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PubMed1982

Intercellular junctions in the hematopoietic compartments of embryonic chick bone marrow.

Avian embryonic marrow is segregated into distinct erythropoietic and granulopoietic compartments. Within each compartment presumptive stem cells and immature blood cells establish intimate contact with their respective stromal cell. In this study we have examined one aspect of potential hematopoietic cell-stromal cell interaction by looking for the presence of intercellular junctions between these two elements. In previous studies, after aldehyde fixation, junctions were not observed, but after perfusion fixation with tannic acid-glutaraldehyde, pentilaminar junctions became evident. These junctions were most characteristically located in the intravascular erythropoietic compartment, but were also found in the extravascular granulopoietic compartment. Junctions frequently joined presumptive stem cells with sinusoidal endothelial cells as well as joining immature erythroblasts with sinusoidal endothelial cells; and less frequently, junctions connected adjacent erythroid cells. However, reticulocytes and erythrocytes were never seen to have formed junctions with any other type of cell. Similar junctions within the extravascular compartment connected contiguous reticular cells and also, on occasion, reticular cells with sinusoidal endothelial cells. Hematopoietic cell-reticular cell junctions were restricted to two classes of blood cells--extravascular presumptive stem cells and mast cells. There was no evidence of junctions connecting mature or maturing granuloid cells and any other cell type. The presence of intercellular junctions between immature blood cells and their respective stromal cells suggests that such interactions might play an important role in avian hematopoiesis. However, further work will be needed to determine if these junctions are merely adherence sites or whether they represent sites of intercellular communication. In either event, these junctions appear to reflect a mechanism whereby the marrow stroma could regulate erythroid maturation.

Animals↗
PubMed1987

Occlusion of hippocampal electrical junctions by intracellular calcium injection.

Low-molecular weight dyes such as Lucifer yellow or carboxyfluorescein have been used to investigate the electrical connectivity of neurons via gap junctions. The interpretation that such dye passage is mediated through intercellular channels has been controversial and difficult to corroborate with direct techniques in mammalian brain. We report here that elevated intracellular free Ca2+, a treatment shown to cause gap junction occlusion in other tissues, significantly blocks dye transfer between hippocampal cells. Furthermore, intracellular injection of FITC-dextran (which is too large to cross gap junctions) never resulted in multiple hippocampal cell fills. These data lend strong support to the argument that the extent of dye-coupling provides a good estimate of the number of intercellular communication channels, and raises the possibility that these channels may be physiologically modulated.

Animals↗
PubMed1970

The fine structure and electrophysiology of heart muscle cell injury.

Injured frog heart cells electrically uncouple from their uninjured neighbors within 30 min after injury. This uncoupling process can be shown by the disappearance of an injury potential measured between such injured and uninjured cells. In the present study, the time course of the decline of injury potentials, and thus of electrical uncoupling, in bullfrog atrial trabeculae was determined. Tissue was fixed with glutaraldehyde and osmium tetroxide at various times after injury to determine the morphological changes which accompany this uncoupling process. In some cases, ruthenium red was included in the fixatives. Normal atrial cells are long and narrow, with intercellular junctions located along the lateral surfaces of the cells. Two types of intercellular junctions have been observed: cardiac adhesion plaques (CAPs), and close junctions. Close junctions occur only infrequently. Ruthenium red penetrates all around the cells, leaving only small areas within the CAPs unstained. After injury, the cells are very dense and the myofilaments disarranged. Both types of intercellular junction remain intact, and only slight changes within CAPs are observed. The results are discussed in relation to current concepts of intercellular communication.

Action Potentials↗
PubMed2006

Viewing chemokines as a third major system of communication in the brain.

There is irrefutable proof that opioids and other classes of centrally acting drugs have profound effects on the immune system. Evidence is mounting that products of the immune system, such as chemokines, can reciprocally alter the actions of these drugs and the endogenous ligands for their receptors. Chemokines are a family of small (8 to 12 kDa) proteins involved in cellular migration and intercellular communication. With a few exceptions, they act on more than one receptor. Although the chemokines and their G protein-coupled receptors are located in both glia and neurons throughout the brain, they are not uniformly distributed. They are found in such brain areas as the hypothalamus, nucleus accumbens, limbic system, hippocampus, thalamus, cortex, and cerebellum. Among the chemokines differentially localized in brain neurons and glia are CCL2/MCP-1, CXCL12/SDF-1alpha, CX3CL1/fractalkine, CXCL10/IP 10, CCL3/MIP-1alpha, and CCL5/RANTES. Functional roles for the chemokine system, composed of the chemokine ligands and their receptors, have been suggested in brain development and heterologous desensitization. The system can alter the actions of neuronally active pharmacological agents such as opioids and cannabinoids and interact with neurotransmitter systems. In this review, we propose that the endogenous chemokine system in the brain acts in concert with the neurotransmitter and neuropeptide systems to govern brain function. It can thus be thought of as the third major system in the brain.

Animals↗
PubMed2004

Gap junction communication dynamics and bystander effects from ultrasoft X-rays.

Gap junctions provide a route for small molecules to pass directly between cells. Toxic species may spread through junctions into 'bystander' cells, which may be exploited in chemotherapy and radiotherapy. However, this may be prevented by junction closure, and therefore an understanding of the dose-dependency of inhibition of communication and bystander effects is important. Low-energy ionising radiation (ultrasoft X-rays) provides a tool for the study of bystander effects because the area of exposure may be carefully controlled, and thus target cells may be clearly defined. Loss of gap junction-mediated intercellular communication between irradiated cells was dose-dependent, indicating that closure of junctions is proportional to dose. Closure was associated with hyperphosphorylation of connexin43. Inhibition of communication occurred in bystander cells but was not proportional to dose. Inhibition of communication at higher radiation doses may restrict the spread of inhibitory factors, thus protecting bystander cells. The reduction in communication that takes place in bystander cells was dependent on cells being in physical contact, and not on the release of signalling factors into the medium.

Animals↗
PubMed2006

Flow cytometry analysis of gap junction-mediated cell-cell communication: advantages and pitfalls.

BACKGROUND: Since the first morphological description of the gap junctions use electron microscopy, a considerable number of techniques has been introduced to evaluate gap junction channel functionality, many of which use dye transfer techniques, such as dye injection and fluorescent dye transfer, analyzed by flow cytometry. METHODS: To analyze dye transfer, generally one population of cells is incubated with calcein-AM (0.5 microM) for 30 min at 37 degrees C, and the other population was incubated with the lipophilic dye DiIC(18) (3) (10 microM) for 1 h at 37 degrees C; after incubation, these cells were washed five times with PBS and cocultured for different times, and then the dye transfer was analyzed by flow cytometry. RESULTS: In this short overview, we focus on some advantages and disadvantages of flow cytometry as a technique to investigate gap junction-mediated intercellular communication (GJIC). In addition, we point out some technical pitfalls that we have encountered when applying this technique to study gap junctions in immune system cells. CONCLUSIONS: Analysis of fluorescent dye transfer by flow cytometry is a useful tool to investigate GJIC. However, some points must be taken into consideration before using this methodology, which are discussed herein.

Animals↗
PubMed1991

Biochemical and ultrastructural evidence for the association of basic fibroblast growth factor with cardiac gap junctions.

Basic fibroblast growth factor (bFGF) is a ubiquitous and multifunctional polypeptide that is believed to have a role in tissue repair and to act as a morphogen in embryonic development. Here, we have used immunohistochemical and biochemical methods with antibodies directed against the amino-terminal domain of bFGF, designated IS2, which recognize native and denatured bFGF, to demonstrate that in addition to its known intracellular and extracellular localization in heart, bFGF is also associated with cardiomyocyte gap junctions. In tissue sections, IS2 labeled regions of intercalated discs, producing an immunofluorescence pattern virtually indistinguishable from that obtained with antibodies against the heart gap junction protein connexin-43. By electron microscopy, gap junctions but not other regions of plasma membrane were heavily immunolabeled with this antibody. By solid phase immunoassay, bFGF was found to be more concentrated in a fraction enriched in cardiac gap junctions than in whole sarcolemmal preparations. Finally, an 18-kDa protein was recognized by several different antibodies specific for bFGF on Western blots of heart subcellular fractions enriched in gap junctions. We suggest that bFGF-like peptides are either an integral part of, or exist in close association with, cardiac gap junctions and thus may play a role in modulating gap junctional intercellular communication.

Animals↗
PubMed1992

Neurotransmitters as neurotrophic factors: a new set of functions.

At the start of this review, factors were deemed trophic if they stimulated mitosis, permitted neural cell survival, promoted neurite sprouting and growth cone motility, or turned on a specific neuronal phenotype. The in vitro evidence from cell cultures is overwhelming that both neurotransmitters and neuropeptides can have such actions. Furthermore, the same chemical can exert several of these effects, either on the same or on different cell populations. Perhaps the most striking example is that of VIP, which can stimulate not only mitosis, but also survival and neurite sprouting of sympathetic ganglion neuroblasts (Pincus et al., 1990a,b). The in vivo data to support the in vitro experiments are starting to appear. A role for VIP in neurodevelopment is supported by in vivo studies that show behavioral deficits produced in neonatal rats by treatment with a VIP antagonist (Hill et al., 1991). The work of Shatz' laboratory (Chun et al., 1987; Ghosh et al., 1990) suggests that neuropeptide-containing neurons, transiently present, serve as guideposts for thalamocortical axons coming in to innervate specific cortical areas. Along similar lines, Wolff et al. (1979) demonstrated gamma-aminobutyric acid-accumulating glia in embryonic cortex that appeared to form axoglial synapses and suggested the possibility that gamma-aminobutyric acid released from the glia might play a role in synaptogenesis by increasing the number of postsynaptic thickenings. Meshul et al. (1987) have provided evidence that astrocytes can regulate synaptic density in the developing cerebellum. The work of Zagon and McLaughlin (1986a,b, 1987) has shown that naltrexone, an antagonist of the endogenous opioid peptides, affects both cell number and neuronal sprouting. Lauder's laboratory (Lauder et al., 1982) has shown a role for 5-HT in regulation of the proliferation of numerous cell types. These studies illustrate another important point, that neurotransmitters and neuropeptides function in communication not only between neurons, but also between neurons and glial cells, and between glial cells. Given that astrocytes can express virtually all of the neural receptors and can produce at least some of the neurotransmitters and neuropeptides, they must now be considered equal partners in the processes of intercellular communication in the nervous system, including the trophic responses. The actions of neurotransmitters and neuropeptides have to be considered in terms of a broad spectrum of actions that range from the trophic actions described in this review, to the classic transmitter actions, to potential roles in neurotoxicity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

Feedback control of intercellular signalling in development.

The intercellular communication that regulates cell fate during animal development must be precisely controlled to avoid dangerous errors. How is this achieved? Recent work has highlighted the importance of positive and negative feedback loops in the dynamic regulation of developmental signalling. These feedback interactions can impart precision, robustness and versatility to intercellular signals. Feedback failure can cause disease.

Animals↗
PubMed1999

Compartmentalization of signaling in neurons: evolution and deployment.

The localization of signal transduction machinery at synapses is a fundamental organizational feature of the nervous system that allows for highly complex integration of information coding processes. Synaptic communication evolved as multicellular organisms became more complex, and as selection pressures were placed on such organisms such that those capable of responding rapidly and specifically to environmental demands survived. Two obvious advantages of synaptic transmission (as opposed to endocrine or paracrine signaling) are that it provides for rapid intercellular communication over great distances and that it provides a high level of spatial specificity. There are several structural and functional aspects of synapses that set them apart from other cellular compartments, with many of the specializations subserving roles in synaptic signal transduction (e.g., neurotransmitter release from the presynaptic terminal and postsynaptic receptor activation and second messenger production). However, studies of developing nervous systems have shown that many synaptic signaling mechanisms are operative prior to synaptogenesis and play important roles in regulating growth cone behaviors, synaptogenesis, and even programmed cell death. Indeed, the concept that "ontogeny recapitulates phylogeny" can be effectively applied to the evolution of the synapse. As the embryo rapidly grows, neurons must elaborate axons and dendrites, establish functional synaptic connections, and maintain and adjust those connections as the organism matures. The purpose of this introductory article is to set the stage for the following articles by briefly reviewing fundamental aspects of the molecular and cellular biology of synapses in an evolutionary context.

Animals↗
PubMed2005

Lessons learned about slow discontinuous conduction from models of impulse propagation.

Propagation of excitation in the heart involves action potential generation by cardiac cells and its propagation in the multicellular tissue. Action potential conduction is the outcome of complex interactions between cellular processes (membrane ion channels and transporters), electrical communication between cells, and the macroscopic architecture of cardiac tissue. This high level of complexity and non linearity requires computer modeling in order to elucidate mechanisms and explain experimentally observed behaviors. This article reviews studies that we have conducted in 1-dimensional models that contain both, cellular ionic processes and intercellular communication through gap junctions. We have defined and computed a quantitative measure of the robustness of conduction, the safety factor, as a function of gap junction coupling and showed that reduced coupling can support very slow and very safe conduction. Such conduction is highly discontinuous and is supported by the L-type calcium current. We also show that gap junction coupling and the associated load has a strong effect on spatial repolarization gradients in cardiac tissue.

Action Potentials↗
PubMed2003

Regulated portals of entry into the cell.

The plasma membrane is the interface between cells and their harsh environment. Uptake of nutrients and all communication among cells and between cells and their environment occurs through this interface. 'Endocytosis' encompasses several diverse mechanisms by which cells internalize macromolecules and particles into transport vesicles derived from the plasma membrane. It controls entry into the cell and has a crucial role in development, the immune response, neurotransmission, intercellular communication, signal transduction, and cellular and organismal homeostasis. As the complexity of molecular interactions governing endocytosis are revealed, it has become increasingly clear that it is tightly coordinated and coupled with overall cell physiology and thus, must be viewed in a broader context than simple vesicular trafficking.

Actins↗
PubMed1998

Gap junctional communication modulates gene expression in osteoblastic cells.

Bone-forming cells are organized in a multicellular network interconnected by gap junctions. In these cells, gap junctions are formed by connexin43 (Cx43) and connexin45 (Cx45). Cx43 gap junctions form pores that are more permeable to negatively charged dyes such as Lucifer yellow and calcein than are Cx45 pores. We studied whether altering gap junctional communication by manipulating the relative expression of Cx43 and Cx45 affects the osteoblast phenotype. Transfection of Cx45 in cells that express primarily Cx43 (ROS 17/2.8 and MC3T3-E1) decreased both dye transfer and expression of osteocalcin (OC) and bone sialoprotein (BSP), genes pivotal to bone matrix formation and calcification. Conversely, transfection of Cx43 into cells that express predominantly Cx45 (UMR 106-01) increased both cell coupling and expression of OC and BSP. Transient cotransfection of promoter-luciferase constructs and connexin expression vectors demonstrated that OC and BSP gene transcription was down-regulated by Cx45 cotransfection in ROS 17/2. 8 and MC3T3-E1 cells, in association with a decrease in dye coupling. Conversely, cotransfection of Cx43 in UMR 106-01 cells up-regulated OC and BSP gene transcription. Activity of other less specific osteoblast promoters, such as osteopontin and osteonectin, was less sensitive to changes in gap junctional communication. Thus, altering gap junctional permeability by manipulating the expression of Cx43 and Cx45 in osteoblastic cells alters transcriptional activity of osteoblast-specific promoters, presumably via modulation of signals that can diffuse from cell to cell. A communicating intercellular network is required for the full elaboration of a differentiated osteoblastic phenotype.

Animals↗
PubMed2005

Effects of Gingko biloba extract on gap junction changes induced by reperfusion/reoxygenation after ischemia/hypoxia in rat brain.

Gap junction communication between astrocytes plays an important role in the brain. The purpose of this study was to investigate the effects of Gingko biloba extract (GBE) on the changes of connexin 43 (Cx43) mRNA and protein expression levels of rat cortex and hippocampus induced by ischemia-reperfusion and astrocyte gap junction intercellular communication (GJIC) induced by hypoxia-reoxygenation. After 2 hours of middle cerebral artery occlusion (MCAO) followed by 24 hours of reperfusion, there was obvious neurological deficit in rats. Cx43 mRNA and protein expression levels of rat cortex and hippocampus in the ischemia hemisphere were decreased significantly. When GBE at doses of 50 and 100 mg/kg body weight was administrated by p.o. daily for 7 days, the neurological deficit was improved, and lower Cx43 mRNA and protein expression levels induced by ischemia-reperfusion were recovered to normal. The i.p. injection of nimodipine (0.7 mg/kg weight body) also showed improvement on neurological deficit and Cx43 expression levels. Astrocyte GJIC was measured by the fluorescence recovery after photobleaching (FRAP). Hypoxia-reoxygenation induced a significant decrease in GJIC. Pretreatment with GBE (100 mg/l) and nimodipine (1.6 mg/l) significantly prevented the hypoxia-reoxygenation inhibition of GJIC. These results suggest that GBE could exert its neuroprotective effects by improvement of Cx43 expression and GJIC induced by hypoxia/ischemia-reoxygenation/ reperfusion injury.

Animals↗
PubMed1991

Gap junction distribution in adult mammalian myocardium revealed by an anti-peptide antibody and laser scanning confocal microscopy.

A polyclonal antiserum, raised against a synthetic peptide matching part of the sequence of connexin43 (a rat cardiac gap-junctional protein), was used in combination with laser scanning confocal microscopy to investigate gap junction distribution in cardiac tissues from a range of mammalian species. Comparison of the localised punctate staining patterns obtained in ventricular tissue with the distribution of intercalated disks as viewed by conventional light microscopy and electron microscopy, and with the staining observed by standard light-microscope immunofluorescence using the same anti-serum, demonstrated highly specific labelling of clearly resolved individual gap junctions. Laser scanning confocal microscopy of ventricular myocardium showed the immunostained gap junctions to be confined to well-defined intercalated disks bisecting the long axis of the muscle fibre, whereas in the atrial myocardium, gap junctions were commonly distributed widely over the lateral surfaces of the myocyte body. Rat atrial gap junctions were significantly larger (as measured by the longest axial lengths of fluorescent spots), and showed a narrower spread of sizes, than their counterparts in the ventricle. Ventricular myocardium from six mammalian species including man gave similar immunostaining patterns, indicating conservation both of the epitope(s) detected by the antiserum, and of the general organisation of the cell-to-cell pathways for electrical propagation, in the mammalian heart. Optical section series obtained by laser scanning confocal microscopy permitted the quantification and mapping of the three-dimensional distribution of gap junctions in ventricular intercalated disks with high clarity over substantial specimen depths. A consistent feature of gap junction organisation within disks of ventricular myocardium in all species studied was the presence of a conspicuous ring of large gap junctions around the periphery of the disk. Immunostained gap junctions lying within the interior zone delineated by the peripheral junctions generally occurred at lower numerical densities and were significantly smaller. In all species, less than 3% of all immunolabelled gap junctions measured were greater than 2 microns in maximal length, though a small proportion (0.06%) exceeded 4 microns. The numerical density of immunolabelled gap junctions in the disk was similar between species; however, within species there was a significant decrease in numerical density with increasing disk size. The new features of intercalated disk structure revealed in this study may have an important part to play in the intercellular communication and electrical propagation properties of the mammalian heart.

Analysis of Variance↗
PubMed1983

Are messenger molecules in microbes the ancestors of the vertebrate hormones and tissue factors?

Peptides very similar to hormones and other messenger molecules of vertebrates have been detected in extracts of unicellular eukaryotes (and prokaryotes). We present arguments to suggest the possibility that these molecules 1) originated evolutionarily in unicellular microbes, 2) serve as intercellular messenger molecules in these organisms, and 3) represent the phylogenetic ancestors of the hormones and neurotransmitters as well as paracrine and other tissue factors of the vertebrates. We suggest that the biochemical elements of intercellular communication arose very early in evolution and are highly conserved; evolution largely changed the anatomy, i.e., the nature of the secretory cell, the target cell, and the fluid compartment that carries the messenger molecule from one to the other. Such an approach suggests a more rational relationship between different modes of intercellular chemical signaling in vertebrates.

Animals↗
PubMed1997

ADP-ribose. A historical overview.

ADP-ribosylation of proteins was first detected as a modification of nuclear proteins by polymeric ADP-ribose residues derived from NAD+. Subsequently, the field developed into three destinct sections: (i) Possible function(s) of poly-ADP-ribosylation with increasing evidence for participation in DNA excision repair and perhaps in DNA recombination; (ii) Mono-ADP-ribosylation as a mechanism to inactivate (by some toxins) or to regulate enzymes/proteins (e.g. in bacterial nitrogen fixation, in protein traffic through membranes, in intercellular communication); (iii) Intramolecular ADP-ribosylation converting NAD+ to cyclic ADP-ribose, a possible Ca(2+)-mobilizing agonist. Thus, NAD+ first known as a cofactor of oxidoreductases has experienced an impressive metamorphosis from a housekeeping coenzyme to a multifunctional group transfering metabolite involved in an increasing number of intracellular and intercellular regulatory loops.

Adenosine Diphosphate Ribose↗
PubMed2002

[Abnormal shift of connexin 43 gap-junction protein induced by 50 Hz electromagnetic fields in Chinese hamster lung cells].

OBJECTIVE: To study the effects of extremely low frequency magnetic fields(ELF MF) on the amount and localization of connexin 43(Cx43) gap-junction protein in the Chinese hamster lung(CHL) cells, and to explore the mechanism of ELF MF suppression on gap-junctional intercellular communication(GJIC). METHODS: The cells were irradiated for 24 h with 50 Hz sinusoidal magnetic field at 0.8 mT without or with 12-O-tetrade-canoylphorbol-3-acetate(TPA), 5 ng/ml for 1 h. The localization of Cx43 proteins were performed by indirect immunofluorescence histochemical analysis and detected by confocal microscopy. The second experiment was conducted to examine the quantity of Cx43 proteins level in nuclei or cytoplasm and detected by Western blotting analysis. RESULTS: The cells exposed to TPA for 1 h displayed less bright labelled spots in the regions of intercellular junction than the normal cells. Most of Cx43 labelled spots occurred in the cytoplasm and aggregated near the nuclei. At the same time, the amount of Cx43 protein in cytoplasm were increased[(2.03 +/- 0.89) in ELF group, (2.43 +/- 0.82) in TPA group] as compared to normal control(1.04 +/- 0.17) (P < 0.01). CONCLUSION: Inhibition on GJIC function by ELF MF alone or combined with TPA may be related with the shift of Cx43 from the regions of intercellular junction to the cytoplasm.

Animals↗