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At least 685 records · Page 38Linked to original sources
PubMed1984

Intercellular communication and the control of growth: XI. Alteration of junctional permeability by the src gene in a revertant cell with normal cytoskeleton.

To learn whether the reduction of cell-to-cell communication in transformation is a possible primary effect of pp60src phosphorylation or secondary to a cytoskeletal alteration, we examined the junctional permeability in transformed cells with normal cytoskeleton. The permeability to fluorescent-labelled mono- and diglutamate was compared in clones of Faras' vole cells--clones transformed by Rous sarcoma virus and reverted from that transformation. One revertant clone (partial revertant), had the high level of pp60src kinase activity and tumorigenicity of the fully transformed parent clone, but had lost the cytoskeletal alterations of that clone. Another revertant clone (full revertant) had lost the tumorigenicity and most of the pp60src kinase activity, in addition (J.F. Nawrocki et al., 1984, Mol. Cell Biol. 4:212). The junctional permeability of the partial revertant with normal cytoskeleton was similar to that of the fully transformed parent clone with abnormal cytoskeleton. The permeabilities of both were lower than those of the full revertant and the normal uninfected cell, demonstrating that the junctional change by the src gene is independent of the cytoskeletal one.

Animals↗
PubMed1994

Intercellular communication between epithelial and fiber cells of the eye lens.

Results of electrical, dye-coupling and morphological studies have previously suggested that gap junctions mediate communication between the anterior epithelium of the lens and the underlying lens fiber cells. This connection is believed to permit 'metabolic cooperation' between these dissimilar cell types and may be of particular importance to the fiber cells, which are thought incapable of autonomous ionic homeostasis. We reinvestigated the nature of the connection between epithelial and fiber cells of the embryonic chicken lens using fluorescence confocal microscopy and freeze-fracture analysis. In contrast to earlier studies, our data provided no support for gap-junction-mediated transport from the lens epithelium to the fibers. Fluorescent dyes loaded biochemically into the lens epithelium were retained there for more than one hour. There was a decrease in epithelial fluorescence over this period, but this was not accompanied by an increase in fiber cell fluorescence. Diffusional modeling suggested that these data were inconsistent with the presence of extensive epithelium-fiber cell coupling, even if the observed decrease in epithelial fluorescence was attributed exclusively to the diffusion of dye into the fiber mass via gap junctions. Furthermore, the rate of loss of fluorescence from isolated epithelia was indistinguishable from that measured in whole lenses, suggesting that decreased epithelial fluorescence resulted from photobleaching and leakage of dye rather than diffusion, via gap junctions, into the fibers. Analysis of freeze-fracture replicas of plasma membranes at the epithelial-fiber cell interface failed to reveal evidence of gap-junction plaques, although evidence of endocytosis was abundant. These studies were done under conditions where the location of the fracture plane was unambiguous and where gap junctions could be observed in the lateral membranes of neighboring epithelial and fiber cells. Paradoxically, tracer molecules injected into the fiber mass were able to pass into the epithelium via a pathway that was not blocked by incubation at 4 degrees C or by treatment with octanol and which excluded large (approximately 10 kDa) molecular mass tracers. Together with previous measurements of electrical coupling between fiber cells and epithelial cells, these data indicate the presence of a low-resistance pathway connecting these cell types that is not mediated by classical gap junctions.

Animals↗
PubMed1984

Inhibition of intercellular communication between normal human embryonal palatal mesenchyme cells by teratogenic glycol ethers.

Cell-cell communication, possibly through gap junctions, is a fundamental event for the differentiation of embryonal tissues. Chemical substances which can interfere with this process may be able to disrupt embryogenesis. We have examined the response of a normal diploid human embryonal palatal mesenchymal (HEPM) cell line to glycol ethers. These cells have gap junctions whose function in cell-cell communication was inhibited by a model teratogen. Potential HEPM donor cells (2000 to 4000) were pulse labeled with 3H-uridine (10 microCi/mL; 3 hr) and then cocultured for 3 hr with 200,000 to 400,000 potential recipient cells in the absence or presence of 2-methoxyethanol (ME; 0.13-0.30 M) or 2-isopropoxyethanol (IPE; 0.05-0.1 M). Computer-assisted quantitative autoradiography was applied to assess the effects on metabolic cooperation. Although this phenomenon was inhibited by ME, the effect was probably not attributable to interference with gap junction-mediated transfer of labeled nucleotides but rather to the lack of formation of gap junctions resulting from cytotoxicity and poor physical contact between cells. The inhibition obtained with IPE was apparently not due to adverse effects on HEPM cells as judged by light microscopy and cell counts of recipients surrounding a given donor. The results suggest that HEPM cells are suitable to study disruption of cell-cell communication as a mechanism responsible for teratogenesis and offer the unique possibility to apply human embryonal cells. However, care has to be taken to assess potential cytotoxicity of xenobiotics, and further refinement of the criteria to detect adverse effects is required.

Autoradiography↗
PubMed1980

Inhibition of intercellular communication by tumor-promoting phorbol esters.

Cocultures were established of mouse epidermal cells (HEL/37) and mouse fibroblast cells (PG-19) deficient in the enzyme hypoxanthine-guanine phosphoribosyltransferase. Metabolic cooperation between the cocultured cells was detected as labeling of PG-19 cells on incubation of cocultures with [3H]-hypoxanthine. The transfer of label from HEL/37 cells to PG-19 cells was inhibited by the tumor prmoters 12-O-tetra-decanoylphorbol-13-acetate (10(-8) M) and phorbol-12,13-di-decanoate (10(-7) M) but not by nonpromoting derivatives of these phorbol esters. The inhibition was partially prevented by the antiinflammatory steroid fluocinolone acetonide, which is an antagonist of mouse skin tumor promotion, and by prolonged exposure of the cocultures to 12-O-tetradecanoylphorbol-13-acetate.

Animals↗
PubMed1999

Cytomegalovirus-induced transendothelial cell migration. a closer look at intercellular communication mechanisms.

A variety of cells such as leukocytes and tumor cells may adhere to endothelial cells and subsequently transmigrate into the solid tissue by involving specific intercellular molecular pathways. One important prerequisite for transendothelial migration is the loosening of endothelial cell-to-cell contact sites, which can be triggered by extravasating cells. Cytomegalovirus (CMV) has obviously evolved the ability not only to influence host cells floating in the blood stream to adhere to endothelial cells, but also to induce the formation of intercellular gaps within the endothelium, resulting in transendothelial migration. These features allow the virus to disseminate and evade the immune system. In coculture experiments with human endothelial monolayers and human CMV (HCMV)-infected neuroblastoma cells or leukocytes, changes in the integrity of the monolayer were observed and further analyzed on the molecular level. For example, HCMV may activate the integrin beta1alpha5 (VLA-5) that triggers adhesion to endothelial cells with subsequent focal disruption of endothelial cell-to-cell connections. It is hypothesized that a Ca(2+)-independent pathway following VLA-5 binding disconnects the cadherin-catenin-actin complex within the endothelial cells. The loss of cadherin function causes the loss of contact to the neighboring endothelial cells and thus could represent an important mechanism in HCMV-induced cellular transendothelial migration and disruption of the endothelial integrity.

Cell Adhesion↗
PubMed1994

Intercellular communication is reduced by TPA and Ki-ras p21 in quiescent, but not proliferating, NRK cells.

We investigated whether the growth state of NRK cells (proliferating or quiescent by serum deprivation) affected the ability of oncogenic Ki-ras p21 and the protein kinase C activator, 12-O-tetradecanoylphorbol-13-acetate (TPA), to alter gap junctional communication. We evaluated gap junctional permeance by rate analysis of the transfer of a fluorescent dye, Lucifer Yellow, between cell pairs. We found that while the gap junctions of proliferating NRK cells were unresponsive to both TPA and to Ki-ras p21, junctional communication in quiescent cells was significantly inhibited by brief exposures to 100 ng/ml TPA. Furthermore, activity of Ki-ras p21 2 h prior to TPA exposure enhanced the inhibitory effect of TPA in quiescent cells. Junctional sensitivity to TPA was transient, with inhibition of junctional communication detected at 10 min and refractory after 60 min of continuous exposure. The suppression of junctional communication by TPA was completely prevented if the oncogenic p21 had been active for a longer period of time (48 h). The application of a phorbol ester derivative (4 alpha-PDD), which does not activate protein kinase C, did not affect the ability of quiescent cells to communicate. From these results we conclude that there is a cell-state dependence of junctional sensitivity to TPA in NRK cells and that ras p21 activity potentiates the junctional response to TPA. One interesting possibility is that this involved a cell-cycle effect.

Animals↗
PubMed1988

Intercellular communication in the eight-cell stage of Xenopus laevis development: a study using dye coupling.

We report an investigation of dye coupling in the eight-cell stage of Xenopus laevis development. Our results indicate that fluorophors injected into micrometers at this stage pass only to sister cells (the corresponding macromeres) and that detectable dye transfer occurs only via cytoplasmic bridges, which persist for about the first two-thirds of the fourth cell cycle. We had previously shown that the dorsoventral polarity of the Xenopus embryo is regulated by a cell interaction that occurs at the end of the fourth cell cycle and we conclude that this cell interaction probably does not require cytoplasmic bridges or gap junctions.

Animals↗
PubMed1991

Mutagenicity and effect on gap-junctional intercellular communication of 4,4'-methylenebis(2-chloroaniline) and its oxidized metabolites.

Oxidized metabolites of 4,4'-methylenebis(2-chloroaniline) (MBOCA) were tested for direct mutagenicity in a Salmonella typhimurium assay and for effects on gap-junctional communication of WB-F344 rat liver cells. The mutagenicities of the N-hydroxy, mononitroso and o-hydroxy (ring) metabolites of MBOCA were assayed without adding activating enzyme systems, using the frame-shift sensitive strain TA98 and the base pair substitution sensitive strain TA100. The mutagenicity of the hydroxylamine was demonstrated by a linear increase in the formation of mutant colonies in both strains, with a formation of two revertants/nmol by TA98 and 21 revertants/nmol by TA100. The mononitroso metabolite showed a slight positive effect on TA100, but effects were masked by its cytotoxicity towards this strain. This metabolite was neither mutagenic nor cytotoxic to TA98. The o-hydroxy and the dinitroso metabolites were negative for mutagenicity at concentrations up to 50 and 500 micrograms/plate, respectively. The effects of parent MBOCA and N-hydroxy, mononitroso and o-hydroxy metabolites on cell-cell communication were determined by a scrape loading/fluorescent dye transfer technique. Cytotoxicity was assessed by determination of colony-forming efficiency and lactate dehydrogenase release. MBOCA itself caused an inhibition of dye transfer at concentrations of 7.5, 11.3 and 15 nmol/ml, whereas measures of cytotoxicity were not seen until 15 and 30 nmol/ml for LDH release and plating efficiency, respectively. None of the oxidized metabolites were active in inhibiting dye transfer at non-cytotoxic concentrations.

Animals↗
PubMedDate not supplied

Inhibition of gap junctional-mediated intercellular communication in vitro by aldrin, dieldrin, and toxaphene: a possible cellular mechanism for their tumor-promoting and neurotoxic effects.

Several mechanisms have been postulated to be responsible for the pleiotropic effects of toxic chemicals. Although the cytotoxicity and mutagenicity of chemicals are well studied and relatively easily detected, the noncytotoxic and nonmutagenic (i.e., epigenetic) mechanisms of chemical toxicity are less well understood. An in vitro assay, using cocultures of Chinese hamster cells to measure metabolic cooperation between V79 6-thioguanine-sensitive (6TGs) and resistant (6TGr) cells, has been developed to detect noncytotoxic and nonmutagenic chemicals that inhibit, quantitatively, gap junctional communication. The insecticides aldrin, dieldrin, and toxaphene, known to have pleiotropic toxic effects in animals, were shown to inhibit gap junctional communication. Interpretation of results suggests that chemical inhibition of gap junctional communication could be a possible mechanism to explain their tumor-promoting and neurotoxic effects.

Aldrin↗
PubMed2001

PGE(2) is essential for gap junction-mediated intercellular communication between osteocyte-like MLO-Y4 cells in response to mechanical strain.

We have observed, in our previous studies, that fluid flow increases gap junction-mediated intercellular coupling and the expression of a gap junction protein, connexin 43, in osteocyte-like MLO-Y4 cells. Interestingly, this stimulation is further enhanced during the poststress period, indicating that a released factor(s) is likely to be involved. Here, we report that the conditioned medium obtained from the fluid flow-treated MLO-Y4 cells increased the number of functional gap junctions and connexin 43 protein. These changes are similar to those observed in MLO-Y4 cells directly exposed to fluid flow. Fluid flow was found to induce PGE(2) release and increase cyclooxygenase 2 expression. Treatment of the cells with PGE(2) had the same effect as fluid flow, suggesting that PGE(2) could be responsible for these autocrine effects. When PGE(2) was depleted from the fluid flow-conditioned medium, the stimulatory effect on gap junctions was partially, but significantly, decreased. Addition of the cyclooxygenase inhibitor, indomethacin, partially blocked the stimulatory effects of mechanical strain on gap junctions. Taken together, these studies suggest that the stimulatory effect of fluid flow on gap junctions is mediated, in part, by the release of PGE(2). Hence, PGE(2) is an essential mediator between mechanical strain and gap junctions in osteocyte-like cells.

Animals↗
PubMed1989

Inhibition of gap-junctional intercellular communication between Chinese hamster lung fibroblasts by di(2-ethylhexyl) phthalate (DEHP) and trisodium nitrilotriacetate monohydrate (NTA).

Di(2-ethylhexyl)phthalate and trisodium nitrilotriacetate monohydrate, two apparently nongenotoxic carcinogens, were tested for effects on gap-junctional communication between Chinese hamster V79 lung fibroblasts. Both compounds inhibited gap-junctional communication in a concentration-dependent manner. The inhibiting effects of these chemicals on gap-junctional communication in vitro correlate with their tumor-promoting activity. Such results further support the hypothesis that inhibition of gap-junctional communication is an in vitro biomarker for some tumor-promoting chemicals.

Acetates↗
PubMed1982

Intercellular communication, three-dimensional cell contact and radiosensitivity.

When electrically coupled mammalian cells are cultured as spherical clones (spheroids) and exposed to ionizing radiation they are less radiosensitive than monolayers of the same cell line. Investigations into the possible role of coupling (gap junctions) and three-dimensional contact in the expression of this phenomenon revealed 1) a correlation between cell coupling and the activity of adenylate cyclase in monolayers, 2) a sharp drop of cyclase activity in spheroids of coupled cells compared to monolayers, and 3) a decrease of coupling with age ("maturation") of the spheroids. These results suggest profound physiological alterations in communicating cells induced under conditions of tight three-dimensional contact as a possible cause for the reduced radiosensitivity of spheroids.

Adenylyl Cyclases↗