liquid chromatography on a C18 hydrophobic support, and high-performance liquid chromatography on a gel-filtration column. The purified factor gave a single band of protein with a molecular weight of 62,000 on sodium dodecyl sulfate-polyacrylamide gel electrophoresis which coincided with biological activity. Its half-maximal concentration for inducing differentiation of M1 cells into macrophages was 1.7 X 10(-11) M. Even at 2.6 X 10(-9) M, it did not induce colony formation of normal bone marrow cells, suggesting that it was distinct from the growth factor for normal precursors of macrophages and/or granulocytes.

Animals↗
PubMed1983

Prolongation by interferon preparation of the survival time of mice implanted with differentiation-inducible mouse myeloid leukemia cells.

The effect of L-cell interferon (IFN) preparation on the survival times of mice implanted with two different clones (T-22 and R-4) of mouse myeloid leukemic M1 cells were examined. T-22 cells, but not variant R-4 cells, can be induced to differentiate in vitro or in vivo into macrophages and granulocytes. In vitro growth of R-4 cells was markedly suppressed by IFN, but that of T-22 cells was resistant to IFN. The survival times of mice with implanted T-22 cells were prolonged by treatment with IFN but those of mice with implanted R-4 cells were not.

Animals↗
PubMed1983

Effect of mouse interferon on growth and differentiation of mouse bone marrow cells stimulated by two different types of colony-stimulating factor.

The effects of mouse L-cell interferon (IFN) on growth of mouse bone marrow cells and their differentiation into macrophages and granulocytes were investigated in a liquid suspension culture system with two different types of colony-stimulating factor (CSF). Within 7 days, most bone marrow cells differentiated into macrophages in the presence of macrophage colony-stimulating factor (M-CSF) derived from mouse fibroblast L929 cells, but into both granulocytes (40%) and macrophages (23%) in the presence of a granulocyte-macrophage colony-stimulating factor (GM-CSF) from mouse lung tissue. IFN inhibited growth of bone marrow cells with both M-CSF and GM-CSF, but had 20 times more effect on bone marrow cells stimulated with M-CSF than on those stimulated with GM-CSF. A low concentration of IFN (50 IU/ml) stimulated production of macrophages by GM-CSF in liquid culture medium, whereas it selectively inhibited colony formation of macrophages in semisolid agar culture. IFN caused no detectable block of late stages of differentiation; mature macrophages and granulocytes were produced even when cell proliferation was inhibited by IFN. These results indicate that IFN preferentially affects growth and differentiation of the cell lineage of macrophages among mouse bone marrow cells.

Animals↗
PubMed1982

Interferon production in mixed cultures of mouse spleen cells and tumor cells: IFN-gamma as the main component.

Interferon (IFN) production in mixed cultures of mouse spleen cells and tumor cells was investigated, mainly using mouse myeloid leukemic cells, M1, and spleen cells from syngeneic SL mice. Spleen cells from other mouse strains (C57BL/6, BALB/c nude and C57BL/6 beige) and other tumor cells (L929 and YAC-1) were similarly effective for IFN production, but mouse mammary carcinoma FM3A cells were not. As the IFN-inducing stimulus, mycoplasma contaminating the tumor cells, or endogenous retrovirus in them, may possibly be involved. The type of IFN produced was identified as IFN-gamma as a major component and IFN-alpha and -beta as minor ones, by acid stability tests and neutralization by antisera with defined specificities against alpha, beta, and gamma. Depletion of natural killer cells from spleen cells did not appreciably affect IFN production, but depletion of Thy 1.2 antigen-bearing cells greatly reduced IFN-gamma production, indicating that T cells were the main IFN producers.

Animals↗
PubMed1982

Macrophage activating factor is not identical with immune interferon or a factor inducing differentiation of mouse myeloid leukemic cells.

Conditioned media of mitogen- or antigen-stimulated spleen cells have been found to contain various lymphokines including macrophage activating factor (MAF), immune interferon (IFN-gamma) and a factor inducing differentiation of mouse myeloid leukemic M1 cells into macrophages and granulocytes (D-factor). We examined the properties and mutual relations of these lymphokines. Conditioned media of concanavalin A (Con A)-stimulated spleen cells and of purified protein derivative (PPD)-stimulated Bacillus Calmette-Guérin (BCG)-immune spleen cells contained the activities of D-factor, MAF and IFN. These lymphokines were similarly eluted on Sephadex G-100 in a peak corresponding to a molecular weight of 40,000 approximately 60,000. However, a rapidly eluted fraction contained MAF but not activities of D-factor and IFN. Treatment of conditioned medium of Con A-stimulated spleen cells at pH 2 abolished the activities of MAF and IFN but did not affect the activity of D-factor. Moreover, addition of cytochalasin B suppressed the productions of MAF and IFN but not that of D-factor by Con A-stimulated spleen cells. Antiserum against mouse IFN-gamma neutralized IFN activity but not MAF activity in the conditioned medium of Con A-stimulated spleen cells. These results indicate that D-factor, MAF and IFN-gamma are all distinct substances.

Animals↗