Biomedical subjects

J Okabe

Publications and source records attributed to J Okabe.

28 records · Page 2Linked to original sources

PubMed1977

Glucocorticoid binding and mechanism of resistance in some clones of mouse myeloid leukemic cells resistant to induction of differentiation by dexamethasone.

Several clones of dexamethasone-resistant cells, which could not differentiate even in a high concentration of dexamethasone, were isolated from glucocorticoid-sensitive myeloid leukemic cells. Some of them were shown to be deficient in steroid binding to specific cytoplasmic receptors, while the others contained glucocorticoid-specific cytoplasmic receptors that might be the same as those in sensitive cells. One of the resistant clones was found to be almost completely deficient in nuclear acceptor sites for cytoplasmic steroid-receptor complexes. The remaining clones were also characterized by significantly reduced amounts of nuclear-bound glucocorticoid. These results suggest that resistibility to glucocorticoids in the resistant clones of myeloid leukemic cells is due mainly to a defect in some steps of intracellular transfer of the steroid. Dexamethasone-sensitive cells, which could differentiate in the presence of dexamethasone, could be also induced to differentiate by protein factor(s) in ascitic fluid. Although all the resistant cells showed a low response to ascitic fluid, some of them showed 10-fold enhancement of phagocytic activity which is a typical character of differentiated cells. These results suggest that response to steroids is not directly correlated with that to protein inducer(s).

Animals↗

PubMed1977

Role of leucocytes in ascites in the production of factor(s) stimulating differentiation of mouse myeloid leukemia cells.

Although the ascitic fluid of animals bearing various tumors and that of mice induced by complete Freund's adjuvant had high activity for inducing differentiation of myeloid leukemic cell line (M1) from an SL mouse to macrophages and granulocyte-like cells, the activity in the ascitic fluid of syngeneic mice bearing the M1 cells was markedly reduced. Macrophages and granulocytes were abundant in the active ascites of animals bearing tumors (8 to 12% of the total ascites cells) while in the ascites of syngeneic mice bearing the M1 cells they were not (0.1 to 0.7% of the total ascites cells). Appearance of lymphocytes in the ascites of both types was not significantly different. Although the conditioned media of the Ehrlich tumor cells, M1 cells, and whole ascites cells with the M1 cells were not active in inducing differentiation of the M1 cells, the conditioned media of all the ascites cells with Ehrlich tumor cells and those of peritoneal macrophages and granulocytes in mice did show a high activity. These results indicate that the peritoneal macrophages and granulocytes in the ascites are responsible for the production of factors stimulating differentiation of the M1 cells.

Animals↗

PubMed1977

Differentiation of a resistant clone of mouse myeloid leukemia cells with dimethyl sulfoxide and ascitic fluid.

Mouse myeloid leukemia line cells, M1, could be induced to differentiate in vitro into macrophages and granulocytes with ascitic fluid of animals bearing various tumors. M1 cells could not be induced to differentiate with dimethyl sulfoxide alone. During the culture of M1 cells, spontaneously appearing cells resistant to factors stimulating differentiation (D-factor) in ascitic fluid were isolated. These resistant cells were more refractile to the toxic action of dimethyl sulfoxide than sensitive cells and grew in culture medium with 1% dimethyl sulfoxide. Although the resistant cells were not induced to differentiate with dimethyl sulfoxide alone, they were sensitized with the aid of dimethyl sulfoxide to undergo differentiation with the D-factor in ascitic fluid.

Animals↗

PubMed1977

Glucorticoid-induced differentiation of cultured mouse myeloid leukemia cells.

Mouse myeloid leukemia cells were induced by some corticoid hormones to migrate in agar, phagocytize, and change into forms which were morphologically similar to macrophages and granulocytes. Inducing ability of corticoids was correlated with glucocorticoid activity, not mineralocorticoid activity. Other steroids were ineffective to induce differentiation of myeloid leukemia cells. Glucocorticoid-resistant cells, which could not differentiate even in a high concentrations of dexamethasone, were selected from steroid-sensitive cells by stepwise increase in concentrations of dexamethasone in culture medium.

Animals↗

PubMed1973