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Y Shiba

Publications and source records attributed to Y Shiba.

At least 91 records · Page 5Linked to original sources
PubMed1985

Characteristics of a BHK cell variant defective in the cell-substratum contact process.

In this paper we document the phenotypic characteristics of a novel BHK cell adhesion variant designated FN-2. Unlike parental cells, FN-2 cells did not attach to fibronectin (pFN)-coated dishes, even after 4-hr incubations on dishes treated with 100 micrograms/ml of pFN. Mixing experiments with the variant and parental cells revealed that the parental cells attached normally in the presence of a ninefold excess of variant cells and the variant cells failed to attach in the presence of a ninefold excess of parental cells. Therefore, the defect in FN-2 cells could not be explained by secretion of a factor inhibiting attachment or lack of secretion of a factor required for attachment. Also, the inability of FN-2 cells to attach to pFN-coated dishes could not be explained by an absence of cell pFN receptors since the variant cells bound normal numbers of small (ca. 0.8 micron) pFN-coated latex beads, although they phagocytosed the beads poorly compared to parental cells. Also, the variant cells were not able to bind large (5.7 or 16.8 microns) pFN-coated beads. When tested on dishes coated with ligands that, unlike fibronectin, have a high affinity for cell surface receptors, e.g., lectins and anti-BHK antibodies, FN-2 cells were observed to attach at a rate similar to that of parental cells but spread much more slowly. The phenotypic characteristics of FN-2 cells suggest that they are deficient in what previously has been called the "cell contact" process in cell adhesion. It is proposed that the cell contact process is the initial formation by an individual cell of a sufficient number of cell-substratum bonds to resist the shear forces operationally used to define "attachment," and that more cell-substratum bonds are necessary for cell attachment to large substrata (dishes or large beads) than for attachment to small substrata (small beads). The molecular defect in FN-2 cells was studied by electroblotting analysis. A high molecular weight (ca. 370 kd) glycoprotein detected by blotting with anti-BHK antibodies and ConA that was present in parental cell membranes was reduced or absent in the variant cells.

Animals↗
PubMed1985

Intercellular communication capacity as a possible determinant of transformation sensitivity of BALB/c 3T3 clonal cells.

While clonal cell variants of BALB/c 3T3 with high and low susceptibilities to ultraviolet radiation- and benzo(a)pyrene-induced transformation show similar intercellular communication capacities when they are in the growing phase, a significant loss in communication occurs at confluence only in transformation-sensitive clonal variant cells. A potent tumor promoter, 12-O-tetradecanoylphorbol-13-acetate, which also enhances BALB/c 3T3 cell transformation induced by methylcholanthrene, inhibited intercellular communication of these variants to a similar extent. These results suggest that intrinsic differences in the control of intercellular communication may be a determinant of the susceptibility of these variants to the induction of transformation.

Animals↗
PubMed1984

Protective effect of cAMP on tumor promoter-mediated inhibition of cell-cell communication.

The formation and maintenance of electrical cell coupling is inhibited by 100 ng/ml 12-O-tetradecanoylphorbol-13-acetate (TPA). This inhibition could be prevented by db-cAMP and aminophylline when added together with TPA, though they did not restore the cell coupling once it had already been blocked by TPA. It is suggested that db-cAMP affects the early membrane effects of TPA in FL cells.

Aminophylline↗
PubMed1984

Monoclonal antibody ECCD-1 inhibits intercellular communication in teratocarcinoma PCC3 cells.

The monoclonal antibody ECCD-1 recognizing a certain class of cell surface proteins inhibits the Ca2+-dependent cell-to-cell adhesion in teratocarcinoma stem cells. In this paper, we studied the effect of ECCD-1 on cell-to-cell communication in PCC3 cells by measuring the transfer of lucifer yellow between cells. To this aim, PCC3 cells were cultured in the presence of ECCD-1 for various periods, and then the fluorescent dye was injected into a cell located in the center of cell colonies, followed by counting number of cells to which the dye was transferred. The results showed that ECCD-1 inhibits the dye transfer between cells, suggesting that the Ca2+-dependent cell-to-cell adhesion system (CDS) is essential for the functions of gap junction.

Animals↗
PubMed1983

Tumour promoter-mediated reversible inhibition of cell-cell communication (electrical coupling). Relationship with phorbol ester binding and de novo macromolecule synthesis.

A tumour promoter, 12-O-tetradecanoyl phorbol-13-acetate (TPA), reversibly inhibits the onset and maintenance of cell-cell communication measured by electrophysiological method. We have now studied the mechanism by which TPA inhibits communication of human cells (FL) in culture. Using [3H]phorbol-12,13-dibutyrate [( 3H]PDBu), we found a class of specific, high-affinity, saturable binding sites in intact FL cells; they have a dissociation constant of 15.4 nM, and at saturation about 3 X 10(5) PDBu molecules were bound to each cell. The binding of [3H]PDBu to FL cells was inhibited by TPA, phorbol-12-13-didecanoate and mezerein, whereas phorbol and 4 alpha-phorbol-12-13-didecanoate had no effect. There is a close correlation between the ability of the former compounds to inhibit [3H]PDBu binding and their capacity to inhibit cell-cell communication. When FL cells are dispersed with EDTA and plated onto a culture dish, they start to couple electrically within 2 h; such cell coupling was not affected by the presence of cycloheximide or actinomycin D. TPA inhibits the formation of electrical cell coupling as well as its maintenance, even in the presence of cycloheximide; the recovery of cell-cell communication after the removal of TPA was not significantly affected by the addition of cycloheximide or actinomycin D. Taken together, these results suggest that TPA-mediated reversible inhibition of intercellular communication is mediated by specific binding of TPA to cellular receptors and that macromolecular synthesis is not necessary.

Binding Sites↗
PubMed1982

Tumor-promoting phorbol esters and mezerien induce contraction in hydra.

12-O-tetradecanoyl phorbol-13-acetate (TPA, 1-100 ng/ml) induced a reversible contraction in the hydra, Hydra japonica. Another tumor-promoting phorbol ester, phorbol-12, 13-didecanoate (PDD), and mezerein also induced contraction, but non-tumor-promoting derivatives such as 4alpha-PDD and phorbol did not.

Animals↗
PubMed1981

Tumor promoters cause a rapid and reversible inhibition of the formation and maintenance of electrical cell coupling in culture.

The effect of tumor promoters on electrical coupling between human FL cells was investigated with a microelectrode technique. When a low concentration (100 ng/ml) of 12-O-tetradecanoylphorbol 13-acetate (TPA) was added to culture medium, only 6% of the cells showed electrical coupling after 5 hr, whereas in control medium more than 90% of the cells were coupled. In the presence of TPA, cell coupling remained suppressed for at least another 19 hr. When TPA was washed out from the culture medium, the cells commenced electrical coupling: 90% of the cells were coupled within 4 hr of the removal of TPA, a rate very similar to that of nontreated control cells. Therefore, TPA-mediated inhibition of cell coupling is reversible. When TPA was added to a culture in which more than 90% of the cells had already established electrical coupling, the percentage of coupled cells decreased to 6% within 8 hr, indicating that TPA can also diminish already established cell coupling. Inhibition of cell coupling also was achieved with other mouse skin tumor promoters--phorbol 12,13-didecanoate, ingenol dibenzoate, and mezerein--whereas nonpromoting derivatives--phorbol and 4 alpha-phorbol 12,13-didecanoate-showed no effect. None of these compounds changed the membrane potential, membrane resistance, or growth rate of FL cells. Thus, it appears that TPA and structurally-related tumor promoters specifically disturb the formation or function, or both, of cell-cell junctions, without significantly affecting the general properties of the surface membrane or the growth of FL cells.

Cell Division↗
PubMed1981

Inhibition of the formation of electrical cell coupling of FL cell by tumor promoters.

The effect of tumor promoters on the formation of electrical cell coupling between human FL cells was investigated by means of a microelectrode technique. In culture medium containing 100 ng/ml of 12-O-tetradecanoyl phorbol-13-acetate (TPA), only 6% of the cells were coupled after 24 hr while more than 90% of the cells were coupled in control medium. The formation of cell coupling was also inhibited by other tumor promoters, phorbol-12,13-didecanoate, ingenol-13, 20-dibenzoate and mezerein, whereas non-promoting derivatives, phorbol and 4 alpha-phorbol-12, 13 didecanoate did not affect cell coupling formation. 7, 12-Dimethylbenz [a] anthracene, benzo [a] pyrene and N-methyl-N'-nitro-N-nitrosoguanidine did not affect the cell coupling. None of the chemicals used changed any electrical properties of the cell membrane, such as membrane potential and membrane resistance, of FL cells. Thus, it appears that TPA and other related tumor promoters inhibit the formation of cell coupling without changing the physiological properties of the membrane significantly.

Amnion↗
PubMed1979

A scanning and transmission electron microscope study of the premetamorphic papillae: possible chemoreceptive organs in the oral cavity of an anuran tadpole (Rana japonica).

Premetamorphic papillae of an anuran tadpole (Rana japonica) were studied by scanning and transmission electron microscopy. Premetamorphic papillae of several shapes are seen in and around the oral cavities of tadpoles during late larval and early metamorphic stages. These papillae are composed of three parts: the apical cellular part, the underlying connective tissue core and the epithelial covering. In the apical cellular part, two populations of cells are observed: apical and basal cells. The apical cell has a slender cytoplasmic process whose apical surface is exposed in the oral cavity. The basal cell is located at the basal portion of the apical cellular part of the papilla without researching the oral cavity. A long solitary microvillus and a bunch of short microvilli are seen on the apical surface of each apical cell. The apical cells contain dense-cored vesicles of 100 nm diameter and make synaptic contacts at their basal membranes with terminals of nerve fibers. Possible chemoreceptive function of the premetamorphic papilla is discussed.

Animals↗