Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cell Communication”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed1990

Carcinogenic implications of the neighborhood coherence principle (NCP).

A new hypothesis on carcinogenesis is set forth on the basis of the neighborhood coherence principle (NCP). NCP constitutes a general rule of pattern formation and maintenance. According to this principle, a system of interacting cells can produce and maintain a spatial organization by virtue of cell-cell communication. This hypothesis suggests that this homeostasis primarily results from a NCP-like process implying cell-cell communication. Each cell is constrained by its neighbors to maintain the mature phenotype despite its inherent individual variability. If the cell-cell mature communication happens to be impaired, tissue homeostasis is disrupted and a proliferative state can be initiated. A further potential effect may result from the establishment of NCP-like communication specific for proliferative cells allied to paracrine and outocrine factors which can lock the cells into the proliferative mode. Most mechanisms implied in this hypothesis have already been investigated. There is a large body of experimental results supporting the role of junctional communication in cooperative metabolism, growth, differentiation and tumour-related events. This new hypothesis provides a framework within which these known facts may be put in a theoretical perspective; it might well constitute the unifying theory--as yet missing--in carcinogenesis.

Animals↗
PubMed2002

Cripto, a multifunctional partner in signaling: molecular forms and activities.

Within a multicellular organism, communication between cells is essential during development to ensure proper execution of cell migration, cell fate decisions, and differentiation events. It is also essential in the adult for the coordination of many physiological functions. Cell-to-cell communications often rely on the interaction of cell surface receptors with soluble or membrane-bound ligands. Receptors or ligands may interact with additional partners to trigger specific signaling cascades inside the cell. In most cases, partners act in a specific configuration, either as a diffusible "co-ligand" or a membrane-bound co-receptor. Here, we examine the case of Cripto, a signaling molecule that has prominent functions during vertebrate development. Conflicting results have suggested that Cripto has the unusual capacity to act both as a secreted ligand and as a cell surface component to control a single signaling pathway. Here, we review the recent experiments that attempt to reconcile those results. Furthermore, three reports have described the fact that Cripto is modified by the addition of sugar residues, including a rare case of fucosylation. These modifications are essential for Cripto function, suggesting that, as is the case for other key developmental or physiological regulators such as Notch or selectins, the activity of Cripto may be controlled by the extent of its glycosylation or fucosylation (or both).

Animals↗
PubMed2001

Connexin-43 expression in oral-derived human osteoblasts after transforming growth factor-beta and prostaglandin E2 exposure.

Dental implant placement stimulates a response in the supporting tissue; the response involves bone remodeling and release of wound-healing factors, including cytokines. Important factors such as transforming growth factor-beta (TGF-beta), which promotes matrix synthesis, and prostaglandin E2 (PGE2), a mediator of inflammation, have the potential to alter the communication between bone cells and interfere with implant site healing. Cells responsible for the formation of bone are interconnected to form a multicellular network. Cell-to-cell communication in this network occurs in part via gap junctions. In bone cells, the predominant gap junction protein is connexin-43. TGF-beta is a growth modulator produced by osteoblasts and released from the matrix in response to resorption and may influence the progression of periodontal disease. TGF-beta also promotes the synthesis of extracellular matrix proteins such as collagen, fibronectin, and adhesion molecules. PGE2 is a mediator of inflammation produced in response to periodontal pathogens. PGE2 levels in the gingival sulcular fluid have been correlated with attachment loss and bone resorption. The relationship between these factors and connexin-43 is unclear. Oral-derived (alveolar) bone was used because the phenotype of bone can differ between species and between different sites in the body. For our studies, explants of human osteoblasts were cultured on eight well plates and characterized by their expression of osteocalcin, osteonectin, alkaline phosphatase, type 1 collagen, and connexin-43. Cells were grown to near confluence on 12 well plates in 20% fetal bovine serum (FBS) Dulbecco modified Eagle medium (DMEM) and then cultured for 24 hours in 0.5% FBS DMEM before exposure to either 1, 5, or 10 ng/mL of TGF-beta in serum-free DMEM for 12 or 24 hours or to 20, 80, or 300 ng/mL of PGE2 in serum-free DMEM for 12 or 24 hours. After incubation, cells were removed from plates by scraping and assayed for connexin-43 protein, first by Western blot to confirm the specificity of the anti-connexin-43 antibody and then by slot blot analysis for quantitative comparison of connexin-43 expression. Our studies showed no significant changes in connexin-43 expression in response to either factor. These studies suggest that exogenous TGF-beta and PGE2 do not alter connexin-43 expression.

Alveolar Process↗
PubMed1990

The genetic control of cell proliferation in Drosophila imaginal discs.

The imaginal discs of Drosophila provide a favorable system for the analysis of the mechanisms controlling developmental cell proliferation, because of the separation in time between cell proliferation and differentiation, and the facility with which controlling genes can be identified and characterized. Imaginal discs are established in the embryo, and grow by cell proliferation throughout the larval period. Proliferation terminates in a regular spatial pattern during the final stages of larval development and the first day of pupal development. Cell proliferation can be locally reactivated in growth-terminated imaginal discs by removing part of the disc and culturing the remaining fragment in an adult host. The pattern of proliferation in these fragments suggests that cell proliferation in imaginal discs is controlled by direct interactions between cells and their neighbors. Proliferation appears to be stimulated by positional information differences, and these differences are reduced by the addition of new cells during tissue growth. Genes involved in cell proliferation control have been identified by collecting and analyzing recessive lethal mutations which cause overgrowth of imaginal discs. In some of these mutants (fat, lgd, c43, dco) the overgrowing tissue is hyperplastic; it retains its single-layered epithelial structure and is capable of differentiating. In two of the hyperplastic mutants (dco and c43), the imaginal discs show a failure of gap-junctional cell communication, suggesting that this form of cell communication may be involved in termination of proliferation. In other mutants the overgrowing disc tissue is neoplastic: it loses its structure and ability to differentiate, becoming a tumorous growth. The two genes that give a neoplastic phenotype (dlg and lgl) have been cloned and cDNAs of one of them (lgl) sequenced. The lgl gene encodes a cell surface molecule with significant homology to calcium-dependent cell adhesion molecules (cadherins). The expression of lgl at the time of termination of cell proliferation suggests that there are changes in the way that cells interact with one another at these times, and that these changes may be implemented by cell adhesion molecules. Direct cell contact within the epithelium, as well as signalling through gap junctions, appears to be involved in the cell interactions needed for the termination of cell proliferation. Mutations in genes encoding the Drosophila homologs of growth factors, growth factor receptors and oncogenes usually show an effect on cell-fate decisions rather than cell proliferation control, but this may be because oncogenic mutations in these genes would be dominant lethals and would therefore not be identified by conventional genetic analysis.

Aging↗
PubMed2003

Effect of mouse uterine stromal cells on epithelial cell transepithelial resistance (TER) and TNFalpha and TGFbeta release in culture.

Recognizing that uterine stromal cells regulate several uterine epithelial cell function(s), the current study was undertaken to more fully define cell-cell communication in the uterus and to examine the role of uterine stromal cells in regulating epithelial cell monolayer integrity and cytokine release. Uterine epithelial and stromal cells from adult intact mice were isolated and cultured separately on cell culture inserts and/or in culture plates. Epithelial cells, which reach confluence as indicated by high transepithelial resistance (TER > 1000 ohms/well), preferentially release transforming growth factor-beta (TGFbeta) into the basolateral chamber ( approximately 70% > apical) and tumor necrosis factor-alpha (TNFalpha) into the apical compartment ( approximately 30% > basolateral). When epithelial cells on cell culture inserts were transferred to plates containing stromal cells, coculture for 24-48 h increased epithelial cell TER ( approximately 70% higher than control) and decreased TNFalpha release into both the apical and basolateral chambers ( approximately 30%-50%). In contrast, TGFbeta release was not affected by the presence of stromal cells. In other studies, the effects of stromal cells on epithelial cell TER and TNFalpha release persisted for 5-7 days following the removal of stromal cells and were also seen in coculture studies in which conditioned stromal media (CSM) was placed in the basolateral chamber. These studies indicate that uterine stromal cells produce a soluble factor(s) that regulates epithelial cell TER and release of TNFalpha without effecting TGFbeta release. These results suggest that uterine stromal cells communicate with epithelial cells via a soluble factor(s) to maintain uterine integrity and epithelial secretory function.

Analysis of Variance↗
PubMed1993

[Role of intercellular communications in hepatic differentiation and carcinogenesis].

The liver epoch like other tissue epochs, occurs after that different events have induced heterogeneity in embryonic cells which result in distinct evolutionary processes. These events and those of organogenesis like "induction", are deeply dependent on cell-cell communications. Cell-cell interactions involve either soluble factors (hormones, growth factors), extracellular matrix or plasma membrane proteins responsible for cell-cell recognition and/or adhesion. All these plasma membrane signals are transduced to the nucleus and modulate the expression of groups of genes. To be functionally stable along the adult stage the liver has to maintain an ordered activity of cell renewal. This balance between proliferation and differentiation is at least in part, controlled by cell-cell communications. Therefore, it is not surprising that intercellular communications are altered during hepatocarcinogenesis. They involve changes in the distribution of junctions, in the amounts of extracellular matrix components and/or growth factors which all result in modifying the differentiation/proliferation balance. Cell culture models have been used for these different studies; new in vitro systems should be set up in the near future by taking advantage of the targeted hepatocarcinogenesis in transgenic mouse.

Cell Communication↗
PubMed2004

Inhibition of gap junction intercellular communications in cell culture by polycyclic aromatic hydrocarbons (PAH) in the absence of PAH metabolism.

We have studied the effect of polycyclic aromatic hydrocarbons (PAH) on gap junction intercellular communications (GJIC) in culture of hepatoma cells Hep G2 and G27. Carcinogenic PAH inhibited GJIC in both cultures in contrast to non-carcinogenic PAH. We showed that both constitutive and inducible expressions of mRNAs of Ah receptor and cytochrome P4501A1 (the main isoform involved in PAH metabolism) were absent in hepatoma G27 cells. We concluded that the initial, non-metabolized molecules of carcinogenic PAH are responsible for changes in GJIC through interaction with an unknown factor in the cellular membrane.

Base Sequence↗
PubMed2001

Regeneration of rabbit cornea following excimer laser photorefractive keratectomy: a study on gap junctions, epithelial junctions and epidermal growth factor receptor expression in correlation with cell proliferation.

Corneal wound repair was investigated in rabbits following excimer laser ablation of a 6 mm diameter and 90 microm deep disc. In the healing process particular attention was focused on the epithelium where gap junction expression and the rearrangement of desmosomes and hemidesmosomes were correlated with cell proliferation and epidermal growth factor receptor expression. Immunofluorescence-based confocal laser scanning microscopy, semithin resin section morphology and electron microscopy were utilized. In resting cornea two isotypes of gap junctions, confined to different regions in the same basal epithelial cells, were detected. Particulate connexin43 (alpha1) immunostaining was concentrated on the apical while the connexin26 type (beta2) in the baso-lateral cell membranes. This is the first report of connexin26 in the cornea. Connexin43 was found also in corneal keratocytes and endothelial cell. Since the two connexins do not form functioning heteromeric channels and have selective permeabilities they may serve alternative pathways for direct cell-cell communication in the basal cell layer. During regeneration both connexins were expressed throughout the corneal epithelium including the migrating cells. They also showed transient up-regulation 24 hr after wounding in the form of overlapping relocation to the upper cell layers. At this time, basal epithelial cells at the limbal region, adjacent to the wound and those migrating over the wounded area all expressed membrane bound epidermal growth factor receptor and they were highly proliferating. In conclusion, like in other stratified epithelia connexin26 is also expressed in the cornea. Transient up-regulation and relocation of connexins within the regenerating epithelium may reflect the involvement of direct cell-cell communication in corneal wound healing. Mitotic activity in the migrating corneal epithelial cells is also a novel finding which is probably the sign of the excessive demand for new epithelial cells in larger wounds not met alone by the proliferating limbal stock.

Animals↗
PubMed1986

Growth inhibition of transformed cells correlates with their junctional communication with normal cells.

The growth of various chemically and virally transformed cell types in culture is inhibited when they are in contact with normal cell types. We show that this growth inhibition is contingent on the presence of junctional communication between the normal and transformed cells (heterologous communication), as probed with a 443 dalton microinjected fluorescent tracer. In cell combinations where heterologous communication is weak or absent there is no detectable growth inhibition; the inhibition appears when communication is induced by cyclic AMP-dependent phosphorylation, and only then. In cell combinations where heterologous communication is spontaneously strong, the growth inhibition is present, but it is abolished when the communication is blocked by retinol or retinoic acid. The cell-to-cell membrane channels of gap junctions are the likely conduits of the signals for this growth control.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed2000

Formation of three-dimensional thyroid follicle-like structures by polarized FRT cells made communication competent by transfection and stable expression of the connexin-32 gene.

Pig thyrocytes, either in the intact gland or cultured under conditions leading to thyroid follicle reconstitution, coexpress two gap junction proteins, connexin-32 (Cx32) and connexin-43 (Cx43). As thyrocytes cultured in the form of a monolayer only express Cx43, we hypothesized that Cx32 could play a role in thyroid folliculogenesis. In the present work, we analyzed the ability of polarized FRT cells (that are gap junction deficient) to form follicle-like structures after stable transfection with either Cx32 or Cx43 genes. Wild-type and transfected FRT cells, while growing, showed the capacity to form three-dimensional structures corresponding to domes that result from the accumulation of fluid underneath limited areas of the cell layer. The number of domes formed by FRT cells expressing Cx32 (FRT-Cx32) was 2- to 3-fold higher than that obtained with either wild-type or Cx43-transfected FRT cells (FRT-Cx43). Domes generated by FRT-Cx32 cells were stable (beyond 3 weeks of culture), whereas those formed from wild-type or FRT-Cx43 cells were transient, disappearing when cells reached confluence. Inspection of the cell organization within domes formed from FRT-Cx32 cells by phase contrast and confocal microscopy revealed a progressive transition from domes toward closed structures with a lumen. The tightness of the lumen was demonstrated by the retention of a fluorescent probe, lucifer yellow, introduced by microinjection. Electron microscope examinations showed that the neoformed follicle-like structures had an inside-out polarity. Analyses of cell motion and division with time, by fluorescence video microscopy, indicated that the transformation of domes into inside-out follicles brings into play the migration of cells and, to a lesser extent, cell multiplication underneath the domes. In conclusion, FRT cells forced to express Cx32 give rise to domes that transform into closed inside-out follicles. This gain of function appears Cx specific, as FRT-Cx43 cells did not form similar structures. Our data suggest that the formation and/or functioning of Cx32 gap junctions might represent a key event in thyroid epithelium morphogenesis, i.e. formation of a lumen from a tight epithelial cell layer.

Animals↗
PubMed1999

Transfection with different connexin genes alters growth and differentiation of human choriocarcinoma cells.

To examine the role of cell-cell communication via gap junctions in controlling proliferation and differentiation we transfected the malignant trophoblast cell line Jeg-3, which exhibits extremely low cell-cell communication mediated by endogenously expressed connexin40, with connexin26, connexin40, and connexin43, respectively. In vitro growth of all cell clones transfected with connexin genes was significantly reduced compared to controls. This effect corresponded to a significant increase in total junctional conductance of all clones. Single-channel conductances for channels formed by the transfected connexins were in the range of the values published previously. Though total junctional conductance varied highly among clones and even within one clone, differentiation of the cells indicated by beta-hCG secretion was most prominent in the clones that revealed the largest amount of well-coupled cell pairs. Connexin26 channels enable cells of one clone to reduce drastically growth rate and produce significantly higher secretion of beta-hCG. Connexin43 had only moderate effects on the differentiation properties of Jeg-3 cells. These findings suggest that restoration of cell-cell communication plays a role in growth reduction and in differentiation of tumor cells and that different channel proteins might have different effects.

Cell Communication↗
PubMed1986

A fluorescence photobleaching assay of gap junction-mediated communication between human cells.

Gap junction-mediated communication between contiguous cells has been implicated in the regulation of cell proliferation and differentiation. This report describes a new technique to measure cell-cell communication, gap fluorescence redistribution after photobleaching, which is based on the diffusion-dependent return of 6-carboxyfluorescein-mediated fluorescence in a photobleached cell that is in contact with other fluorescently labeled cells. Fluorescence recovery rates are interpreted as dye transport across gap junctions. Results of experiments on normal human fibroblasts and human teratocarcinoma cells show that this technique can measure rapid dye transfer and detect inhibition of communication (between teratocarcinoma cells) by the tumor promoters 12-O-tetradecanoyl-phorbol-13-acetate and the pesticide dieldrin.

Cell Communication↗
PubMed1990

Cytokines of the lung.

Communication between cells determines the steady-state composition of the lung in health and becomes a critical determinant of outcome in pathologic processes resulting in anatomic remodeling. This review presents the evolving concepts of the biology of cytokines (also known as peptide growth factors or biological response modifiers) in maintaining normal tissue growth and homeostasis. How these extracellular signaling proteins are involved in such pathologic disorders as spontaneous pulmonary fibrosis, sarcoidosis, pneumoconiosis, and the evolution and recovery from acute lung injury is also discussed. During the past decade the cytokines have come to the fore as important multifunctional mediators of cell behavior and cell-cell communication. A wide range of cellular responses are influenced or triggered when cytokines interact with cells. These include mitosis, chemotaxis, angiogenesis, cytoskeleton arrangement, immunomodulation, and extracellular matrix production. Cytokines influence cell behavior by binding to specific high affinity surface receptors on target cells. These receptors are linked in turn at the cell membrane to a complex array of intracellular signaling pathways. Individual cytokines may inhibit as well as promote cellular functions such as mitosis and thereby play a critical role in homeostasis of normal tissue elements. Hence, cytokines are intimately involved in normal tissue homeostasis as well as in processes eventuating in growth and remodeling. All cells produce and secrete cytokines at some time during their life. Each cytokine is capable of modulating more than one cellular function. Although produced by a variety of cell types, the triggers that induce a specific cytokine to be produced differ between cells. Many of the cytokines share regions of homologous nucleic acid sequences, suggesting that they are members of larger gene families. Given that tissues and cells are exposed to complex cytokine mixtures rather than to individual cytokines, recent attention has turned to understanding how cytokines interact. The combined effects of cytokine mixtures have proved to be both complex and unpredictable based on knowledge of the separate actions of the individual cytokines involved. In studies of the role of cytokines in lung disease, early research attention has focused on those cytokines released by alveolar macrophages (the so-called macrophage-derived growth factors). However, structural cells as well as immune effector cells of the lung are capable of cytokine production and release. The cytokines receiving the most attention to date in relation to pulmonary diseases include platelet-derived growth factor (PDGF), interleukin-1 (IL-1), transforming growth factor-beta (TGF-beta), tumor necrosis factor-alpha (TNF-alpha), insulinlike growth factor I (IGF-I), and, most recently, interleukin-6 (IL-6).(ABSTRACT TRUNCATED AT 400 WORDS)

Biological Factors↗
PubMed1993

Gap junctional intercellular communication and cell proliferation during rat liver carcinogenesis.

During multistage liver carcinogenesis, there is a sequential decrease in gap junctional intercellular communication (GJIC), associated with reduced expression of a major liver gap-junction protein (connexin 32). There are also several lines of evidence indicating that the induction of cell proliferation plays an important role during liver carcinogenesis. The relationship between GJIC and cell proliferation and their roles in liver carcinogenesis are not yet known. Results from various experiments suggest that there is a close relationship between the inhibition of GJIC and stimulation of liver cell proliferation. However, our results also suggest that different stimuli may affect cell proliferation and GJIC differentially by different mechanisms.

Animals↗
PubMed1996

New insights into lung growth and development.

Lung development requires a complex series of developmentally controlled interactions that involve mechanical forces, genetic and endocrine influences, and cell-cell communication. At each step, cell-matrix or cell-cell signaling mediated by peptide growth factors and extracellular matrix components is crucial in directing cell proliferation, differentiation, and migration. Although a comprehensive understanding of how these components interact to guide lung organogenesis has been elusive, the action and control of peptide growth factors in autocrine and paracrine signaling, mesenchymal-epithelial interactions in controlling branching morphogenesis, cell-cell communication in the regulation of cellular differentiation, and factors regulating pattern formation are being clarified.

Animals↗
PubMed1982

Permeability of gap junctions at the segmental border in insect epidermis.

We have examined cell-cell communication between epidermal cells of fifth-instar larvae of the milkweed bug Oncopeltus fasciatus and those of maggots of the blowfly Calliphora erythrocephala. Ionic coupling and the transfer of injected Lucifer Yellow (molecular weight 450) and lead-EDTA (molecular weight 374) were used to map the pattern of communication. All epidermal cells, regardless of their position with respect to the segmental border, were ionically coupled. In both species Lucifer yellow was transferred freely between cells lying in the same segment--that is, in the same developmental compartment as defined by cell lineage. Dye injections close to the segmental border showed that Lucifer Yellow was not transferred between cells in adjacent segments--that is, across the compartmental border. In Calliphora failure of Lucifer Yellow transfer at the segmental border was always observed; in Oncopeltus Lucifer Yellow was not transferred in 90% of preparations examined. Injections of PbEDTA2- in Calliphora showed that this anion was transferred freely from cell to cell and did not respect the segmental boundary. Previous studies of the distribution of gap junctions at and away from the segmental border make it unlikely that the failure of Lucifer Yellow to cross from segment to segment is due to reduced number of gap-junctional channels at the border. We conclude that gap junctions at the segmental borders may have different permeability properties from those between cells in the same segment.

Animals↗
PubMed1991

[Observation of cellular communication in the corneal endothelium using a small molecular weight fluorescent dye].

The metabolic and functional connection between corneal endothelial cells is thought to depend on the transfer of small molecules via gap junctions, as has been reported for other tissues. Cell-to-cell communication in the corneal endothelium was studied by monitoring the spread of fluorescence following the direct injection of Lucifer Yellow CH into single endothelial cells of the excised rabbit cornea. The image of the endothelial cells was observed during the injection and post-injection periods using specular microscopy and fluorescence microscopy. In the fresh cornea, the dye transferred readily from the injected endothelial cell to its neighbors. In damaged cells, dye transfer was slower or did not occur. After 5 hours of incubation in tissue culture medium 199, the specular microscopic image degraded, lowered cell membrane potential and decreased dye transfer rate were measured. This study showed that in normal corneal endothelial cells there were efficient cell communication channels between neighboring cells, and as the endothelium becomes less viable, cell communication is inhibited.

Animals↗
PubMed1984

Inhibition of metabolic cooperation between Chinese hamster V79 cells by structurally diverse teratogens.

Cell-cell communication through chemical messengers is a fundamental event required for the differentiation of embryonal cells. Interference with this process by xenobiotics may disrupt embryogenesis. Chinese hamster cells (V79) which display a specific form of cell-cell communication called metabolic cooperation were cultured in the presence of structurally diverse chemical teratogens. Among them were 12-O-tetradecanoyl-phorbol-13-acetate (TPA), diphenylhydantoin (DPH), warfarin, and a series of monoalkyl ethers of ethylene glycol with alcohol chain lengths from methyl to butyl. Sodium saccharin and ascorbic acid were examined to represent two chemicals which have been thoroughly tested for teratogenic effects in laboratory animals and cause no birth defects. Recovery of 100 6-thioguanine-resistant V79 (6-TGr) cells in coculture with 400,000 6-thio-guanine-sensitive V79 (6-TGs) cells in the presence of 6-thioguanine (6-TG) and the chemical agent was measured. In amounts that neither interfered with colony forming ability nor caused cytostasis when 100 6-TGr cells were plated alone, all of the substances except for saccharin and vitamin C increased the number of surviving 6-TGr cells in a concentration-related manner. The recovery was increased by the presence of TPA (to 100% by 4 ng/ml), DPH (from 26% at 91 microM to 43% at 274 microM), warfarin (from 15.5% at 162 microM to 44.5% at 487 microM) and to variable extents by all five glycol ethers. The most efficacious in the latter group of compounds was the isopropyl ether which raised 6-TGr recovery from 8% at 0.017 M to 66% at 0.087 M. Based on the evidence accumulated by previous studies involving TPA, we postulate that the teratogens employed inhibited metabolic cooperation. These observations suggest that V79 cells may be suitable to study inhibition of cell-cell communication as a mechanism of teratogenesis.

Animals↗