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PubMed2005

[Effects and the mechanism of carvedilol on gap junctional intercellular communication in rat myocardium].

OBJECTIVE: To examine the effects of carvedilol on myocardial ischemia and reperfusion injury and on gap junctional intercellular communication (GJIC). METHODS: The left coronary artery was occluded for 30 min and reperfused for 4 h. The activity of creatine phosphokinase (CK), lactate dehydrogenase (LDH) and the infarct size were measured. Isolated buffer-perfused hearts were divided randomly into four groups, sham operation (SO), myocardial ischemia and reperfusion (IR), carvedilol (CV) and heptanol (a gap junctional inhibitor) (HT). The effect of carvedilol on GJIC was measured by a modification of Scrape-loading and dye transfer method, and the state of CX43 phosphorylation was evaluated by Western blot. RESULTS: Compared with the SO group, Increased CK, LDH and infarct size were found in the IR group after 4 h reperfusion. GJIC in the IR group was not inhibited, but dephosphorylated CX43 was increased after 30 minutes of ischemia. Carvedilol decreased CK, LDH and infarct size compared with the IR rats; after 30 minutes of ischemia, both carvedilol and heptanol significantly reduced the GJIC, associated with a significant augmentation of dephosphorylated CX43. CONCLUSIONS: These results suggest that carvedilol reduces GJIC during ischemia presumably by dephosphorylating Cx43, which may be one of the mechanisms of lessening myocardial ischemia-reperfusion injury.

Animals↗
PubMed1990

Modification of gap junctional intercellular communication by changes in extracellular pH in Syrian hamster embryo cells.

Studies were conducted to determine the effect of culture medium pH on gap junctional intercellular communication (GJIC) in early passage Syrian hamster embryo (SHE) cells. Previous studies have demonstrated that SHE cells cultured at a clonal density at pH 6.70 are morphologically transformed by carcinogens at a significantly higher frequency than cells cultured in media of higher pH. Several other cell characteristics consistent with promotion-like effects are observed with pH 6.70 culture of SHE cells. It was postulated that the promotion-like effects observed in SHE cells cultured at acidic pH are mediated in part by a reduction of GJIC. In this study, we evaluated GJIC in SHE cells by fluorescent dye coupling. Results from this study indicate that GJIC decreased as a function of decreased extracellular pH. Cells cultured at pH 6.70, 7.15 or 7.35 exhibited 47, 75 and 85% coupled cells respectively. The decrease in dye coupling occurred by 24 h after switching the cells from pH 7.15 to 6.70 medium. The decreased GJIC observed at pH 6.70 was not due to changes in cell proliferation and was reversible within 24 h when pH 6.70 cultures were refed with pH 7.15 medium. The phorbol ester 12-O-tetradecanoylphorbol-13-acetate inhibited SHE cell GJIC in a pH-dependent manner with cells at pH 6.70 exhibiting the greatest inhibition by TPA and cells at pH 7.35 being unresponsive. The effect of pH on GJIC in SHE cells is consistent with the pH-dependent response to chemically induced morphological transformation and may be mechanistically related to this phenomenon.

Animals↗
PubMed1992

Inhibition of gap-junctional intercellular communication by TPA and airborne particulate matter in primary cultures of rat alveolar type II cells.

Alveolar type II cells were isolated from the lungs of female Wistar rats and were used for studies on inhibition of gap junction mediated intercellular communication (IC). Cells were incubated with 12-O-tetradecanoylphorbol-13-acetate (TPA) or extracts of airborne particulate matter (APM) and subsequently microinjected with the fluorescent dye Lucifer Yellow after which the number of fluorescent (i.e. communicating) cells was determined. Cells exposed to solvent (DMSO), showed an extensive dye coupling. Exposure of cells to TPA or extracts of APM derived from different pollution sources resulted in a strong inhibition of IC. These results show that primary cultures of rat alveolar type II cells can serve pre-eminently as a model in dye-coupling experiments. It further can be concluded that extracts of APM, in addition to the genotoxic activity that has been known for many years, also may have a tumor-promoting potency.

Air Pollutants↗
PubMed2006

Gap junction-mediated intercellular communication between dendritic cells (DCs) is required for effective activation of DCs.

Gap junctions, formed by members of the connexin (Cx) family, are intercellular channels allowing direct exchange of signaling molecules. Gap junction-mediated intercellular communication (GJIC) is a widespread mechanism for homeostasis in organs. GJIC in the immune system is not yet fully understood. Although dendritic cells (DC) reportedly form cell-to-cell contact between DCs in nonlymphoid and lymphoid organs, GJIC between DCs remains unknown. In this study we examined whether DCs form GJIC. XS52 and bone marrow-derived DCs (BMDCs) were tested for GJIC by counting intercellular transfer of Lucifer Yellow microinjected into a cell. Either DC became effectively dye-coupled when activated with LPS plus IFN-gamma or TNF-alpha plus IFN-gamma. LPS- plus IFN-gamma-induced dye-coupling was mediated by DC-derived TNF-alpha. In addition, CpG plus IFN-gamma induced dye-coupling in BMDCs, which was also mediated by DC-derived TNF-alpha. LPS- plus IFN-gamma-induced activation of DCs (assessed by CD40 expression) was observed when there was cell-to-cell contact and was significantly blocked by heptanol, a gap junction blocker. These results indicate that cell-to-cell contact and GJIC are required for effective DC activation. In addition, heptanol significantly inhibited the LPS- plus IFN-gamma-induced up-regulation of the other costimulatory (i.e., CD80 and CD86) and MHC class II molecules expressed by BMDCs, and it significantly reduced their allostimulatory capacity. Among Cx members, Cx43 was up-regulated in dye-coupled BMDCs, and Cx mimetic peptide, a blocker of Cx-mediated GJIC, significantly inhibited the dye-coupling and activation, suggesting the involvement of Cx43. Thus, our study provides the first evidence for GJIC between DCs, which is required for effective DC activation.

Animals↗
PubMed1991

Inhibition of gap junction-mediated intercellular communication by alpha-linolenate.

The purpose of this investigation was to assess whether alterations in the fatty acid composition of rat liver epithelial (WB-F344) cell phospholipids would modulate gap junction-mediated intercellular communication (GJIC). WB-F344 cells were grown to confluency in culture medium supplemented with one of seven different fatty acids at a concentration of 50 microM for 48 h. Only alpha-linoleate (18:3 n-3) significantly inhibited GJIC. Saturated fatty acids (12:0, 16:0, and 18:0), a monounsaturated fatty acid (18:1 n-9), and n-6 polyunsaturated fatty acids (18:2 and 20:4) did not affect GJIC. The alpha-linolenate-induced inhibition of GJIC was not due to the activation of protein kinase C or intracellular hydroperoxide production, two lipid-dependent parameters previously shown to inhibit GJIC. In addition, alpha-linolenate did not alter membrane fluidity. Although the mechanism by which alpha-linolenate inhibits GJIC is unclear, changes in the fatty acid composition of cell phospholipids may be of critical importance. Subsequent to supplementation with alpha-linolenate, WB-F344 cell phospholipids had reduced 20:4 n-6 and elevated n-3 fatty acids. The results of this investigation emphasize the importance of current research into the influence of lipids on cell function and identify a new mechanism by which gap junctions can be modulated.

Animals↗
PubMed2004

Millimeter wave exposure reverses TPA suppression of gap junction intercellular communication in HaCaT human keratinocytes.

The effect of 30.16 GHz millimeter wave (MMW) exposure at 1.0 and 3.5 mW/cm2 on gap junction intercellular communication (GJIC) was studied in cultured HaCaT keratinocytes, using the fluorescence recovery after photobleaching (FRAP) technique and laser confocal scanning microscopy to follow the intracellular movement of 5,6-carboxyfluorescein diacetate dye. While MMW exposure alone for 1 h at either 1.0 or 3.5 mW/cm2 did not affect GJIC, MMW exposure in combination with 5 ng/ml TPA treatment reversed TPA induced suppression of GJIC. Exposure at 1.0 mW/cm2 resulted in a partial reversal, and exposure at 3.5 mW/cm2 resulted in essentially full reversal of the TPA suppression.

Cell Communication↗
PubMed1995

Inhibition of gap junctional intercellular communication and enhancement of growth in BALB/c 3T3 cells treated with connexin43 antisense oligonucleotides.

Many studies have correlated reductions in gap junctional intercellular communication (GJIC) with altered cellular growth, tumor promotion, and neoplastic transformation. To test directly whether reduced GJIC affects cellular growth, GJIC was inhibited in murine BALB/c 3T3 fibroblasts by treatment with a phosphorothioate-modified antisense oligonucleotide targeted against the connexin43 translation start codon, and in vitro cell growth was monitored. The cells were incubated with the oligonucleotide (0.1-0.5 microM) in liposomes in serumless culture medium for 16 h; washed and refed with serum-containing medium; and analyzed for dye-coupling, connexin43 protein and mRNA levels, and cell growth over the next 5 d. The antisense oligonucleotide inhibited dye-coupling and reduced connexin43 protein levels in a concentration-dependent manner but had no effect on connexin43 mRNA levels. Cell growth rate was not affected, but saturation density was increased approximately threefold by the oligonucleotide. These data support a role for GJIC in the establishment of contact inhibition of in vitro cell growth.

3T3 Cells↗
PubMed2002

Aluminum impairs gap junctional intercellular communication between astroglial cells in vitro.

The purpose of the present study was to investigate the effect of aluminum on gap junctional intercellular communication (GJIC) in cultured astrocytes. In the CNS the extracellular environment and metabolic status of neurons is dependent upon astrocytes, which are known to exhibit GJIC. This cell-to-cell communication provides a cytoplasmic continuity between adjacent cells, allowing exchange of diverse ions, second messengers, and metabolites. To study the effects of aluminum intoxication on GJIC in cultured glial cells, astroglial cell cultures obtained from fetal rat brains were exposed to aluminum lactate for 2-6 weeks. To demonstrate the metabolic coupling of neighboring cells, the technique of microinjection of the gap junction permeable substance neurobiotin was performed. Whereas in controls intensive GJIC was observed by dye transfer of neurobiotin from the microinjected cell into the adjacent astrocytes, aluminum treatment significantly impaired this cellular communication. As aluminum is known to affect cytoskeletal elements, additional investigations into the organization of intermediate filaments (glial fibrillary acid protein, GFAP) and microfilaments in control astrocytes and subsequent aluminum exposure were performed with the aid of fluorescence microscopy and rapid-freeze, deep-etch electron microscopy. Aluminum exposure led to an aggregation of GFAP-positive filaments near to the cell nucleus, accompanied by a destruction of the actin cytoskeleton, especially close to the cell membrane. Ultrastructurally these data could be verified as prominent areas without actin filaments contacting the cell membrane detectable in aluminum-treated astrocytes. Immunohistochemical staining of Cx43 revealed an impaired trafficking of this connexin into the cell prolongations following aluminum treatment, although electron-microscopic data revealed that gap junctions between adjacent astrocytes were still present after aluminum incubation for 24 days. In conclusion, in cultured astrocytes the morphological integrity of microfilaments and the intermediate filament network seem to be fundamental for the translocation of connexins from Golgi complex into the cellular prolongation to exhibit proper and extensive cellular communication through gap junctions.

Aluminum↗
PubMed2000

Inhibition of gap-junctional-intercellular communication in intact rat liver by nongenotoxic hepatocarcinogens.

Many nongenotoxic hepatocarcinogens can induce cell proliferation, and inhibit apoptosis and gap-junctional-intercellular communication (GJIC). GJIC, the movement of small molecules (less than 1.2 kD) through membrane channels, is important in regulating cellular homeostasis and differentiation. The inhibition of hepatic GJIC can increase cell proliferation and possibly, inhibit apoptosis. In this study, the relationship between hepatic GJIC, proliferation, and apoptosis was examined in rats treated for 7 days with tumor-promoting doses of the nongenotoxic hepatocarcinogens phenobarbital (PB; 800 ppm), pregnenolone-16alpha-carbonitrile (PCN; 1000 ppm), and Aroclor 1254 (PCB; 100 ppm). In addition, 3-methylcholanthrene (3MC) was included as a negative control. PB, PCN, and PCB increased parenchymal-cell proliferation and inhibited hepatic apoptosis, while no alteration in these growth parameters was observed in 3MC-treated rats. GJIC, as measured by fluorescent-dye transfer through intact liver, was decreased nearly 50% by PB, PCN, and PCB, yet no effect on GJIC was observed in liver from 3MC-treated rats. These data indicate that compounds that inhibit GJIC in liver may be nongenotoxic hepatocarcinogens, which occurs simultaneously during increased cell proliferation and inhibited apoptosis.

Animals↗
PubMed2005

Transgenic disruption of gap junctional intercellular communication enhances early but not late stage hepatocarcinogenesis in the rat.

Much experimental evidence supports the conclusion that loss of gap junctional intercellular communication (GJIC) contributes to carcinogenesis. Transgenic rats featuring a dominant negative mutant of the connexin 32 gene under albumin promoter control (Cx32Delta Tg-High and Cx32Delta Tg-Low lines, respectively with high and low copy numbers of the transgene) have disrupted GJIC, as demonstrated by scrape dye-transfer assay in vivo as previous report by Asamoto et al. (2004). In the present study, we investigated the susceptibility of these transgenic rats to a single intraperitoneal administration of diethylnitrosamine (DEN), and found a significant increase in preneoplastic glutathione S-transferase placental form (GST-P) positive lesions in the livers of Cx32Delta Tg-High but not Cx32Delta Tg-Low rats. However, incidences of adenomas and hepatocellular carcinomas were not elevated at the end of the experiment (52 weeks). In addition, we investigated the promotional effect of phenobarbital (PB) on Cx32Delta Tg-High rats pretreated with DEN and found enhanced formation of GST-P positive lesions, in contrast to the lack of promoting effects reported for Cx32 deficient mice. The results indicate that although both high and low expression of the dominant negative connexin 32 mutant gene in our rats is able to inhibit gap junctional capacity, only high expression is effective at enhancing susceptibility to early stage DEN-induced liver carcinogenesis.

Alkylating Agents↗
PubMed1995

In vitro growth inhibition of neoplastically transformed cells by non-transformed cells: requirement for gap junctional intercellular communication.

We examined whether the inhibition of neoplastically transformed cell growth by co-cultured non-transformed cells involved gap junctional intercellular communication (GJIC). The growth of poorly communicating (approximately 25-35% dye-coupled cells), Ha-ras and neu oncogene-transformed WB-F344 rat liver epithelial cells was inhibited by co-culture with highly communicating (90-95% dye-coupling), non-transformed WB-F344 cells. Inhibition was dependent upon heterologous cell-cell contact and required that the non-transformed cells were GJIC competent. GJIC-deficient mutant WB-F344 cells did not suppress transformed cell growth. Restoration of mutant cell GJIC by transfection with rat connexin43 cDNA restored growth-inhibiting activity. These results clearly demonstrate a role for GJIC in the inhibition of transformed cell growth by non-transformed cells.

Animals↗
PubMed2001

[Effect of inorganic arsenic on gap junctional intercellular communication between human skin fibroblasts].

OBJECTIVE: The aim of this study is to investigate the effect of inorganic arsenic on gap junctional intercellular communication (GJIC) between human skin fibroblasts. METHODS: GJIC between human skin fibroblasts was detected by the scrape loading/dye transfer assay. RESULTS: Arsenite at concentrations from 0.005 micromol/L to 5.0 micromol/L significantly inhibited the dye transfer between human skin fibroblasts in a dose dependent manner. The dye transfer between human skin fibroblasts was also inhibited by arsenate, while the dose-dependent effects were not observed. Further study found that arsenite at concentrations of 0.5 micromol/L and 5.0 micromol/L significantly increased protein kinase C (PKC) activities in cells, especially in the membrane fraction. CONCLUSIONS: Arsenite and arsenate significantly inhibited GJIC between human skin fibroblasts, suggesting that inorganic arsenic may play an important role in the process of tumor promotion. Furthermore, PKC activation may be involved in the mechanisms of GJIC inhibition by inorganic arsenic.

Arsenates↗
PubMed1997

The role of gap junctional intercellular communication (GJIC) disorders in experimental and human carcinogenesis.

There is a growing body of evidence supporting the etiologic implication of gap junctional intercellular communication disorders in carcinogenesis. Substantial progress has recently been made both in molecular biology of gap junction and in the field of cancer research. They provide new insights and conceptions of gap junctional disorders in tumor pathology. Modern understanding of the structure, function and regulation of gap junctions, as well as putative mechanisms of its disorders in human and experimental carcinogenesis are discussed in this review with particular emphasis on fast-moving aspects of this problem.

Animals↗
PubMed1993

Enhancement of gap junctional intercellular communication in tumor promoter-treated cells by components of green tea.

Green tea (Camellia sinensis) has been reported to inhibit tumor promotion in vivo and in vitro. Many tumor promoters inhibit gap junctional intercellular communication (GJIC) which may be an important mechanism of promotion. In the present study, we hypothesized that green tea would enhance GJIC in promoter-treated cells. An aqueous extract of green tea (GTE) and several of its constituents were tested for their effects on GJIC in p,p'-dichlorodiphenyltrichloroethane (DDT)-, 12-O-tetradecanoylphorbol-13-acetate (TPA)- and dieldrin-treated WB-F344 rat liver epithelial cells. All three promoters inhibited GJIC in a dose-responsive manner at non-cytolethal concentrations. (GTE (10-80 gamma/ml) enhanced GJIC 20-80% in promoter-treated cells. (-)-Epigallocatechin gallate and (-)-epicatechin gallate also enhanced GJIC in DDT-treated cells, but no effects were seen with (+)-catechin, (-)-epicatechin, (-)-epigallocatechin, caffeine, or theobromine. These data suggest GTE may inhibit tumor promotion by enhancing GJIC and that the most active components are the catechin gallates.

Animals↗
PubMedDate not supplied

Inhibition of connexin43 gap junctional intercellular communication by TPA requires ERK activation.

The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), is a potent inhibitor of gap junctional intercellular communication (GJIC). This inhibition requires activation of protein kinase C (PKC), but the events downstream of this kinase are not known. Since PKC can activate extracellular signal regulated kinases (ERKs) and these also downregulate GJIC, we hypothesized that the inhibition of GJIC by TPA involved ERKs. TPA treatment (10 ng/ml for 30 min) of WB-F344 rat liver epithelial cells strongly activated p42 and p44 ERK-1 and -2, blocked gap junction-mediated fluorescent dye-coupling, and induced connexin43 hyperphosphorylation and gap junction internalization. These effects were completely prevented by inhibitors of PKC (bis-indolylmaleimide I; 2 microM) and ERK activation (U-0126; 10 microM). These data suggest that ERKs are activated by PKC in response to TPA treatment and are downstream mediators of the gap junction effects of the phorbol ester.

Animals↗
PubMed2002

[Electromagnetic noise blocks the gap-junctional intercellular communication suppression induced by 50 Hz magnetic field].

OBJECTIVE: To explore whether the superposition of an electromagnetic noise can block gap-junctional intercellular communication(GJIC) suppression induced by 50 Hz 0.4 mT extremely low frequency magnetic field(ELF MF). METHODS: Fibroblast cells of mice(NIH 3T3) were exposed to 0.4 mT ELF MF or(and) electromagnetic noise with the same intensity of MF for 24 h, and the GJIC was determined by using fluorescence recovery after photobleaching(FRAP) analysis, which was performed with a laser-scanning confocal microscope(Leica, Germany). RESULTS: ELF MF exposure significantly inhibited GJIC with fluorescence recovery rate of 27.67% +/- 5.12% as compared with the control group(45.57% +/- 9.72%) (P < 0.01), while that of ELF MF plus noise group was (52.61% +/- 8.30%), which was significantly different from ELF MF group(P < 0.01), but not from control(P > 0.05). CONCLUSION: Electromagnetic noise could block the GJIC suppression induced by 50 Hz 0.4 mT MF.

Animals↗
PubMed1990

Inhibitory effect of testosterone on gap junctional intercellular communication of human transitional cell carcinoma cell lines.

A dye transfer method was applied to investigate the effect of testosterone on gap junctional intercellular communication (IC) of two kinds of human transitional cell carcinoma cell lines, JTC-30 and JTC-32. When JTC-30 cells were cultured with testosterone at nontoxic concentrations (17-69 microM), a dose and time dependent inhibition of dye transfer was observed. More than 90% inhibition occurred after exposure to 69 microM testosterone for 96 h. The inhibition was reversed rapidly after testosterone deprivation. Similar results were obtained with JTC-32 cells. 17 beta-Estradiol showed no inhibitory effect on IC of both transitional cell carcinoma cell lines even at toxic levels. Testosterone exhibited no inhibitory effect on IC of human fibroblasts. The inhibitory effect of 5 alpha-dihydrotestosterone was almost similar to that of testosterone. At concentrations examined, cyproterone acetate influenced neither dye transfer nor the inhibitory effect of testosterone, suggesting a mechanism of testosterone action different from that of the known receptor system. Since blockage of IC has been indicated as one reliable evidence for tumor promotion, current results suggest that testosterone is a possible endogenous promoter of the bladder carcinoma and may therefore possibly play a role on the sexually different incidence of bladder carcinoma.

Carcinoma, Transitional Cell↗
PubMed2000

The role of inhibition of gap junctional intercellular communication in rodent liver tumor induction by phthalates: review of data on selected phthalates and the potential relevance to man.

Inhibition of gap junctional intercellular communication (GJIC) has been postulated as a nongenotoxic carcinogenic mechanism, probably related to tumor promotion. Recent studies assessed the role of GJIC in the induction of rodent liver tumors by high levels of phthalate esters. Studies with di(2-ethylhexyl) (DEHP) and diisononyl (DINP) phthalates demonstrated that inhibition of GJIC in rats and mice was well correlated with induction of both liver tumors and markers for peroxisomal proliferation. However, GJIC was unaffected in hamsters and primates, species in which phthalate treatment does not induce peroxisomal proliferation. In vitro studies which extended the database to include human liver cells mirrored the in vivo situation; GJIC was inhibited in rat and mouse cells but not in cells from unresponsive species including humans. Peroxisomal proliferation has been characterized as a species-specific process essential for phthalate-induced rodent liver tumor induction. That GJIC was not inhibited in primate liver or human liver cells provides evidence for a second species-specific carcinogenic process. Thus the GJIC data along with those from studies of peroxisomal proliferation support the view that the carcinogenic effects of DEHP and DINP in rodents are not relevant to humans.

Animals↗