Cell communication reduced by changes in cell surface carbohydrates.
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Results for “Cell Communication”
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Synaptic inhibition and cell communication; impairment of cell-to-cell coupling produced by gamma-aminobutyric acid (GABA) in the somatic musculature of Ascaris lumbricoides.
The influence of gamma-aminobutyric acid (GABA) (10(-5) M) on the electrical coupling of giant somatic muscle cells of Ascaris lumbricoides was investigated. GABA enhanced the resting potential of the cells and abolished the spike activity. The coupling coefficient (V2/V1) was reduced by 58.8% while the input resistance (Rin) was decreased by 38.8%. The decline in Rin was not related to unlinearity of the current-voltage relation. As the time constant of cell membrane was reduced by 28.4% by the addition of GABA the effect of the neurotransmitter on cell-to-cell coupling seems to be mainly related to a decrease in resistance of the non-junctional membrane due to an increase in chloride conductance.
Action Potentials↗
Cell communication in the basal cells of the human epidermis.
Electrotonic spread can be measured in the basal cells of the human epidermis. The communication between neighboring cells is high, whereas no leak to the intercellular spaces could be detected. The specific resistance of the membranes between the cells is about 10 Omegacm(2). This finding suggests that for those particles that are able to pass the cell membrane the intracellular path through the epidermis is at least as suitable as the path through the intercellular spaces.
Blister↗
[Quorum sensing in Pseudomonas aeruginosa: cell to-cell communication to sense the cell density of the same species].
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4-Butyrolactone↗
Regulation of cell-cell communication mediated by connexin 43 in rabbit myometrial cells.
The aim of this study was to evaluate the rapid regulation of cell-cell communication by using the microinjection of purified cAMP-dependent protein kinase (protein kinase A), the Ca(2+)-phospholipid-dependent protein kinase (protein kinase C), or the inhibitor proteins (PKI and CKI) that are, respectively, specific for each of these enzymes. Gap junction phenotypes of myometrial tissue and cells were studied by means of immunocytochemistry with antibody to connexin 43 (alpha 1; Cx43). Cells were enzymatically disaggregated from myometrium of nonpregnant, mid-pregnant (Day 14), and late-pregnant (Day 29) rabbit uteri (n = 8 per group) and seeded at high density such that after 4 days, cultures had the appearance of a cross-sectioned myometrium. Purified proteins and their subunits were microinjected, and intercellular communication was evaluated by monitoring Lucifer Yellow dye transfer. Cultures were treated with 0.5 mM 8Br-cAMP (8-bromo adenosine 3',5' cyclic monophosphate) or 10 microM OAG (1-oleoyl-2-acetyl-sn-glycerol), which, respectively, activate protein kinase A and protein kinase C. Immunoreactive Cx43 and cell-cell communication were examined 5 min to 2 h later. Cx43 was detected in myometrial cryosections and cultured cells by indirect immunofluorescence, and its expression increased with gestation. Exposure to 8Br-cAMP increased the amount of immunoreactive Cx43. Basal dye transfer was minimal in nonpregnant cells, increased in cells of mid-pregnant uteri, and was maximal in late-pregnant cells. Treatment with 8Br-cAMP enhanced transfer in mid- and late-pregnant cells but had no obvious effect on cells from nonpregnant animals. OAG treatment inhibited dye transfer in greater than 95% of the cells tested irrespective of pregnancy status. PKI inhibited cell-cell communication within 2 min and up to 40 min. Injection of free catalytic subunit of protein kinase A following PKI inhibition restored communication within 2-3 min, with maximal transfer in 4-5 min. Protein kinase C inhibited communication, which resumed in < 3 min after injection of CKI. We conclude that rabbit myometrial cells engage in Cx43-mediated cell-cell communication and that this process increases during pregnancy. Further, activators of protein kinase A or injected free catalytic subunit rapidly enhances cell-cell communication, whereas activators of protein kinase C or the enzyme itself diminishes this process.
8-Bromo Cyclic Adenosine Monophosphate↗
Inhibition of cell-cell communication by commercial chlorinated paraffins in rat liver epithelial IAR 20 cells.
The effects of six commercial chlorinated paraffins of different carbon chains length and chlorine content (Cereclor 50LV [C50LV], Hüls 60 [H60], Cereclor S45 [CS45], Cereclor S52 [CS52], Cereclor 42 [C42] and Cereclor 48 [C48] on cell communication have been investigated in the scrape-loading/dye-transfer assay in IAR 20 rat liver epithelial cells, as well as the effects of these compounds on connexin 43 (cx 43), the main gap junction protein in this cell line. The results clearly demonstrated that at non-cytotoxic concentrations C50LV, H60, CS45 and CS52 completely inhibited the cell communication within 1 hr. The short carbon chain length chlorinated paraffins (C50LV and H60) were inhibiting the cell communication at lower concentration than the intermediate carbon chain length chlorinated paraffins (CS45 and CS52). Almost complete inhibition of the cell communication was maintained for at least 24 hrs of H60 exposure. Immunoblots of IAR 20 cell extracts after H60-exposure showed a decreased phosphorylation of cx 43 after 1, 4 and 24 hrs of treatment. The phosphorylation pattern of cx 43 prepared from H60- or CS52-exposed cells was different from that prepared from 12-O-tetradecanoylphobol-13-acetate (TPA)-exposed cells after 1 hr treatment. The results show that the short and intermediate, but not the long carbon chain length chlorinated paraffins, are potent inhibitors of gap junction intercellular communication. Thus, our findings suggest that these compounds may act as tumour promoters.
Animals↗
How do injured cells communicate with the surviving cell monolayer?
Mechanically scratching cell monolayers relieves contact inhibition and induces surviving cells near the wound edge to move and proliferate. The present work was designed to test whether surviving cells passively respond to newly available space, or whether cells are actively stimulated by signals from injured cells nearby. We monitored intracellular free Ca2+ ([Ca2+]i) while scratching confluent monolayers of bovine pulmonary endothelial cells and mouse mammary epithelial cells. Within seconds after wounding, a transient elevation of [Ca2+]i was observed in surviving cells. In endothelial cells, the [Ca2+]i elevation propagated into the monolayer for a distance of 10 to 12 cell rows at a speed of 20 to 28 microm/second. The amplitude of the wave of [Ca2+]i was reduced as it propagated into the monolayer, but the velocity of the wave was nearly constant. Cells that experienced the [Ca2+]i elevation had intact plasma membranes, and survived for over 24 hours post wounding. Removing extracellular Ca2+ decreased the amplitude by two-thirds and reduced the propagation rate by half, suggesting that Ca2+ influx contributed to the increased [Ca2+]i. To determine how [Ca2+]i waves were stimulated, we blocked extracellular communication by fluid perfusion or intercellular communication by breaks in the monolayer. In bovine pulmonary artery endothelial cultures, the [Ca2+]i wave passed over breaks in the monolayer, and was prevented from traveling upstream in a perfusion chamber. Conditioned media from injured cells also elevated [Ca2+]i in unwounded reporter cultures. In mouse mammary epithelial monolayers with established cell-cell contacts, the [Ca2+]i wave passed over breaks in the monolayer, but was only partially prevented from traveling upstream during perfusion. These experiments showed that mechanical wounds lead to long distance, [Ca2+]i-dependent communication between the injured cells and the surviving cell monolayer through at least two mechanisms: first, extracellular release of a chemical stimulus from wounded cells that diffused to neighboring cells (present in both monolayers); second, transmission of an intercellular signal through cell-cell junctions (present in the mammary epithelial monolayers). Thus, mechanical injury provided a direct, chemical stimulus to nearby cells which have not themselves been damaged.
Animals↗
Modulation of cell communication and carcinogenesis.
In this paper, recent studies on the role of cell communication in cancer induction, particularly in two-stage carcinogenesis, were reviewed. Cell communication has been proposed to play an important role in cell growth and differentiation since its discovery. The recent finding that tumor promoters inhibit cell communication supports this possibility. The inhibition of cell communication by phorbol ester tumor promoters was also shown to correlate with enhancement of in vitro carcinogenesis in Balb/c 3T3 cells. This strongly suggests that the blocked cell communication may play a crucial causative role in the process of carcinogenesis. Accumulated evidence indicates that phorbol ester may induce blockage of cell communication through binding to its membrane receptor which is presumably Ca2+/phospholipid-dependent kinase. cAMP enhances cell communication and protects its inhibition by phorbol ester, presumably through activating cAMP-dependent kinase. This indicates the possibility that the two kinases may be key elements for physiological regulation of cell communication. It is proposed that the disturbance of the kinase systems by endogenous and exogenous factors may be responsible for the promotion phase of cancer induction. However, the true physiological role of cell communication in carcinogenesis remains to be demonstrated more directly. Especially, what kinds of molecules can pass through the gap junction and regulate cell functions in a cell community must be challenged in future. Some such molecules were speculatively described in this review.
Animals↗
Transmission of hormonal stimulation by cell-to-cell communication.
Rat ovarian granulosa cells and mouse myocardial cells respond to cell-specific hormones by cyclic AMP-dependent mechanisms. In coculture, these heterologous cells communicate by means of gap junctions. Exposure of the cocultures to a hormone specific for one cell type causes the heterologous cells to respond through a cell contact-dependent mechanism. These studies suggest that this cross-stimulation results from the intercellular communication of a mediator that is common to both cell types. The communicated mediator may be cyclic AMP.
Cell Communication↗
Inhibition of cell-cell communication by methylsulfonyl metabolites of polychlorinated biphenyl congeners in rat liver epithelial IAR 20 cells.
The effects of three polychlorinated biphenyl (PCB) congeners and their six methylsulfonyl (MeSO2)-metabolites on cell communication have been investigated in the scrape-loading/dye-transfer assay in IAR 20 rat liver epithelial cells. The results demonstrated that at non-cytotoxic concentrations 2,2',4',5-tetrachlorobiphenyl, 2,2',4',5,5'-pentachlorobiphenyl (2,2',4',5,5'-pentaCB), 2,2',4',5,5',6-hexachlorobiphenyl (2,2',4',5,5', 6-hexaCB), and their 3- and 4-MeSO2 derivatives completely inhibited the cell communication within 1 h. 4-MeSO2-2,2',4',5,5'-pentaCB and 4-MeSO2-2,2',4',5, 5',6-hexaCB appeared to inhibit the cell communication at slightly lower concentration than their parental PCB congeners and 3-MeSO2 derivatives. The results show that 3- and 4-MeSO2 derivatives of the PCB congeners tested inhibit gap junction intercellular communication at about the same potency as their parental compounds. Since inhibition of cell communication is often observed after treatment with many tumor promoters, our findings suggest that the metabolites may also act as tumor promoters.
Alkanesulfonates↗
Cell-to-cell communication in cultured rat thyroid monolayer cells is inhibited dose-dependently by methimazole.
We performed monolayer culture of rat thyrocytes and studied gap junctional communication by measuring intercellular fluorescence redistribution after photobleaching. Cell-to-cell communication among thyrocytes gradually developed during the culture. This communication was demonstrated in approximately 60 percent of the cells cultured for 8 days, while it could not be detected in the remaining 40 percent of the cells even after longer culture. When thyrocytes were cultured in the presence of methimazole, the fluorescence recovery after photobleaching was inhibited dose-dependently. Thyroid-stimulating hormone did not affect the fluorescence recovery. We provided, for the first time, that methimazole inhibited the development of cell-to-cell communication of thyrocytes dose-dependently.
Animals↗
Superoxide and nitric oxide--participation in cell communication.
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Animals↗
The loss of gap junctional cell-to-cell communication is coupled with dedifferentiation of retinal pigmented epithelial cells in the course of transdifferentiation into the lens.
Retinal pigmented epithelial cells (PECs) of the chick embryo can be cultured as a monolayer of melanized hexagonal cells. Modifications of the culture condition make the cells lose most of the phenotypes and further transdifferentiate into lentoid bodies within a few weeks. Ultrastructural observations showed that PECs and the lentoids have gap junctions with distinct morphology. Diffusion of a fluorescent dye confirmed the presence of gap junctions in both phenotypes. However, cells in the intermediate stage of transdifferentiation, which show neither the phenotype of the PEC nor that of the lentoid and are called dedifferentiated PECs here, have almost no gap junction structure. We propose the possibility that the dedifferentiation of PECs and the loss of cell-to-cell communication are tightly coupled events. This cell culture system is a suitable material for further studying this relationship by cellular and molecular approaches.
Animals↗
Single cell transplantation reveals interspecific cell communication in Drosophila chimeras.
Cell-cell communication is not only a common strategy for cell fate specification in vertebrates, but plays important roles in invertebrate development as well. We report here on experiments testing the compatibility of mechanisms specifying cell fate among six different Drosophila species. Following interspecific transplantation, the development of single ectodermal cells was traced in order to test their abilities to proliferate and differentiate in a heterologous environment. Despite considerable differences in cell size and length of cell cycle among some of the species, the transplants gave rise to fully differentiated clones that were integrated into the host tissue. Clones comprised cells of epidermal and/or neural histotypes, indicating that mechanisms mediating the epidermal/neural dichotomy in the ectoderm are conserved between the species. Cells of the neural lineages differentiated into neurones, glia, or both. Moreover, heterologous neurones sent out axons that followed major pathways along nerves and within the neuropile, demonstrating their ability to recognize positional cues in the heterologous CNS of the host.
Animals↗
Role of Cx43 phosphorylation and MAP kinase activation in EGF induced enhancement of cell communication in human kidney epithelial cells.
Epidermal growth factor (EGF) has been found to induce enhanced gap junctional intercellular communication (GJIC) in the human kidney epithelial cell line K7. This is in contrast to what is reported for other cell types, which all show decreased GJIC in response to EGF. In the present study it is shown that 12-O-tetradecanoylphorbol-13-acetate (TPA) and EGF induce similar phosphorylation pattern of the gap junction protein connexin43 (Cx43) in K7 cells, although their effects on GJIC are opposite. Tyrosine phosphorylation of a 42 kD protein was observed to be induced concomitantly with phosphorylation of Cx43. EGF was however found to induce only serine phosphorylation of Cx43, indicating that the tyrosine kinase activity of the EGF receptor was not directly affecting the gap junction protein. The 42 kD protein phosphorylated on tyrosine was identified to be a mitogen activated protein (MAP) kinase. Both EGF and TPA was found to activate MAP kinase in these cells. Phosphorylation of Cx43 and enhancement of GJIC in response to EGF occurred with difference in time course. Phosphorylation of Cx43 was completed within 15 min, while the enhanced GJIC appeared 2-3 h later. It is therefore possible that regulation of synthesis or transport of Cx43 is responsible for the increase in GJIC, rather than direct involvement of Cx43 phosphorylation. This is in support of our previous finding that protein synthesis is necessary for EGF induced upregulation of GJIC in K7 cells.
Antibodies↗
Roles of cell-to-cell communication in development.
Possible roles of cell-to-cell communication mediated by intercellular bridges and gap junctions in development of the female gamete and embryo are discussed. Synchronization of cell cycle events is presumably a role for intercellular bridges between germ cells. The follicle of the Cecropia moth reveals that an electrical polarity exists between nurse cells and oocytes which are connected by intercellular bridges and this polarity may generate differences that result in differentiation of the oogonia to become either the oocyte or nurse cells. Gap junction-mediated transfer of cyclic AMP, made in response to gonadotropin stimulation, between granulosa cells is discussed as a mechanism that allows cells within a tissue to respond to an external stimulus even though all cells in that tissue may not be exposed to the stimulus. A nutritional role for heterologous cell communication between follicle cells and the oocyte in oocyte growth is presented as an example of how gap junction-mediated communication can allow one cell type to influence the behavior of another cell type. During development, a restriction in communication between differentiating cells is frequently observed. Examples of this phenomenon in a mammal and an insect are presented.
Animals↗
Directional specificity of prostate stromal to epithelial cell communication via FGF7/FGFR2 is set by cell- and FGFR2 isoform-specific heparan sulfate.
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Animals↗
Interruption of cell-cell communication in Chinese hamster V79 cells by various alkyl glycol ethers: implications for teratogenicity.
Intercellular communication most likely plays a significant coordinating role in morphogenesis. Blockage of a specific type of intercellular communication, that mediated by gap junctions, has been proposed as a mechanism of action of some teratogens. Several glycol ethers have recently been shown to be teratogenic in laboratory animals. Because these compounds are negative in genotoxic assays, it is suggested that they may act by nongenetic, perhaps membrane-mediated mechanisms. In the present study several structurally related alkyl glycol ethers were examined for their ability to block junction-mediated intercellular communication. Interruption of intercellular communication was measured in vitro by an assay that depends on the transfer of metabolites via gap junctions, i.e., metabolic cooperation. All compounds tested--ethylene glycol (EG), ethylene glycol monomethyl ether (EGME), ethylene glycol monoethyl ether (EGEE), ethylene glycol monopropyl ether (EGPE), and ethylene glycol monobutyl ether (EGBE)--were able to block metabolic cooperation in vitro. The potencies of the compounds were inversely related to the length of the aliphatic chain, the dose required for maximum blockage increasing as the aliphatic chain shortened. Some differences in the maximum amount of blockage were detected, but these were not consistent and hence were not considered significant. Cytotoxicity, as measured by cell survival, was also related to the structure of the compound, generally increasing with increased length of the aliphatic chain. There were structurally related differences in the concentration ranges over which the compounds were effective.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗