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At least 685 records · Page 38Linked to original sources
PubMed1986

Retinoic acid inhibits junctional communication between animal cells.

Retinoic acid inhibits junctional communication between a variety of vertebrate cell types in culture. It reduces the intercellular transfer of 3H-nucleotides between Syrian hamster kidney fibroblasts (BHK 21/13), Chinese hamster lung fibroblasts (V79), rat liver epithelial cells (BRL), Swiss mouse embryo fibroblasts (3T3), rainbow trout gonadal fibroblasts (RTG2) and Xenopus embryo fibroblasts (Xen). It also reduces metabolic cooperation between hypoxanthine-guanine phosphoribosyl transferase deficient mutant and wild-type BHK cells. The inhibition is rapid (intercellular transfer of iontophoretically injected Lucifer Yellow CH between BRL cells is completely blocked after the cells have been exposed to 10(-4) M retinoic acid for 5 min), and is fully reversed when the drug is removed. Based on these results and the observation that the amount of gap junctional protein isolated from cells grown in the presence of retinoic acid for 1 h is the same and after 24 h is increased (1.3- to 3.1-fold) compared with the amount isolated from untreated cells, we suggest that the inhibitory effect is mediated by the reversible closure of junctional channels.

1-Octanol↗
PubMed1983

F-actin aggregates may activate transformed cell surfaces.

Observations on the role of transformation-specific F-actin aggregates [Carley et al, 1981] in altering morphology, adhesion and intercellular interaction in transformed cells are reported here. The appearance and disappearance of membrane- and substrate-associated F-actin aggregates (MAG and SAG, respectively) are followed in a cell line temperature-sensitive for transformation. Since MAG structures also appear near the membrane in suspension cultures of transformed cells and in transformed cells in coculture with untransformed cells, they appear to function at cell-cell contacts. Unlike microfilament bundles in untransformed cells, MAG and SAG do not contain the F-actin regulatory protein tropomyosin. The lack of tropomyosin in these structures near the membrane is reminiscent of areas of an exceptionally active actin cytoskeleton usually associated with motile processes of the normal cell membrane. Such areas of membrane-cytoskeletal interaction may be involved in the aberrant cell-cell communication as well as the aggressive behavior often seen in transformed cells.

Actins↗
PubMed1996

Reduction of gap junction protein connexin 32 in rat atrophic gastric mucosa as an early event in carcinogenesis.

This study was conducted to examine the possible relationship among connexin 32 (Cx32) expression, cell proliferation and differentiation in the normal stomach, N-methyl-N'-nitro-nitrosoguanidine (MNNG)-induced atrophic gastritis, and carcinoma in rats. Atrophic gastritis and adenocarcinoma were induced by the administration of MNNG for 8 and 30 weeks, respectively. Cell proliferation was detected by staining with 5-bromo-2'-deoxyuridine (BrdU). The proliferative zone (BrdU-positive zone), located in the lower third of the gastric gland in controls, was elongated in atrophic gastritis. In adenocarcinoma, BrdU-positive cells were distributed diffusely. Cx32 expression was investigated by an indirect immunofluorescence method. In both control and atrophic gastritis specimens, Cx32 fluorescence was abundant in the surface epithelium, but was rarely detected in the glandular portion or the proliferative zone. The length of the Cx32-positive mucosa was significantly less than the control value in atrophic gastritis and no such positive mucosa was visible in adenocarcinoma. The results of this study indicate that the loss of cell-cell communication through the gap junction, associated with elongation of the proliferative cell zone, may be manifested much earlier than carcinoma. We regard this model as useful for investigating the development of atrophic gastritis into gastric carcinoma.

Adenocarcinoma↗
PubMed1989

Cell-cell interactions in Dictyostelium development.

The development of an organism requires extensive cell-cell communication; however, little is known about the signals transmitted among differentiating cells. Observations of Dictyostelium amoebae reveal that transmembrane signaling systems have been highly conserved in evolution. The signals that cause these cells to differentiate are processed by mechanisms similar to those that process sensory and hormonal stimuli in higher animals.

Cell Communication↗
PubMed1985

Metabolic cooperation between vascular endothelial cells and smooth muscle cells in co-culture: changes in low density lipoprotein metabolism.

A microcarrier co-culture system for aortic endothelial cells and smooth muscle cells (SMCs) was developed as a model for metabolic interactions between cells of the vessel wall. Low density lipoprotein (LDL) metabolism in SMCs was significantly influenced by co-culture with endothelium. The numbers of high affinity receptors for LDL was increased more than twofold (range, 2.1-5.6), with concomitant increases in LDL receptor-mediated endocytosis and degradation. These effects reached a plateau at an endothelial cell/SMC ratio of 1. Kinetic analysis of the endocytic pathway for LDL in SMCs indicated that, in co-culture with endothelium, there was no alteration in the binding affinity of LDL to its receptors but that the internalization rate constant declined and the rate constant for degradation increased. This analysis suggested that the formation and migration of endocytic vesicles was the rate-limiting step of enhanced LDL metabolism under co-culture conditions. Two mechanisms by which endothelial cells influenced smooth muscle LDL metabolism were identified. First, mitogen(s) derived from endothelial cells stimulated entry of SMCs into the growth cycle, and the changes in LDL metabolism occurred as a consequence of G1-S transition. Second, SMC lipoprotein metabolism was stimulated in the absence of mitogens by a low molecular weight (less than 3,500) factor or factors. Co-culture was a required condition for the latter effect, suggesting that the mediator(s) may be unstable or that cell-cell communication was necessary for expression. These results (a) demonstrate that vascular cell interactions can modify LDL metabolism in SMCs, (b) provide some insights into the mechanisms responsible, and (c) identify co-culture as an experimental approach appropriate to certain aspects of vascular cell biology.

Animals↗
PubMed1990

Interleukin-8 gene expression by a pulmonary epithelial cell line. A model for cytokine networks in the lung.

Cellular constituents of the alveolar-capillary wall may be key participants in the recruitment of polymorphonuclear leukocytes to the lung through the generation of the novel neutrophil chemotactic peptide interleukin-8 (IL-8). This interaction appears to occur via the ability of human alveolar macrophage (AM)-derived monokines, tumor necrosis factor (TNF), and interleukin-1 (IL-1) to induce gene expression of IL-8 from pulmonary type II-like epithelial cells (A549). Northern blot analysis demonstrated that steady-state IL-8 mRNA expression, by either TNF- or IL-1 beta-treated A549 cells, occurred in both a dose- and time-dependent fashion. Similarly, extracellular antigenic IL-8, as assessed by specific ELISA, was expressed from TNF- or IL-1 beta-stimulated epithelial cells in a time-dependent fashion with maximal IL-8 antigen detected at 24 h poststimulation. Immunohistochemical staining utilizing rabbit anti-human IL-8 antibody identified immunoreactive, cell-associated IL-8 antigen as early as 8 h post-TNF or IL-1 beta stimulation. A549-generated neutrophil chemotactic bioactivity paralleled IL-8 steady-state mRNA levels. Signal specificity was demonstrated in this system as IL-8 mRNA or protein expression by lipopolysaccharide (LPS)-treated A549 cells was not different from unstimulated cells. Although LPS did not serve as a direct stimulus for the production of IL-8 by type II-like epithelial cells, the condition media from LPS-challenged AM induced a significant expression of IL-8 mRNA by the A549 cells. 24-h conditioned media from LPS-treated cells was as potent as either IL-1 beta or TNF in generating steady-state IL-8 mRNA by A549 cells. Preincubation of LPS-treated AM-conditioned media with anti-human TNF or IL-1 beta neutralizing antibodies resulted in significant abrogation of IL-8 gene expression by A549 pulmonary epithelial cells. These findings demonstrate potential cell-to-cell communication circuits that may be important between AMs and pulmonary epithelial cells during the recruitment phase of acute lung inflammation.

Blotting, Northern↗
PubMed2004

Analyzing for co-localization of proteins at a cell membrane.

Cell-to-cell communication is mediated by molecular interactions at the surface of the cell by soluble ligands released from distant cells or by cell surface molecules on adjacent cells. These interactions lead to activation of intracellular signaling pathways that subsequently can lead to activation of specific genes. This signal transduction process controls cellular activities as diverse as proliferation, differentiation and apoptosis, so we must understand the underlying molecular events in detail in order to understand broader questions related to development, uncontrolled growth in tumors, tissue regeneration and use of stem cells to name a few. Binding of a ligand in the extracellular space to a transmembrane receptor constitutes the first crucial step for activation of a signaling pathway within the cell. This binding can either lead to oligomerization of individual receptors, to reorganization of existing clusters of receptors or to changes in the protein conformations, which in turn results in recruitment of signaling molecules in the cytoplasm. While different membrane receptors activate different downstream signaling pathways, some receptors can activate more than one pathway and a particular pathway can be activated by different receptors. It appears that these processes are regulated either by agonists and antagonists in the extracellular medium, by receptor-receptor interactions in the membrane or by a number of signaling mediators in the cytoplasm of the cell. Our work has focused on understanding how the intermolecular interactions in the membrane can control the signal transduction process: Are there specialized structures on the surface that facilitate receptor-receptor interactions? Do the receptors exist as monomers or pre-existing complexes that enhance the probability of activation? Do different receptors associate in the same domains or are there distinct organizational principles for each receptor type. In order to address these questions, we seek to develop tools that allow us to examine intermolecular interactions and reactions directly on the cell surface, particularly on live cells in culture or in tissue. This review discusses some of the approaches that are currently available and highlights some of the key advantages and disadvantages they represent with particular focus on image cross correlation spectroscopy as a relatively new quantitative tool developed by us to address some of these issues.

Animals↗
PubMed1996

Function at the junction: dynamic interactions between lung cells and extracellular matrix.

Recent advances are elucidating the mechanisms by which cells communicate with the surrounding matrix. Cells have specific receptors for matrix proteins. A number of intracellular molecules with signalling functions aggregate at specialised focal adhesion points and facilitate transfer of information both into and out of cells. The importance of these signaling processes to cell biology makes it likely that manipulation of these processes will allow innovative therapeutic approaches to lung disease.

Cell Communication↗
PubMed2001

Gap junctional channels regulate acid secretion in the mammalian gastric gland.

Gap junction channels are regarded as a primary pathway for intercellular message transfer, including calcium wave propagation. Our study identified two gap junctional proteins, connexin26 and connexin32, in rat gastric glands by RT-PCR, Western blot analysis, and immunofluorescence. We demonstrated a potential physiological role of the gap junctional channels in the acid secretory process using the calcium indicator fluo-3, and microinjection of Lucifer Yellow. Application of gastrin (10-7 m) to the basolateral membrane resulted in the induction of uniphasic calcium signals in adjacent parietal cells. In addition, single parietal cell microinjections in intact glands with the cell-impermeant dye Lucifer Yellow resulted in a transfer of dye from the injected cell to the adjacent parietal cell following gastrin stimulation, demonstrating gastrin-induced cell-to-cell communication. Both calcium wave propagation and Lucifer Yellow transfer were blocked by the gap junction inhibitor 18alpha-glycyrrhetinic acid. Our studies demonstrate that functional gap junction channels in gastric glands provide an effective means for rapid cell-to-cell communication and allow for the rapid onset of acid secretion.

Animals↗
PubMed2005

Regulation of Sertoli cell and germ cell differentation.

Unwanted childlessness affects approximately one in six couples worldwide. According to the World Health Organization, in nearly 40% of cases the cause can be attributed to the female, in 20% to the male, in 25% to both, and in 15% the cause remains unknown. The incidence of male factor infertility in the general population is approximately 7%. The majority of these men experience irreversible idiopathic infertility and cannot father children without some form of medical intervention. Male factor infertility, in addition, may be caused by testicular germ cell cancer, which is known to represent the most common cancer among young men in Western industrialized countries. There is growing evidence that this cancer originates from fetal germ cells exhibiting an aberrant programme of gene expression and that tumour progression may be favoured by an aberrant Sertoli cell-germ cell communication. The present monograph aims to shed more light on the regulation of Sertoli and germ cell differentiation. Involving knockout and transgenic mouse models, the authors focus on (a) male factor infertility that might be related to altered maturation of Sertoli cells, (b) male factor infertility that might be due to incorrect histone-to-protamine exchange in haploid spermatids, and (c) progression of testicular germ cell cancer that might be favoured by an aberrant Sertoli cell-germ cell communication.

Animals↗
PubMed1996

Effect of antipeptide antibodies directed against three domains of connexin43 on the gap junctional permeability of cultured heart cells.

Cell-to-cell communication can be blocked by intracellular injections of antibodies raised against gap junction proteins, but the mechanism of channel obstruction is unknown. Binding to connexins could lead to a conformational change, interfere with regulatory domains or cause a steric hindrance. To address these questions, the effects on cell-to-cell communication of affinity purified polyclonal antibodies raised against peptides reproducing the intracellular sequences 5-17, 314-322 and 363-382 of rat connexin43 were investigated in cultured rat ventricular cells. The antibodies against sequence 363-382 were characterized by immunoblotting and immunocytochemistry. Characterization of antibodies 5-17 and 314-322 has been previously reported. In a first series of experiments, the effect on gap junctional communication was assessed by injecting a junction-permeant fluorescent dye into cells adjacent to one cell previously microinjected with antibodies. In a second series, junctional permeability was quantitatively determined on records of fluorescence recovery after the photobleaching of 6-carboxyfluorescein-loaded cells. Antibodies 5-17 marked a 43 kDa band on immunoblots, but did not immunolabel gap junctions and had no functional effect. Antibodies 314-322 recognized the 43 kDa protein and labeled the intercalated disks, but failed to interfere with junctional permeability. Antibodies to the nearby sequence 363-382, for which all immunospecific tests had been positive, caused a delayed diffusional uncoupling in 50% of the microinjected cells. It is suggested that the blocking of junctional communication by antibodies results from interference with a regulatory domain of the connexin.

Animals↗
PubMed2001

HSV-2 disrupts gap junctional intercellular communication between mammalian cells in vitro.

Infection by herpes simplex virus-2 (HSV-2) disrupts both dye and electrical coupling in Vero (African green monkey kidney) cell cultures. Vero cells in vitro were iontophoretically injected with the fluorescent dye Lucifer yellow CH, the spread of which revealed that cells throughout the confluent sheet shared open gap junctions. However, 24 h after infection with the virus (but before cells became rounded), dye always remained only within the target cell. Intracellular electrophysiological measurements of ionic coupling revealed a 0.4 coupling coefficient for adjacent cells in uninfected control cultures. By 3 h following infection significant down-regulation of gap junctions had begun, preceding by many hours any signs of infection visible with the light microscope. Measurements between adjacent cells 3 h post-infection, a period when HSV-2 gene expression is known to be at a maximum, yielded an average coupling coefficient of 0.35. By 6 h post-infection (a period of known viral DNA replication) average coupling coefficient for adjacent cells was 0.25, while by 24 h post-infection the average fill still further to <0.08. A coupling coefficient of <0.08 suggests that infection by HSV-2 completely disabled the gap junctions.

Animals↗
PubMed2005

Up-regulation of gap junctional intercellular communication and connexin43 expression by retinoic acid in human endometrial stromal cells.

CONTEXT: Gap junctions, made up of connexins (Cxs), play fundamental roles in coordinating a number of cellular processes through their ability to directly regulate cell-cell communication. Cx43 is the most widely expressed Cx in the endometrium and is known to be important in a variety of physiological and pathological processes in this tissue. OBJECTIVE: In this study, we investigated the ability of the retinoid, all-trans-retinoic acid (RA), to regulate Cx43 expression in human endometrial stromal cells. DESIGN: Primary endometrial stromal cells obtained from patients undegoing surgery for infertility workup were treated in vitro with RA and control compounds for different time periods, up to 48 h. Cx43 mRNA and protein levels, protein phosphorylation, and gap junctional intercellular communication (GJIC) were analyzed. RESULTS: Treatment of the cells with RA showed a dose-dependent increase in Cx43 expression at both the mRNA and protein levels. In addition, RA induced a relative decrease in the phosphorylated species of Cx43 while causing a corresponding increase in the nonphosphorylated form. Concomitant with these changes, RA-treated cells demonstrated up to a 250% enhancement of GJIC as assessed by dye transfer experiments. Augmentation of GJIC and alterations of Cx43 expression were observed over the same range of RA concentrations. Treatment of cells with the protein kinase C activator 12-O-tetradecanoylphorbol-13-acetate increased the phosphorylated species of Cx43 and correspondingly inhibited GJIC. CONCLUSIONS: Phosphorylation of Cx43 is inversely related to GJIC in endometrial stromal cells. Retinoids increase GJIC in endomentrial stromal cells through upregulation of Cx43 expression while inducing a decrease in the phosphorylated species of the protein. The data suggest a novel mechanism by which retinoids can influence endometrial cell biology.

Cell Communication↗
PubMedDate not supplied

In vitro measurement of respiration of choroid plexus cells in communicating hydrocephalus.

Communicating hydrocephalus occurs as a result of inappropriate CSF production in the circumstance of diminished absorption. Ventricular enlargement does not progress as rapidly as the measured normal production of CSF would suggest. Thus, compensatory mechanisms must exist to respond in some manner to the altered pathophysiology. In this experiment the metabolic activity (O2 consumption) of the choroid plexus cells in animals with communicating hydrocephalus was compared with that of normals. The modified Cartesian diver technique of Zeuthen13 was employed. These preliminary measurements show that the metabolic activity of the choroid plexus cells was the same in hydrocephalic animals and normals. Response to experimentally induced increased CSF pressure also showed no difference.

Animals↗
PubMed1995

Transient and restricted expression during mouse embryogenesis of Dll1, a murine gene closely related to Drosophila Delta.

The Drosophila Delta (Dl) gene is essential for cell-cell communication regulating the determination of various cell fates during development. Dl encodes a transmembrane protein, which contains tandem arrays of epidermal-growth-factor-like repeats in the extracellular domain and directly interacts with Notch, another transmembrane protein with similar structural features, in a ligand-receptor-like manner. Similarly, cell-cell interactions involving Delta-like and Notch-like proteins are required for cell fate determinations in C. elegans. Notch homologues were also isolated from several vertebrate species, suggesting that cell-to-cell signaling mediated by Delta- and Notch-like proteins could also underlie cell fate determination during vertebrate development. However, in vertebrates, no Delta homologues have yet been described. We have isolated a novel mouse gene, Dll1 (delta-like gene 1), which maps to the mouse t-complex and whose deduced amino acid sequence strongly suggests that Dll1 represents a mammalian gene closely related to Drosophila Delta. Dll1 is transiently expressed during gastrulation and early organogenesis, and in a tissue-restricted manner in adult animals. Between day 7 and 12.5 of development, expression was detected in the paraxial mesoderm, closely correlated with somitogenesis, and in subsets of cells in the nervous system. In adult animals, transcripts were detected in lung and heart. Dll1 expression in the paraxial mesoderm and nervous system is strikingly similar to the expression of mouse Notch1 during gastrulation and early organogenesis. The overlapping expression patterns of the Dll1 and Notch1 genes suggest that cells in these tissues can communicate by interaction of the Dll1 and Notch1 proteins. Our results support the idea that Delta- and Notch-like proteins are involved in cell-to-cell communication in mammalian embryos and suggest a role for these proteins in cellular interactions underlying somitogenesis and development of the nervous system.

Amino Acid Sequence↗
PubMed2006

Endothelial-cardiomyocyte interactions in cardiac development and repair.

Communication between endothelial cells and cardiomyocytes regulates not only early cardiac development but also adult cardiomyocyte function, including the contractile state. In the normal mammalian myocardium, each cardiomyocyte is surrounded by an intricate network of capillaries and is next to endothelial cells. Cardiomyocytes depend on endothelial cells not only for oxygenated blood supply but also for local protective signals that promote cardiomyocyte organization and survival. While endothelial cells direct cardiomyocytes, cardiomyocytes reciprocally secrete factors that impact endothelial cell function. Understanding how endothelial cells communicate with cardiomyocytes will be critical for cardiac regeneration, in which the ultimate goal is not simply to improve systolic function transiently but to establish new myocardium that is both structurally and functionally normal in the long term.

Animals↗
PubMed1989

Cellular and molecular mechanisms of chemical synaptic transmission.

During the last decade much progress has been made in understanding the cellular and molecular mechanisms by which nerve cells communicate with each other and nonneural (e.g., muscle) target tissue. This review is intended to provide the reader with an account of this work. We begin with an historical overview of research on cell-to-cell communication and then discuss recent developments that, in some instances, have led to dramatic changes in the concept of synaptic transmission. For instance, the finding that single neurons often contain multiple messengers (i.e., neurotransmitters) invalidated the long-held theory (i.e., Dale's Law) that individual neurons contain and release one and only one type of neurotransmitter. Moreover, the last decade witnessed the inclusion of an entire group of compounds, the neuropeptides, as messenger molecules. Enormous progress has also been made in elucidating postsynaptic receptor complexes and biochemical intermediaries involved in synaptic transmission. Here the development of recombinant DNA technology has made it possible to clone and determine the molecular structure for a number of receptors. This information has been used to gain insight into how these receptors function either as a ligand-gated channel or as a G protein-linked ligand recognition molecule. Perhaps the most progress made during this era was in understanding the molecular linkage of G protein-linked receptors to intramembranous and cytoplasmic macromolecules involved in signal amplification and transduction. We conclude with a brief discussion of how synaptic transmission leads to immediate alterations in the electrical activity and, in some cases, to a change in phenotype by altering gene expression. These alterations in cellular behavior are believed to be mediated by phosphoproteins, the final biochemical product of signal transduction.

Animals↗
PubMed1990

Skeletal tissue response to cytokines.

Communication among individual cell types that populate connective tissues such as cartilage or bone is of critical importance in determining the phenotypic properties of these tissues under both physiologic and pathologic conditions. Cytokines, which may be defined as soluble products released from one cell that can modulate the activity of other cells, play a critical role in this process of cell communication. The introduction of molecular biologic techniques has permitted identification of specific cytokines previously characterized on the basis of biologic activities. Cloning and sequencing of these products have provided formal evidence for their existence and allowed identification of the full spectrum of their biologic activities. These results have established that individual cytokines may have multiple biologic activities and that multiple cytokines share common functional properties. Based on these results, the term "cytokine" has been used more generally to include products originally described as growth or differentiation factors, e.g., interleukins, monokines, or lymphokines. Cytokines have an important role in the initiation and control of skeletal tissue growth and development and in regulating bone remodeling in the adult organism. As in other connective tissues, these effects are mediated via paracrine, autocrine, and endocrine mechanisms. In skeletal tissues, cytokines may modulate the activity of resident cells by an additional mechanism. Factors produced locally within bone or arriving via the circulation are incorporated into the mineralized bone matrix, and their release during skeletal remodeling could provide the basis for coupling the activity of bone resorbing and forming cells. The principal cytokines that have been shown to affect skeletal tissues include factors previously described as monokines or lymphokines such as interleukin-1 (IL-1), tumor necrosis factors (TNF-alpha and TNF-beta), and interferon-gamma (IFN-gamma); the colony-stimulating factors; and the so-called growth and differentiation factors including transforming growth factors-alpha and -beta (TGF-alpha and TGF-beta), insulinlike growth factor-I (IGF-I), platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF). Although the effects of the individual cytokines are diverse, it is possible to classify individual factors based on their effects on specific aspects of bone formation or resorption. Significant progress has been made recently toward elucidating the mechanisms of action of the cytokines. Binding studies using radiolabeled ligands have characterized the specific cell surface receptors and defined their distribution and properties among skeletal tissue cells. Various so-called signal transduction pathways have been implicated in mediating these effects...

Animals↗