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PubMed1996

Endothelin-1 regulates glucose utilization in cultured astrocytes by controlling intercellular communication through gap junctions.

The role played by endothelin-1 and intercellular communication mediated by gap junctions in the regulation of glucose disposal by astrocytes has been studied in primary culture. Endothelin-1 increased glucose uptake by astrocytes as did one of its putative messenger arachidonic acid and the non-physiological gap junction uncoupler alpha-glycyrrhetinic acid (AGA). None of these agents increased glucose uptake by C6 glioma cells, a cell line in which gap junction proteins are poorly expressed. In confluent astrocytes, the inhibition of gap junction permeability caused by AGA doubled the activity of the pentose phosphate shunt with minimal changes in the activity of the pyruvate dehydrogenase-catalyzed reaction and that of the tricarboxylic acid cycle. By contrast, these effects were not observed in dissociated astrocytes in which intercellular communication is lacking. The scraped loading dye transfer technique was modified to follow the passage of glucose and its metabolites through astrocyte gap junctions. The diffusion of glucose, the phosphorylated derivative glucose-6-phosphate, the phosphorylisable but not metabolisable derivative ortho-methyl-glucose, and the anaerobic glycolytic product L-lactate was much higher in astrocytes than in C6 glioma cells and was inhibited by the inhibition of gap junction permeability caused by endothelin-1, arachidonic acid, octanol, or AGA. It is concluded that gap junction permeability may regulate brain metabolism by controlling the uptake, utilization, and intercellular distribution of glucose and its metabolites in astrocytes.

Animals↗
PubMedDate not supplied

[Intercellular communication in the astrocyte culture as a measure of therapeutic efficacy in multiple sclerosis treated by interferon].

INTRODUCTION: Measurement of therapeutic efficacy in multiple sclerosis depends on the clinical and magnetic resonance findings on follow up. There are no biological markers. Measurement of interleukins and other markers of inflammation has not proved useful in the follow up of these patients. The response of astrocytes to mediators of inflammation gives rise to modification in their capacity for intercellular communication. OBJECTIVE: To find whether culture of astrocytes in serum from patients with multiple sclerosis at different clinical stages and on different treatments gives rise to modification in intercellular communication. PATIENTS AND METHODS: Astrocytes were cultured in serum from three patients with an untreated acute clinical episode of multiple sclerosis, and the results compared with those obtained after serum culture when the patients had been treated with interferon for a year. RESULTS. In astrocyte culture using serum from patients with an acute episode of multiple sclerosis, but not on treatment with interferon, there was a statistically significant reduction in intercellular communication as compared to astrocytes cultured with serum from these same patients treated with interferon for one year (*p< 0.05; **p< 0.01). CONCLUSION: Measurement of the modifications in intercellular communication on astrocyte culture may be used as a marker for inflammatory activity in the serum of patients with multiple sclerosis, and therefore as an index of therapeutic efficacy.

Adjuvants, Immunologic↗
PubMed1990

Inhibition of gap-junctional intercellular communication and enhanced binding of fibronectin-coated latex beads by stimulation of DNA synthesis in quiescent 3T3-L1 cells.

To clarify the modulation of intercellular communication via gap junctions, associated with the growth induction of quiescent 3T3-L1 cells, we investigated the gap-junctional intercellular communication in growth-stimulated cells that were able to bind fibronectin-coated beads. When quiescent 3T3-L1 cells were incubated with fibronectin-coated beads for the first 2 h after the addition of calf serum, 24.0% of the cells bound and phagocytosed beads. Among the cells with bound beads, the percentage of the cells labeled concurrently with bromodeoxyuridine was 63.7% when examined 13 h after the addition of calf serum. Transient reduction of dye-coupling, measured with Lucifer Yellow CH, was observed only in the cells with bound beads 2 h after addition of calf serum, but it was not observed in the cells without bound beads. When the quiescent cells were incubated with fibronectin-coated beads for 2 h from 4-6 h after the addition of calf serum, the percentage of cells with bound beads increased to 53.1%, but the decrease in dye-coupling among the cells with bound beads was slight. These results suggest that the induction of cell growth causes a transient reduction in gap-junctional intercellular communication in 3T3-L1 cells with bound fibronectin-coated beads.

Animals↗
PubMed2000

Morphological transformation and effect on gap junction intercellular communication in Syrian hamster embryo cells as screening tests for carcinogens devoid of mutagenic activity.

A large fraction of chemicals observed to cause cancer in experimental animals is devoid of mutagenic activity. It is therefore of importance to develop methods that can be used to detect and study environmental carcinogenic agents that do not interact directly with DNA. Previous studies have indicated that induction of in vitro cell transformation and inhibition of gap junction intercellular communication are endpoints that could be useful for the detection of non-genotoxic carcinogens. In the present work, 13 compounds [chlordane, Arochlor 1260, di(2-ethylhexyl)phthalate, 1,1,1-trichloro-2, 2-bis(4-chlorophenyl)ethane, limonene, sodium fluoride, ethionine, o-anisidine, benzoyl peroxide, o-vanadate, phenobarbital, 12-O-tetradecanoylphorbol 13-acetate and clofibrate] have been tested for their ability to induce morphological transformation and affect intercellular communication in Syrian hamster embryo cells. The substances were selected on the basis of being proven or suspected non-genotoxic carcinogens, and thus difficult to detect in short-term tests. The data show that nine of the 13 compounds induced morphological transformation, and seven of the 13 inhibited intercellular communication in hamster embryo cells. Taken together, 12 of the 13 substances either induced transformation or caused inhibition of communication. The data suggest that the combined use of morphological transformation and gap junction intercellular communication in Syrian hamster embryo cells may be beneficial when screening for non-genotoxic carcinogens.

Animals↗
PubMed1985

Inhibited intercellular communication as a mechanistic link between teratogenesis and carcinogenesis.

Teratogenesis and carcinogenesis share many characteristics, leading to the speculation that they may also share pathogenic mechanisms. Direct intercellular communication mediated by membrane junctions is known to occur between a variety of cells and may play an important role in the control of cell growth and differentiation. Inhibition of junctional communication may be a mechanism common to both teratogenesis and carcinogenesis whereby cells and tissues are diverted from their normal differentiation paths. The multistage model of carcinogenesis predicts that the irreversibly initiated cell is at least partially regulated by the surrounding cells of a tissue, and that the initiated cell remains inactive until stimulated to proliferate by a tumor promotor. Tumor promoters may release the initiated cell from control of the surrounding tissue by interrupting intercellular communication, since many tumor promoters have now been shown to interfere with junctional communication in cultured mammalian cells. Furthermore, many tumorigenic cells have compromised junctional communication abilities. Similarly, it has been reasoned that the cells of an embryo must be able to communicate with each other to define tissue specificity and pattern formation, and to coordinate morphogenetic events. Many studies have chronicled alterations in junctional communication that occur coincident with major developmental events and some studies suggest that junctional communication may be modified at boundaries of morphogenetic fields. A recent in vivo study has provided evidence that inhibition of junctional communication may interfere with embryonic development, and several teratogens are known to interrupt junctional communication in mammalian cells in culture. These observations suggest that inhibition of junctional intercellular communication may be a shared mechanism of carcinogenesis and teratogenesis.

Animals↗
PubMed2003

Bystander effect in suicide gene therapy is directly proportional to the degree of gap junctional intercellular communication in esophageal cancer.

Gap junctional intercellular communication (GJIC) has been shown to be involved in the bystander effect through herpes simplex virus thymidine kinase/ganciclovir (HSV-tk/GCV) gene therapy. In this study, we examined the expression of connexins, the components of gap junction, and the degree of GJIC in esophageal cancer cell lines and compared the bystander effect in cells with different capacities of GJIC. We found loss in connexin 26 expression and reduced connexin 43 in esophageal cancer. GJIC capacity varied among cell lines and was dependent on the connexin 43 expression in the cell-cell contact areas. In mixing assay, the extent of the bystander effect was tightly correlated with the degree of GJIC capacity. The effects of retinoic acid and cAMP on the bystander effect were also investigated. Treatment with retinoic acid, but not with cAMP, was associated with augmented bystander killing by increase in GJIC in some esophageal cancer cell lines. Our results indicated that the degree of GJIC was predictive to identify a tumor as suitable for gene therapy with the HSV-tk/GCV system. Also GJIC chemically-enhanced with retinoic acid might be useful to improve response in suicide gene therapy.

Blotting, Western↗
PubMed1987

Alterations of intercellular communication associated with the transformation of C3H/10T1/2 cells.

Cultures of C3H/10T1/2 mouse embryo cells were treated in accordance with several treatment regimens that induced the focal growth of morphologically transformed cells. Intercellular communication between focus cells, and between focus and monolayer cells, was examined in late stages of transformation experiments by microinjection of Lucifer yellow dye into cells and observation of dye transfer to surrounding cells. Transformed foci produced by treatment with 3-methylcholanthrene, by initiation with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA), or by initiation with MNNG and promotion with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were studied. These included focus types thought to possess tumorigenic potential (Types II and III) and those believed to lack such potential (Type I). Cells within all focus types exhibited only limited communication with each other or with surrounding monolayer cells. In contrast, microinjection of monolayer cells typically resulted in dye transfer to an average of approximately 50 other monolayer cells. The presence of the tumor promoters TPA or TCDD did not alter intercellular communication between monolayer cells. These studies demonstrate that alterations in intercellular communication are evident during the growth of transformed foci. These changes are relatively independent of both the treatment regimen used to produce foci and the presumed oncogenic potential of different focus types.

Animals↗
PubMed1989

Inhibition of gap-junctional intercellular communication between epithelial cells transformed by the activated H-ras-1 oncogene.

In order to study the effects of an activated H-ras-1 oncogene on gap-junctional intercellular communication, we introduced the EJ/T24 H-ras-1 oncogene into cells of the epithelial Clone 9-3 cell line. Gap-junctional intercellular communication was significantly reduced in H-ras-1-transformed Clone 9-3 derivatives; this result shows that transformation by the activated H-ras-1 oncogene can inhibit gap-junctional intercellular communication. We postulate that the activated H-ras-1 oncogene product could mediate this effect through a change in the phosphorylation of the major gap-junction protein.

Animals↗
PubMed1989

Herbimycin A suppresses the reduction of gap-junctional intercellular communication induced by tumor-promoting phorbol ester in 3T3-L1 cells.

We have examined the suppressive effect of herbimycin A on the reduction of gap-junctional intercellular communication that is induced by a tumor-promoting phorbol ester in 3T3-L1 cells. Most cells in growth arrest participated in dye-coupling, as evaluated by the transfer between cells of a fluorescent dye (Lucifer Yellow CH). Treatment of cells with 0.25 microgram/ml herbimycin A slightly enhanced the dye-coupling. This enhancement required treatment for periods as long as 24 h. Addition of 100 ng/ml 12-O-tetradecanoylphorbol-13-acetate (TPA) caused a rapid reduction of dye-coupling. However, addition of TPA did not suppress dye-coupling in cells pretreated for more than 24 h with herbimycin A. Pretreatment of cells for less than 6 h with herbimycin A did not suppress the TPA-induced reduction of dye-coupling. These results suggest that herbimycin A suppresses the reduction of gap-junctional intercellular communication that is induced by TPA through enhancement of the ability of the cells to participate in gap-junctional intercellular communication.

Animals↗
PubMed1998

Modulated gap junctional intercellular communication as a biomarker of PAH epigenetic toxicity: structure-function relationship.

Cancer is a multistage multimechanism process involving gene and/or chromosomal mutations (genotoxic events), altered gene expression at the transcriptional, translational, and post-translational levels (epigenetic events), and altered cell survival (proliferation and apoptosis or necrosis), resulting in an imbalance of the organism's homeostasis. Maintenance of the organism's homeostasis depends on the intricate coordination of genetic and metabolic events between cells via extracellular and intercellular communication mechanisms. The release of a quiescent cell, whether normal or premalignant, from the suppressing effects of communicating neighbors requires the downregulation of intercellular communication via gap junctions, thereby allowing factors that control intracellular events to exceed a critical mass necessary for the cell to either proliferate or undergo apoptosis. Therefore, determining the role an environmental pollutant must play in the multistage carcinogenic process includes mechanisms of epigenetic toxicity such as the effects of a compound on gap junctional intercellular communication (GJIC). A classic example of a class of compounds in which determination of carcinogenicity focused on genotoxic events and ignored epigenetic events is polycyclic aromatic hydrocarbons (PAHs). The study of structure-activity relationships of PAHs has focused exclusively on the genotoxic and tumor-initiating properties of the compound. We report on the structure-activity relationships of two- to four-ringed PAHs on GJIC in a rat liver epithelial cell line. PAHs containing a bay or baylike region were more potent inhibitors of GJIC than the linear PAHs that do not contain these regions. These are some of the first studies of determine the epigenetic toxicity of PAHs at the epigenetic level.

Animals↗
PubMed1992

Evolutionary origins of intercellular communication systems: implications for mammalian biology.

Traditionally, the two major systems of intercellular communication (i.e. the nervous and endocrine systems) were considered separate functional and anatomical entities. Recent studies have provided evidence that the biochemical elements of these systems have common early phylogenetic origins and have suggested that, with the exception of their anatomical diversity, all the systems of intercellular communication are biochemically similar. On the basis of these findings, we suggest that the overlaps between the nervous and endocrine systems, the widespread tissue production of hormones, and other phenomena are now more easily understood.

Animals↗
PubMed1984

Effects of 12-O-tetradecanoylphorbol-13-acetate (TPA), retinoic acid and diazepam on intercellular communication in a monolayer of rat liver epithelial cells.

We have studied the influence of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), the vitamin A derivative retinoic acid and the benzodiazepine diazepam on intercellular communication via established gap junctions in a monolayer of rat liver epithelial cells (RLB) at various times of incubation. Intercellular communication was measured as the transfer of [3H]hypoxanthine-derived nucleotides between RLB hypoxanthine guanine phosphoribosyl transferase+ (HPRT+) and RLB HPRT- cells. TPA only showed transient inhibition of metabolic cooperation: after 4 h of treatment, intercellular communication was reduced to about 40% of the control and longer treatments showed progressively less effect until 24 h of treatment, when no difference was seen between TPA-treated and control preparations. Retinoic acid was a more effective inhibitor: both 3 X 10(-6) M applied for 24 h and 10(-4) M applied for 6.5 h, caused a 50% inhibition of label transfer. The junctional communication could only be blocked at very high concentrations (5 X 10(-4) M) in short-exposure experiments, but this is possibly a consequence of non-specific effects on the cell membrane. When the incubation time was 24 h, a considerable portion of the gap junctions appeared to persist in the 'open' state. Diazepam showed no significant inhibitory effect in the experiments performed.

Animals↗
PubMed1995

Basic fibroblast growth factor stimulates connexin-43 expression and intercellular communication of cardiac fibroblasts.

Gap junctions (GJ) are membrane specializations responsible for intercellular communication and for ensuring electrical and/or metabolic coupling between cells. They are composed of connexins, a family of related proteins. Connexin-43 (Cx43) is a major connexin of the rat heart, expressed by myocytes as well as non-muscle cells. In this communication we have examined expression of Cx43 by cardiac fibroblasts and regulation of its expression by an endogenous mitogen, basic fibroblast growth factor (bFGF). Recombinant human bFGF, administered to cultured cells which had been maintained in 0.5% serum for 48 h, induced dose-dependent and statistically significant increases in Cx43 mRNA as well as protein accumulation, at 6 h after addition. Intercellular communication was also increased at 6 h but not 30 min after bFGF treatment, as assessed using a scrape-loading protocol. It is concluded that the bFGF-induced stimulation of Cx43 expression caused increased coupling between cardiac fibroblasts. This would be of importance in injured myocardium, the increased bFGF content of which might stimulate electrical coupling involving fibroblasts of the scar tissue.

Animals↗
PubMed1995

Intercellular communication in the brain: wiring versus volume transmission.

During the past two decades several revisions of the concepts underlying interneuronal communication in the central nervous system have been advanced. We propose here to classify communicational phenomena between cells of the central neural tissue under two general frames: "wiring" and "volume" transmission. "Wiring" transmission is defined as intercellular communication occurring through a well-defined connecting structure. Thus, wiring transmission is characterized by the presence of physically identifiable communication channels within the neuronal and/or glial cell network. It includes synaptic transmission but also other types of intercellular communication through a connecting structure (e.g., gap junctions). "Volume" transmission is characterized by signal diffusion in a three-dimensional fashion within the brain extracellular fluid. Thus, multiple, structurally often not well characterized extracellular pathways connect intercommunicating cells. Volume transmission includes short- (but larger than synaptic cleft, i.e. about 20 nm) and long-distance diffusion of signals through the extracellular and cerebrospinal fluid. It must be underlined that the definitions of wiring and volume transmission focus on the modality of transmission and are neutral with respect to the source and target of the transmission, as well as type of informational substance transmitted. Therefore, any cell present in the neural tissue (neurons, astroglia, microglia, ependyma, tanycytes, etc.) can be a source or a target of wiring and volume transmission. In this paper we discuss the basic definitions and some distinctive characteristics of the two types of transmission. In addition, we review the evidence for different types of intercellular communication besides synaptic transmission in the central nervous system during phylogeny, and in vertebrates in physiological and pathological conditions.

Animals↗
PubMed1995

Delayed inhibition of gap-junctional intercellular communication in the acinar cells of rat submandibular glands induced by parasympathectomy and cholinergic agonists.

In this study, the effects of parasympathectomy and cholinergic agonists on gap-junctional intercellular communication and salivary secretion were investigated to clarify the involvement of salivary secretion in delayed uncoupling between acinar cells of rat submandibular glands. Gap-junctional intercellular communication was monitored as dye-coupling in the acinar cells of isolated acini by the transfer of Lucifer Yellow CH. Parasympathectomy induced dye-uncoupling in the acinar cells isolated from denervated salivary glands 12 hr after parasympathectomy-induced salivary secretion. Intraperitoneal application of carbachol (CCh), acetylcholine, pilocarpine, but not isoproterenol, stimulated salivary secretion, and then induced dye-uncoupling in the acinar cells 12 hr later. Atropine suppressed both the salivary secretion and delayed dye-uncoupling induced by parasympathectomy and CCh, when atropine was applied intraperitoneally before the induction of salivary secretion. However, atropine did not suppress the delayed dye-uncoupling by intraperitoneal application of CCh, when atropine was injected after the cessation of CCh-induced secretion. These results suggest that delayed inhibition of gap-junctional intercellular communication by parasympathectomy and cholinergic agonists in rat submandibular glands might be related to the change of secretory function after salivary secretion.

Animals↗
PubMed2000

Modulation of intercellular communication by differential regulation and heteromeric mixing of co-expressed connexins.

Intercellular communication may be regulated by the differential expression of subunit gap junction proteins (connexins) which form channels with differing gating and permeability properties. Endothelial cells express three different connexins (connexin37, connexin40, and connexin43) in vivo. To study the differential regulation of expression and synthesis of connexin37 and connexin43, we used cultured bovine aortic endothelial cells which contain these two connexins in vitro. RNA blots demonstrated discordant expression of these two connexins during growth to confluency. RNA blots and immunoblots showed that levels of these connexins were modulated by treatment of cultures with transforming growth factor-ss1. To examine the potential ability of these connexins to form heteromeric channels (containing different connexins within the same hemi-channel), we stably transfected connexin43-containing normal rat kidney (NRK) cells with connexin37 or connexin40. In the transfected cells, both connexin proteins were abundantly produced and localized in identical distributions as detected by immunofluorescence. Double whole-cell patch-clamp studies showed that co-expressing cells exhibited unitary channel conductances and gating characteristics that could not be explained by hemi-channels formed of either connexin alone. These observations suggest that these connexins can readily mix with connexin43 to form heteromeric channels and that the intercellular communication between cells is determined not only by the properties of individual connexins, but also by the interactions of those connexins to form heteromeric channels with novel properties. Furthermore, modulation of levels of the co-expressed connexins during cell proliferation or by cytokines may alter the relative abundance of different heteromeric combinations.

Animals↗
PubMed2000

Quantitative determination of gap junction intercellular communication by scrape loading and image analysis.

Gap junction intercellular communication (GJIC) consists of intercellular exchange of low molecular weight molecules. Chemically induced alterations of this communication have been suggested to result in abnormal cell growth and tumour promotion. Several in vitro assays have been developed to determine the effect of chemicals on gap junction communication in cultured cells. The scrape loading dye transfer technique is based on studying the transfer of the fluorescent dye Lucifer Yellow in cells where the dye is loaded through a cut in the cell monolayer. This technique is rapid and relatively uncomplicated, but has only been used to qualitatively demonstrate communication, due to lack of an appropriate method for quantification of the dye spreading. We show here that analysis of digital fluorescence images of cells scrape loaded with Lucifer Yellow can be used for quantitative determination of GJIC. We have analysed the images both by means of distance of diffusion of the dye in the cell monolayer, as well as by area of dye-coupled cells. The results are consistent with that obtained using microinjection of Lucifer Yellow and the method offers a simple way for quantitative determination of GJIC.

Animals↗
PubMed2001

[Cytokines and chemokines: mediators for intercellular communication in the brain].

The brain includes glial cells (astrocytes, microglia and oligodendrocytes) and endothelial cells in addition to neurons. Under some pathological conditions, it is invaded by leukocytes such as neutrophils, monocytes/macrophages and lymphocytes. Intercellular communication across these cell species is supposed to play crucial roles both in the brain functions and dysfunctions. However, the molecular basis of such intercellular communication remains unclear. We have studied the roles of cytokines and chemokines, which have been investigated as essential mediators in the immune and inflammatory systems, in intercellular communication across neurons, glial cells, endothelial cells and leukocytes. Messenger RNA expression of cytokines such as interleukin-1 beta was induced in brain microglia by i.p. injection of excitotoxin and neurostimulant, at least, partly via catecholaminergic systems. Messenger RNA of other cytokines such as leukemia inhibitory factor was induced in astrocytes. This cytokine specifically induced nociceptin mRNA in the cultured cortical neurons. Constitutive expression of some chemokines such as fractalkine and stromal cell derived factor-1 alpha was observed in the brain, suggesting that they play important roles in maintenance of brain homeostasis or determination of the patterning of neurons and/or glial cells in the developing and adult brains. Cytokines such as interleukin-1 beta and chemokines such as monocyte chemoattractant protein-1 and macrophage inflammatory protein-1 alpha were produced in ischemic brain and implicated in ischemic brain injury. In addition to ischemia, cytokines, chemokines and their receptors have been shown to be involved in various neurodegenerative diseases such as multiple sclerosis, Alzheimer's disease and AIDS dementia syndrome. They are potential targets for therapeutic intervention for neurodegenerative diseases.

Animals↗