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PubMed1987

Inverse correlation between the metastatic capacity of cell clones derived from a rat mammary carcinoma and their intercellular communication with normal fibroblasts.

We used three highly and two weakly metastatic clones obtained from a rat mammary carcinoma cell line (c-SST-2) to examine the relationship between the metastatic capacity of tumor cells and their intercellular communication with normal fibroblasts. By employing the dye-transfer method, we found that the frequency of intercellular communication between weakly metastatic clone cells and fibroblasts was significantly higher than that between highly metastatic clone cells and fibroblasts. These results suggest that normal fibroblasts may regulate the metastatic capacity of tumor cells by intercellular communication.

Animals↗
PubMed1987

Effect of biological toxins on gap-junctional intercellular communication in Chinese hamster V79 cells.

Since chemical modulation of gap-junctional intercellular communication has been implicated in several toxicological endpoints, a study to examine the ability of several biological toxins to inhibit this process was undertaken. Eight biological toxins were tested for their ability to inhibit metabolic cooperation, a measure of gap-junctional intercellular communication, in the Chinese V79 cell system. Aplysiatoxin, anhydrodebromoaplysiatoxin and debromoaplysiatoxin showed the strongest ability to inhibit metabolic cooperation while T2-toxin and vomitoxin inhibited metabolic cooperation to a lesser degree. Aflatoxin B1, aflatoxin B2 and palytoxin were inactive in the Chinese V79 system. Palytoxin, which was extremely cytotoxic, might act as a tumor promoter if it induces compensatory hyperplasia in vivo.

Animals↗
PubMed1996

Mechanistical studies of the inhibition of intercellular communication by organochlorine compounds.

Many hydrocarbons are environmental pollutants that, due to their lipophilicity and chemical stability, accumulate in biological systems including milk and body fat. A number of investigations have demonstrated that many organochlorine compounds can act as tumour promoters in vivo and inhibit gap junctional intercellular communication between cells in culture. In the present study we have investigated the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), different polychlorinated biphenyls, chlorinated paraffins and the pesticide endosulfan. Using techniques of scrape loading dye/transfer and Western blot analysis the function, expression and phosphorylation of different connexins in vitro and in vivo were studied. The results show a good correlation between the ability to act as a tumour promoter and to interfere with gap junctional intercellular communication. All tested compounds inhibited the intercellular communication in a liver derived cell line (IAR 20). However, the results show that the time to inhibition varies between the different agents. Endosulfan and chlorinated paraffins inhibit the communication within one hour, whereas dioxin like substances need to expose the cells for 48 hours before the communication is affected.

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↗
PubMed1988

Anchored cell analysis/sorting coupled with the scrape-loading/dye-transfer technique to quantify inhibition of gap-junctional intercellular communication in WB-F344 cells by 2,2',4,4',5,5'-hexabromobiphenyl.

Inhibition of intercellular communication has been hypothesized to play a role in tumor promotion. The compound 2,2',4,4',5,5'-hexabromobiphenyl (245-HBB) is a tumor promoter in vivo and blocks intercellular communication in vitro. The scrape-loading/dye-transfer (SL/DT) assay was used to assess this in vitro effect at varying concentrations of 245-HBB. The SL/DT technique is based on the intracellular loading of a fluorescent dye, lucifer yellow (LY), and monitoring its transfer into adjacent cells via patent gap junctions. Confluent WB-F344 (rat epithelial) cells were exposed to various noncytolethal concentrations of 245-HBB. Transfer of LY was then quantified with anchored cell analysis/sorting (ACAS 470, Meridian Instruments, Okemos, Mich.). The results indicate an inverse correlation between the degree of fluorescence in secondary LY-recipient cells and the treatment concentration. The coupling of these two new methods of cellular biology provided rapid quantitative analysis of dye transfer in measuring the concentration/response of modulation of gap-junctional permeability in cultured cells.

Animals↗
PubMed1989

Reliability of the "kiss of death" method for evaluation of intercellular communication: effect of cloning and culture technique.

I explored the effect of genetic (cloning) and non-genetic (arrangement of the method and quality of culture serum) factors upon variability of the results obtained by using the "kiss of death" method for evaluation of intercellular communication in Chinese hamster cells V79-4. Cloning had neither quantitative (intraspecies communication) nor qualitative (interspecies communication) effects. Of the non-genetic factors, the time interval of application of transferred agent (thioguanine) after plating the cells and the agent concentration were investigated. These factors did not influence significantly the results. Intercellular communication was more intensive in a less rich medium containing bovine serum than in a richer medium containing foetal calf serum. On the basis of the results obtained I conclude that the higher variability of intercellular communication values determined by the "kiss of death" method is not due to an error in the experimental method used but probably reflects the real changes in these values that occur with time in cell populations.

Blood↗
PubMed2005

Analysis of avian bone response to mechanical loading. Part two: Development of a computational connected cellular network to study bone intercellular communication.

Mechanical loading-induced signals are hypothesized to be transmitted and integrated by connected bone cells before reaching the bone surfaces where adaptation occurs. A computational connected cellular network (CCCN) model is developed to explore how bone cells perceive and transmit the signals through intercellular communication. This is part two of a two-part study in which a CCCN is developed to study the intercellular communication within a grid of bone cells. The excitation signal was computed as the loading-induced bone fluid shear stress in part one. Experimentally determined bone adaptation responses (Gross et al. in J Bone Miner Res 12:982-988, 1997 and Judex et al. in J Bone Miner Res 12:1737-1745, 1997) are correlated with the fluid shear stress by the CCCN, which adjusts cell sensitivities (loading and signal thresholds) and connection weights. Intercellular communication patterns extracted by the CCCN indicate the cell population responsible for perceiving the loading-induced signal, and loading threshold is shown to play an important role in regulating the bone response.

Algorithms↗
PubMed1990

Mechanical stimulation and intercellular communication increases intracellular Ca2+ in epithelial cells.

Intercellular communication of epithelial cells was examined by measuring changes in intracellular calcium concentration ([Ca2+]i). Mechanical stimulation of respiratory tract ciliated cells in culture induced a wave of increasing Ca2+ that spread, cell by cell, from the stimulated cell to neighboring cells. The communication of these Ca2+ waves between cells was restricted or blocked by halothane, an anesthetic known to uncouple cells. In the absence of extracellular Ca2+, the mechanically stimulated cell showed no change or a decrease in [Ca2+]i, whereas [Ca2+]i increased in neighboring cells. Iontophoretic injection of inositol 1,4,5-trisphosphate (IP3) evoked a communicated Ca2+ response that was similar to that produced by mechanical stimulation. These results support the hypothesis that IP3 acts as a cellular messenger that mediates communication through gap junctions between ciliated epithelial cells.

Animals↗
PubMed2002

Cx32 formation and/or Cx32-mediated intercellular communication induces expression and function of tight junctions in hepatocytic cell line.

Gap junctional intercellular communication (GJIC) is thought to play a crucial role in cell differentiation. Small gap junction plaques are frequently associated with tight junction strands in hepatocytes, suggesting that gap junctions may be closely related to the role of tight junctions in the establishment of cell polarity. To examine the exact role of gap junctions in regulating tight junctions, we transfected connexin 32 (Cx32), Cx26, or Cx43 cDNAs into immortalized mouse hepatocytes derived from Cx32-deficient mice and examined the expression and function of the endogenous tight junction molecules. In transient wild-type Cx32 transfectants, immunocytochemistry revealed that endogenous occludin was in part localized at cell borders, where it was colocalized with Cx32, whereas neither was detected in parental cells. In Cx32 null hepatocytes transfected with Cx32 truncated at position 220 (R220stop), wild-type Cx26, or wild-type Cx43 cDNAs, occludin was not detected at cell borders. In stable wild-type Cx32 transfectants, occludin, claudin-1, and ZO-1 mRNAs and proteins were significantly increased compared to parental cells and all of the proteins were colocalized with Cx32 at cell borders. Treatment with a GJIC blocker, 18 beta-glycyrrhetinic acid, resulted in decreases of occludin and claudin-1 at cell borders in the stable transfectants. The induction of tight junction proteins in the stable transfectants was accompanied by an increase in both fence and barrier functions of tight junctions. Furthermore, in the stable transfectants, circumferencial actin filaments were also increased without a change of actin protein. These results indicate that Cx32 formation and/or Cx32-mediated intercellular communication may participate in the formation of functional tight junctions and actin organization.

Actin Cytoskeleton↗
PubMed2005

Effect of byproducts from the ozonation of pyrene: biphenyl-2,2',6,6'-tetracarbaldehyde and biphenyl-2,2',6,6'-tetracarboxylic acid on gap junction intercellular communication and neutrophil function.

In this study, biphenyl-2,2',6,6'-tetracarbaldehyde, an initial byproduct formed from the ozonation of pyrene, and biphenyl-2,2',6,6'-tetracarboxylic acid, a subsequent pyrene ozonation byproduct, were evaluated using two toxicology assays to compare the toxicity of ozonation byproducts with that of the parent compound. The first assay measured the potential for the compounds to block gap junctional intercellular communication (GJIC) using the scrape loading/dye transfer technique in normal WB-344 rat liver epithelial cells. The second assay evaluated the ability of the compounds to affect neutrophil function by measuring the production of superoxide in a human cell line (HL-60). Pyrene significantly blocked intercellular communication (f = 0.2-0.5) at 40 microM and complete inhibition of communication (f < 0.2) occurred at 50 microM. Gap junctional intercellular communication in cells exposed to biphenyl-2,2',6,6'-tetracarbaldehyde reached f < 0.5 at a concentration of 15 microM. At concentrations greater than 20 microM, biphenyl-2,2',6,6'-tetracarbaldehyde was cytotoxic and the inhibition of GJIC was caused by cell death. Biphenyl-2,2',6,6'-tetracarboxylic acid was neither cytotoxic nor inhibitory to GJIC at the concentrations tested (10-500 microM). Exposure to biphenyl-2,2',6,6'-tetracarbaldehyde resulted in a concentration-dependent decrease in phorbol 12-myristate 13-acetate-stimulated O2- production. Neither exposure to pyrene nor biphenyl-2,2',6,6'-tetracarboxylic acid caused a significant toxic effect on neutrophil function.

Aldehydes↗
PubMed1998

Downregulation of connexin32 protein and gap-junctional intercellular communication by cytokine-mediated acute-phase response in immortalized mouse hepatocytes.

In the present study, we have analyzed the direct effects of cytokines, which mediate the acute-phase response in liver, on connexin expression and gap-junctional intercellular communication in immortalized MHSV12 mouse hepatocytes. When these cells were stimulated for 24 h with interleukin 1 and interleukin 6, the amount of connexin26 (Cx26) mRNA increased together with beta-fibrinogen mRNA, as expected for this positive acute-phase gene. In contrast, connexin32 (Cx32) mRNA expression was not affected under these conditions. Indirect immunfluorescence revealed a drastic decrease in Cx32 signals, whereas slightly more Cx26 signals were found. Stronger stimulation with interleukin 1 and tumor necrosis factor alpha gave a dose-dependent increase in steady state levels of Cx26 and beta-fibrinogen mRNA, but no further change in Cx32 mRNA level was seen. However, when Cx32 protein was analyzed on immunoblots, we found a 5-fold decrease in expression even at low cytokine doses that did not affect Cx32 mRNA expression. Under these conditions, cell to cell transfer of Lucifer yellow, microinjected into immortalized hepatocytes, was decreased by 70%, suggesting that intercellular communication through Cx32 channels was partially inhibited earlier than other genetic alterations characteristic of the acute-phase response. Thus, the major hepatic gap junction protein was largely downregulated at the beginning of the experimental inflammatory reaction, but about 30% of gap-junctional intercellular communication was maintained. This suggests that, during the acute-phase response, the second hepatic Cx26 protein may compensate in part for the downregulation of the Cx32 protein.

Acute-Phase Reaction↗
PubMed2003

Gap junction-mediated intercellular communication in a long-term primary mouse hepatocyte culture system.

Gap junction-mediated intercellular communication (GJIC) is critical for maintaining integral cellular processes including differentiation and growth control. The disruption of GJIC has been correlated with aberrant function in many cell types, including hepatocytes in vivo; therefore it is imperative that cellular model systems support intercellular communication to simulate normal cellular functions. Functional GJIC has been shown in long-term primary rat hepatocyte cultures, which have been implemented widely to study various aspects of hepatocellular function; however, the onset of transgenic technology in murine species has necessitated the development of a primary mouse hepatocyte system. In this report, we analyze GJIC in a dimethylsulfoxide (DMSO)-containing long-term primary mouse hepatocyte culture system. The cells retain morphologic and biochemical characteristics of differentiated hepatocytes through day 30 post plating, including liver-specific gene expression. We further show that connexin32 and connexin26 expression and gap junction plaque formation increase over time in culture concomitant with an increase in GJIC between adjoining primary mouse hepatocytes. In conclusion, the findings described in this study make it possible to maintain differentiated primary mouse hepatocytes that also show GJIC in long-term culture for 30 days. In addition, this system has the potential to be extended to study primary mouse hepatocytes isolated from genetically engineered mice.

Animals↗
PubMed1997

The biological conditions of assessment of ethylene glycol-induced inhibition of gap junctional intercellular communication by metabolic cooperation assay.

Ethylene glycol (EG) has been previously shown to inhibit gap junctional intercellular communication. In this paper we examine conditions under which the effect of EG on gap junctional communication is assessed by metabolic cooperation assay. The later, after the start of metabolic cooperation assay, EG was added, the lower its inhibitory effect was. If treatment with EG began 12 h or even later after plating of cells, no significant effect on gap junctional communication was observed. Short EG treatments (2-8 h) induced a reversible inhibition of cell-to-cell communication, provided that the cells could communicate freely after the drug was removed. However, if further cell-to-cell communication was excluded, the effect of short exposures was irreversible. Using Scrape loading method we observed that after a 60 min exposure to EG the standard gap junctional intercellular communication was completely restored in a few hours.

Animals↗
PubMed2000

Dynamics of intercellular communication during melanoma development.

Melanoma development involves processes determined collectively by various microenvironmental factors, among which intercellular communication has drawn increased attention. Cell-cell crosstalk mediated by cadherins and connexins results in coordinated regulation of cell growth, differentiation, apoptosis and migration. Abnormal expression of adhesion receptors and dysregulated intercellular communication appears to drive tumor development and progression.

Animals↗
PubMed1994

Expression of cell adhesion molecules and connexins in gap junctional intercellular communication deficient human mesothelioma tumour cell lines and communication competent primary mesothelial cells.

Gap junctional intercellular communication (GJIC) has been reported to be markedly reduced in human mesothelioma tumour cell lines compared with primary mesothelial cells. Immunofluorescence stainings have shown that the gap junction protein connexin43 (Cx43) is expressed in both malignant and normal mesothelial cells. In this study the mRNA expression of Cx43 and three different connexins--Cx37, Cx40 and Cx45, which are highly expressed in lung tissue--was investigated in eight human mesothelioma cell lines, and in human primary mesothelial cells from several donors. The expression of the intercellular adhesion molecules A-CAM (N-cadherin) and L-CAM (E-cadherin) was studied at the protein level. No mRNA expression of Cx37, Cx40 or Cx45 in either mesothelioma tumour cells or the primary mesothelial cells was detected. Cx43 was expressed at both the mRNA and the protein level, in seven out of eight mesothelioma cell lines, as well as in all the primary mesothelial cell cultures. The well as in all the primary mesothelial cell cultures. The intercellular adhesion molecule A-CAM was expressed at the cell-cell borders in six out of seven mesothelioma cell lines, as well as in normal mesothelial cells. No expression of L-CAM was observed in these cells. The results suggest that Cx43 and A-CAM are the major proteins in gap and adherens junctions respectively in human mesothelial cells. Most mesothelioma tumour cell lines with markedly reduced GJIC still express both Cx43 and A-CAM. Only one of our mesothelioma tumour cell lines severely deficient in GJIC lacks both the gap junction protein Cx43 and the cell adhesion molecule A-CAM.

Cell Adhesion Molecules↗
PubMed1997

Dimethylsulfoxide maintains intercellular communication by preserving the gap junctional protein connexin32 in primary cultured hepatocyte doublets from rats.

Intercellular communication via gap junctions is one of the differentiated functions of cells. Dimethylsulfoxide (DMSO) is known to induce cell differentiation and maintain differentiated cellular functions in primary hepatocyte culture, but the mechanism of action of DMSO is unknown. Therefore, we investigated the effect of DMSO on cell-cell communication via gap junctions of hepatocyte doublets, which are differentiated cells that lose differentiated functions with time in culture. In isolated rat hepatocyte doublets, we assessed the effects of 1, 2 and 3% DMSO in culture medium on morphological changes and dye-coupling activity between pairs of cells by microinjection with fluorescent dye (Lucifer Yellow CH). The distribution of gap junction protein connexin32 (Cx32) was assessed by indirect immunofluorescence analysis and the Cx32 mRNA was detected by the reverse transcription-polymerase chain reaction method. Dimethylsulfoxide delayed the morphological change of hepatocyte doublets from a spherical to a flattened shape. Dye-coupling efficiency significantly decreased with time in culture in the control group, whereas in groups treated with 2 and 3% DMSO, dye-coupling efficiency was retained after 6 and 9 h of inoculation (P < 0.05 and P < 0.01, respectively). Analysis by indirect immunofluorescence showed few fluorescent spots for Cx32 in the control group at 9 h of incubation, whereas many punctate fluorescent spots were seen in the 3% DMSO group at 9 h of incubation. The detection of Cx32 mRNA in the 3% DMSO group was also stronger than in controls. Dimethylsulfoxide significantly maintained intercellular communication via gap junctions in primary cultured rat hepatocytes through the preservation of functional Cx32 protein, thus maintaining cell differentiation.

Animals↗
PubMed2001

[Studies of intercellular communication in human rhabdomyosarcoma cell lines of different metastatic potential].

OBJECTIVE: To investigate the relationship between intercellular communication and three human rhabdomyosarcoma (RMS) cell lines of different metastatic potential. METHODS: Indirect immunofluorescent staining and laser scanning confocal microscope (ISCM) were used to detect connexin 43 (CX43), a molecule related with gap junctional intercellular communication (GJIC). Fluorescence redistribution after photobleaching (FRAP) was used to detect function of GJIC. RESULTS: A high level of CX43 protein expression was revealed in normal human myoblasts. CX43 protein was mainly localized on the surface of cells and sometimes in cytoplasm. CX43 expression was decreased in RMS cells. Both the detection rates and fluorescent intensity of CX43 decreased when the metastatic potential of RMS increased (P < 0.05). In contrast to normal, the fluorescence recovery rates of the RMS cells decreased and there was a negative correlation between the function of GJIC and malignancy of RMS cell lines (P < 0.05). CONCLUSION: Varying degrees of GJIC inhibition may correlate with different metastatic potential of RMS. This may help to determine the malignant behavior of RMS and be used as a prognostic index of RMS.

Animals↗
PubMed2004

[Influence of acetylcholine on cytoplasma Ca2+ signals and gap junctional intercellular communication of rat hippocampus cells].

OBJECTIVE: To investigate the influence of acetylcholine (Ach) on gap junctional intercellular communication in rat hippocampus. METHODS: Ach was applied to primary co-cultured hippocampus neurons and glial cells. Laser scanning confocal microscopy was used to monitor the change of Ca(2+) in the cytoplasma. The effect of Ach on gap junctional intercellular communication(GJIC) was measured by scrape loading method. RESULTS: Ach(0.05-0.10 mmol/L) induced all changes in cytoplasmic Ca(2+) concentration and calcium waves and calcium oscilation in cytoplasma. The Ca(2+) change could be blocked by scopolamine. Using scrape-loading method, we found GJIC notably enhanced 60 h after applying Ach to these cultured cells. CONCLUSION: Ach can enhance GJIC in hippocampus cells.

Acetylcholine↗