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PubMedDate not supplied

Pretreatment with the gap junction uncoupler heptanol does not limit infarct size in rabbit heart.

Previous findings indicate that heptanol, an agent well-recognized to disrupt chemical signaling between myocytes by uncoupling of gap junctions, significantly limited infarct size when administered at the time of reperfusion. Our aim was to assess on the potential role of cell--cell communication via gap junctions during ischemia by investigating whether "loading" the soon-to-be ischemic territory with heptanol would limit myocardial necrosis. Five isolated buffer-perfused rabbit hearts were pretreated with heptanol (0.5 mM) for 10 min, while 12 served as controls. In the final 30 s of treatment, a large marginal branch of the left circumflex coronary artery was occluded for 30 min followed by 2 h of reperfusion, and infarct size was delineated by tetrazolium staining. Heptanol had no significant effect on the extent of infarct: area of necrosis (AN, expressed as a percentage of the myocardium at risk) was 75+/-3% and 72+/-8% in vehicle- and heptanol-treated groups (P=.76). Thus, our results suggest that cell-to-cell communication via gap junctions during coronary artery occlusion does not contribute importantly to the development of necrosis in rabbit heart.

Animals↗
PubMed2001

Effect of the factor inhibiting germinal vesicle breakdown on the disruption of gap junctions and cumulus expansion of pig cumulus-oocyte complexes cultured in vitro.

The present study was undertaken to explore the regulatory mechanisms for meiotic resumption of pig cumulus-oocyte complexes (COCs) by assessing the nuclear status of oocytes, the degree of gap junction cell-to-cell communication and cumulus expansion after culture of various numbers of COCs in 10 microl droplets of medium for 24 h. Gap junction communication was examined by confocal laser scanning microscopy after injection of a fluorescent dye, lucifer yellow, into the oocytes. When one, three or six COCs were cultured in a 10 microl droplet, germinal vesicle breakdown was observed in > 70% of oocytes; increasing the number of COCs in a droplet further actually decreased the proportion of oocytes undergoing germinal vesicle breakdown (10 COCs: 49%; 20 COCs: 21%; 40 COCs: 13%). When six COCs were cultured in a 10 microl droplet of conditioned medium (prepared previously by culturing 20 intact and oocytectomized COCs for 24 h), the proportion of oocytes undergoing germinal vesicle breakdown was significantly reduced compared with the proportion in fresh medium. An increase in the proportion of category 1 COCs (all gap junctions within cumulus cells and between cumulus cells and oocyte are functionally maintained) was achieved by increasing the number of COCs cultured in a 10 microl droplet. The addition of conditioned medium to the fresh medium at a concentration of 50% significantly inhibited cumulus expansion. From these results, it is concluded that the factors secreted by cumulus cells regulate the disruption of gap junctions and cumulus expansion, and concurrently control the incidence of germinal vesicle breakdown in pig COCs.

Animals↗
PubMed2003

Tumor necrosis factor alpha in the bovine oviduct during the estrous cycle: messenger RNA expression and effect on secretion of prostaglandins, endothelin-1, and angiotensin II.

Tumor necrosis factor (TNF) alpha is an important physiological mediator of cell-to-cell communication. Recent observations suggest that TNFalpha is involved in the control of reproductive functions. The present study examined the role of TNFalpha in the secretion of factors involved in regulating smooth muscle contraction, such as prostaglandin E2 (PGE2), prostaglandin F2alpha (PGF2alpha), endothelin-1 (ET-1), and angiotensin II (Ang II), as it was in the original by the cow oviduct at different stages of the estrous cycle using an in vitro microdialysis system. Expression of mRNA for TNFalpha and its receptors (TNFalpha-R) was also evaluated. For microdialysis, the lumen of a portion (length, 10 cm) of the each oviductal segment was implanted with a dialysis capillary membrane, and TNFalpha (100 ng/ml) was infused for 4-8 h during a 16-h incubation period. The microdialysis system maintains cell-to-cell integrity and cell-to-cell communication, and it enables real-time observation of physiological changes in the luminal release of different substances. Concentrations of PG, ET-1, and Ang II in 4-h fractions were measured using second-antibody enzyme immunoassays. Infusion of TNFalpha stimulated oviductal secretion of PG, ET-1, and Ang II during the follicular and postovulatory stages, but not during the luteal stage. Expression of TNFalpha, TNFalpha-R type I, and TNFalpha-R type II mRNA was detected in the bovine oviduct by reverse transcription-polymerase chain reaction. High expression of both TNFalphaR types and ligands was detected during the follicular and postovulatory stages, whereas low expression was detected during the luteal stage. The results of the present study provide, to our knowledge, the first direct evidence that TNFalpha stimulates PG, ET-1, and Ang II secretion and that up-regulation of the TNFalpha system occurs in the cow oviduct during the periovulatory period. In conclusion, the TNFalpha system may optimize the release of contraction-related substances and modulate local contraction to regulate the oviductal transport of the gametes and embryo.

Angiotensin II↗
PubMed2005

Transcriptional profiling reveals evidence for signaling and oligodendroglial abnormalities in the temporal cortex from patients with major depressive disorder.

Major depressive disorder is one of the most common and devastating psychiatric disorders. To identify candidate mechanisms for major depressive disorder, we compared gene expression in the temporal cortex from 12 patients with major depressive disorder and 14 matched controls using Affymetrix HgU95A microarrays. Significant expression changes were revealed in families of genes involved in neurodevelopment, signal transduction and cell communication. Among these, the expression of 17 genes related to oligodendrocyte function was significantly (P < 0.05, fold change > 1.4) decreased in patients with major depressive disorder. Eight of these 17 genes encode structural components of myelin (CNP, MAG, MAL, MOG, MOBP, PMP22, PLLP, PLP1). Five other genes encode enzymes involved in the synthesis of myelin constituents (ASPA, UGT8), or are essential in regulation of myelin formation (ENPP2, EDG2, TF, KLK6). One gene, that is, SOX10, encodes a transcription factor regulating other myelination-related genes. OLIG2 is a transcription factor present exclusively in oligodendrocytes and oligodendrocyte precursors. Another gene, ERBB3, is involved in oligodendrocyte differentiation. In addition to myelination-related genes, there were significant changes in multiple genes involved in axonal growth/synaptic function. These findings suggest that major depressive disorder may be associated with changes in cell communication and signal transduction mechanisms that contribute to abnormalities in oligodendroglia and synaptic function. Taken together with other studies, these findings indicate that major depressive disorder may share common oligodendroglial abnormalities with schizophrenia and bipolar disorder.

Adult↗
PubMed1988

Cluster formation in PHA-stimulated mononuclear cells from peripheral blood: effects of colcemid and taxol.

Mononuclear cells from peripheral blood were incubated with phytohemagglutinin (PHA) for 24-72 hours. The cells formed dense cell clusters with firm cell-to-cell attachment and signs of cell communication, proliferation and differentiation. At the end of a 72-hour period of incubation, the test preparations were treated for 90 minutes with the classical microtubule antagonist Colcemid and the new microtubule antagonist taxol. Taxol produced approximately twice as many mitoses as Colcemid. Chromosomes in taxol-blocked mitoses appeared to be more contracted than chromosomes in Colcemid-blocked mitoses. It is suggested that one beneficial side effect of Colcemid preparation of chromosomes is stretching due to microtubule disassembly.

Alkaloids↗
PubMed1996

[Gap junctions in the thyroid gland: distribution, regulation, function].

As in most organized tissues, cells of the thyroid gland, thyrocytes, are connected by various types of intercellular junctions, among which gap junctions. Gap junctions are composed of channels that allow the direct cell-to-cell exchange of small cytoplasmic molecules (Mr < 1000). Proteins forming gap junction channels are the connexins (Cx). Thyrocytes coexpress two Cx: Cx32 and Cx43 that form distinct channels localized in different regions of the lateral plasma membrane domain; gap junctions formed of Cx43 are localized in tight junctions. The tissue-specific hormone, TSH, increases the synthesis of these two Cx and induces the opening of gap junction channels. Gap junction-mediated cell-to-cell communication is likely involved in the control of thyroid cell proliferation since the reinduction of cell-to-cell coupling in communication-deficient thyroid cell lines, by stable transfection of the Cx32 cDNA, induces a decrease of the proliferation rate of these cells.

Animals↗
PubMed1998

Intercellular protein trafficking through plasmodesmata.

During plant morphogenesis, groups of cells differentiate to form specialized tissues possessing distinct structures and functions. Cell specialization is a result of specific gene expression at the individual cell level. Coordination of differential gene expression among cells requires that cells communicate with one another. Plasmodesmata provide a cytoplasmic pathway for direct intercellular communication. Recent discoveries that macromolecules such as transcription factors, viral proteins, and plant defense-related proteins can traffic through plasmodesmata suggest that intercellular protein trafficking is potentially an important means to regulate plant developmental processes, physiological functions, plant-pathogen interactions, and plant defense reactions. Thus, elucidating the specific functions and mechanisms of intercellular protein trafficking has broad implications in understanding how a plant develops and functions at the molecular level. This review is to provide an update on this rapidly developing area of plant biology, with emphasis on the discussion of possible mechanisms underlying intercellular protein trafficking.

Biological Transport↗
PubMed2002

A conserved mechanism for extracellular signaling in eukaryotes and prokaryotes.

Epidermal growth factor receptor (EGFr) is a key mediator of cell communication during animal development and homeostasis. In Drosophila, the signaling event is commonly regulated by the polytopic membrane protein Rhomboid (RHO), which mediates the proteolytic activation of EGFr ligands, allowing the secretion of the active signal. Until very recently, the biochemical function of RHO had remained elusive. It is now believed that Drosophila RHO is the founder member of a previously undescribed family of serine proteases, and that it could be directly responsible for the unusual, intramembranous cleavage of EGFr ligands. Here we show that the function of RHO is conserved in Gram-negative bacteria. AarA, a Providencia stuartii RHO-related protein, is active in Drosophila on the fly EGFr ligands. Vice versa, Drosophila RHO-1 can effectively rescue the bacterium's ability to produce or release the signal that activates density-dependent gene regulation (or quorum sensing). This study provides the first evidence that prokaryotic and eukaryotic RHOs could have a conserved role in cell communication and that their biochemical properties could be more similar than previously anticipated.

Amino Acid Sequence↗
PubMed2001

Intercellular communication in cultured human vascular smooth muscle cells.

Intercellular communication through gap junction channels plays a fundamental role in regulating vascular myocyte tone. We investigated gap junction channel expression and activity in myocytes from the physiologically distinct vasculature of the human internal mammary artery (IMA, conduit vessel) and saphenous vein (SV, capacitance vessel). Northern and Western blots documented the presence of connexin43 (Cx43) in frozen tissues and cultured cells from both vessels. Northern blots also confirmed the presence of Cx40 mRNA in cultured IMA and SV myocytes. Dual whole cell patch-clamp experiments revealed that macroscopic junctional conductance was voltage dependent and characteristic of that observed for Cx43. In the majority of records, in both vessels, single-channel activity was dominated by a main-state conductance of 120 pS, with subconducting events comprising less than 10% of the amplitude histograms. However, some records showed "atypical" unitary events that had a conductance similar to Cx40 (approximately 140-160 pS), but gating behavior like that of Cx43. As such, it is conceivable that the presence and coexpression of Cx40 and Cx43 in IMA and SV myocytes may result in heteromeric channel formation. Nonetheless, in terms of gating, Cx43-like behavior clearly dominates.

Aged↗
PubMed1995

Gap junctions in blood forming tissues.

More than ten research groups have now reported the presence of gap junctions in blood-forming tissue or cultured cells. It is time to accept that these cell-coupling structures are present in this tissue. To find out what they are doing here we need to develop appropriate experimental techniques. This review covers the particular problems of investigating direct cell-cell communication by gap or other junctions in undisturbed haemopoietic tissue. It then describes and assesses the published reports of haemopoietic gap junctions. Recently, in the author's laboratory, three means of increasing the number of gap junctions 50- to 100-fold in mouse marrow have been described, as well as techniques for doing so in culture. There is a complete report of this work here. At present it is quite unclear what function gap junctions serve in blood-formation, perhaps it is some consolation that 30 years after their ultramicroscopic discovery it is also true for all other unexcitable tissues. Possibly the ability to up-regulate their expression in haemopoietic tissue will help us find out what their role is in blood formation.

Animals↗
PubMed2002

Disruption of Gja8 (alpha8 connexin) in mice leads to microphthalmia associated with retardation of lens growth and lens fiber maturation.

The development of the vertebrate lens utilizes a sophisticated cell-cell communication network via gap junction channels, which are made up of at least three connexin isoforms, alpha8 (Cx50), alpha3 (Cx46) and alpha1 (Cx43), and which are encoded by three different genes. In a previous study, we reported that, with a disruption of Gja3 (alpha3 connexin), mice developed nuclear cataracts with a normal sized lens. We show that Gja8tm1 (alpha8-/-) mice develop microphthalmia with small lenses and nuclear cataracts, while the alpha8 heterozygous (+/-) mice have relatively normal eyes and lenses. A comparative study of these alpha3 and alpha8 knockout mice showed that the protein levels of both alpha3 and alpha8 were independently regulated and there was no compensation for either the alpha3 or alpha8 protein from the wild-type allele when the other allele was disrupted. More interestingly, western blotting data indicated that the presence of alpha8 in the lens nucleus is dependent on alpha3 connexin, but not vice versa. The staining of the knock-in lacZ reporter gene showed the promoter activity of alpha8 connexin is much higher than that of alpha3 connexin in embryonic lenses and in adult lens epithelium. More importantly, a delayed denucleation process was observed in the interior fibers of the alpha8-/- lenses. Therefore, alpha8 connexin is required for proper fiber cell maturation and control of lens size.

Animals↗
PubMed1999

Aortic connexin43 is decreased during hypertension induced by inhibition of nitric oxide synthase.

Connexin43 (Cx43), the predominant gap junction protein in vessels and heart, is involved in the control of cell-to-cell communication and is thought to modulate the contractility of the vascular wall and the electrical coupling of cardiac myocytes. We have investigated the effects of arterial hypertension induced by inhibition of nitric oxide synthase on the expression of Cx43 in aorta and heart as well as on the distensibility of the carotid artery. Administration of 0.4 g/L NG-nitro-L-arginine methyl ester (L-NAME) to rats in their drinking water for 4 weeks increased intra-arterial mean blood pressure, wall thickness of aorta and carotid artery (25%), and heart weight (17%). Analysis of heart mRNA demonstrated increased expression of the fetal skeletal alpha-actin and of atrial natriuretic peptide but not of Cx43. In contrast, Cx43 mRNA and protein were decreased by 50% in the aortas of L-NAME-treated rats that did not show increased carotid distensibility. Because these data contrasted with those obtained in the 2-kidney, 1 clip model of rat hypertension, which is characterized by increased arterial distensibility and Cx43 expression in aorta, we investigated by Western blot analysis the posttranslational modifications of Cx43. We found that Cx43 was more phosphorylated in the aorta of 2-kidney, 1 clip rats than in that of L-NAME or control rats, which indicated a differential regulation of Cx43 in different models of hypertension. The data suggest that the cell-to-cell communication mediated by Cx43 channels may help regulate the elasticity of the vascular wall.

Animals↗
PubMed1993

Osteocytes, strain detection, bone modeling and remodeling.

One of the characteristic features of mammalian and avian bone is a population of live cells of the osteoblast lineage distributed both on the surface and throughout the matrix. These cells communicate with one another via gap junctions. A number of roles have been proposed for both osteocytes and the lacunar/canalicular labyrinth they occupy. These include arrest of fatigue cracks, mineral exchange, osteocytic osteolysis, renewed remodeling activity after release by resorption, stimulation, and guidance of osteoclastic cutting cones involved in mineral exchange and the repair of microdamage, strain detection, and the control of mechanically related bone modeling/remodeling. The question of whether osteocytes control or influence modeling and remodeling is of major importance. Such influence could be crucial in relation to three importance consequences of remodeling activity: calcium regulation, microdamage repair, and mechanically adaptive control of bone architecture. Mechanically adaptive control of bone architecture requires feedback concerning the relationship between current loading and existing architecture. This feedback is most probably derived from the strain in the matrix. The arrangement of the osteocyte network seems ideally suited to both perceive strain throughout the matrix and to influence adaptive modeling and remodeling in a strain-related manner. The hypothesis that osteocytes perform this role has growing experimental support.

Animals↗
PubMed2003

Ligand-receptor pairs in plant peptide signaling.

Extensive studies on plant signaling molecules over the past decade indicate that plant cell-to-cell communication, as is the case with animal systems, makes use of small peptide signals and specific receptors. To date, four peptide-ligand-receptor pairs have been identified and shown to be involved in a variety of processes. Systemin and phytosulfokine (PSK), the first and second signaling peptides identified in plants, were isolated by biochemical purification based on their biological activities. Furthermore, their receptors have been biochemically purified from plasma membranes on the basis of specific ligand-receptor interactions. By contrast, the two other peptide signals, CLAVATA3 (CLV3) and the pollen S determinant SCR/SP11, were genetically identified during searches for specific ligands for receptors that had already been cloned. Systemin functions in the plant wound response, whereas PSK appears to cooperate with auxin and cytokinin to regulate cellular dedifferentiation and redifferentiation. CLV3 is important for meristem organization, binding to a heterodimeric receptor comprising the CLV1 and CLV2 proteins. SCR/SP11 instead plays a role in self-incompatibility, where it activates a signalling cascade that leads to rejection of pollen with the same S haplotype. These ligands all seem to bind to receptors that possess intrinsic kinase activity, and al least two of them are generated by proteolytic processing of larger precursor proteins.

Amino Acid Sequence↗
PubMed1994

Expression of cell adhesion molecules and connexins in gap junctional intercellular communication deficient human mesothelioma tumour cell lines and communication competent primary mesothelial cells.

Gap junctional intercellular communication (GJIC) has been reported to be markedly reduced in human mesothelioma tumour cell lines compared with primary mesothelial cells. Immunofluorescence stainings have shown that the gap junction protein connexin43 (Cx43) is expressed in both malignant and normal mesothelial cells. In this study the mRNA expression of Cx43 and three different connexins--Cx37, Cx40 and Cx45, which are highly expressed in lung tissue--was investigated in eight human mesothelioma cell lines, and in human primary mesothelial cells from several donors. The expression of the intercellular adhesion molecules A-CAM (N-cadherin) and L-CAM (E-cadherin) was studied at the protein level. No mRNA expression of Cx37, Cx40 or Cx45 in either mesothelioma tumour cells or the primary mesothelial cells was detected. Cx43 was expressed at both the mRNA and the protein level, in seven out of eight mesothelioma cell lines, as well as in all the primary mesothelial cell cultures. The well as in all the primary mesothelial cell cultures. The intercellular adhesion molecule A-CAM was expressed at the cell-cell borders in six out of seven mesothelioma cell lines, as well as in normal mesothelial cells. No expression of L-CAM was observed in these cells. The results suggest that Cx43 and A-CAM are the major proteins in gap and adherens junctions respectively in human mesothelial cells. Most mesothelioma tumour cell lines with markedly reduced GJIC still express both Cx43 and A-CAM. Only one of our mesothelioma tumour cell lines severely deficient in GJIC lacks both the gap junction protein Cx43 and the cell adhesion molecule A-CAM.

Cell Adhesion Molecules↗
PubMed1998

Signaling complexes: biophysical constraints on intracellular communication.

This review surveys the kinds of protein complex that participate in cell communication and identifies, where possible, general principles by which they form and act. It also advances the notion that biophysical constraints imposed by macromolecular crowding and diffusion have had a controlling influence on the evolution of cell signaling pathways. Complexes associated with the bacterial aspartate receptor, with eucaryotic tyrosine kinase receptors, with T-cell receptors, and with focal contacts are examined together with proteins that serve as adaptors, anchors, and scaffolds for signaling complexes. The importance of diffusion in controlling the numbers and locations of signaling complexes is discussed, as is the special role played by membranes in signaling pathways.

Animals↗
PubMed1992

Intercellular communication and cell-cell adhesion.

In developmental biology, binary cell-cell interactions often determine the fate of one or both cell partners. The two cells must adhere to one another to allow chemical signals to be transmitted in one or both directions across the regions of cell-cell contact. The molecular mechanisms of cell-cell adhesion and intercellular communication, even if they are mediated by different cell surface components, may be functionally integrated in several different ways. Studies of helper T cells with antigen-presenting B cells in culture have illuminated such binary interactions. The possible application of similar mechanisms to other binary developmental systems is briefly explored.

Animals↗
PubMed2005

Adhesion, migration and communication in melanocytes and melanoma.

Under normal conditions, homeostasis determines whether a cell remains quiescent, proliferates, differentiates, or undergoes apoptosis. In this state of homeostasis, keratinocytes control melanocyte growth and behaviour through a complex system of paracrine growth factors and cell-cell adhesion molecules. Alteration of this delicate homeostatic balance and can lead to altered expression of cell-cell adhesion and cell communication molecules and to the development of melanoma. Melanoma cells escape from this control by keratinocytes through three major mechanisms: (1) down-regulation of receptors important for communication with keratinocytes such as E-cadherin, P-cadherin, desmoglein and connexins, which is achieved through growth factors produced by fibroblasts or keratinocytes; (2) up-regulation of receptors and signalling molecules not found on melanocytes but important for melanoma-melanoma and melanoma-fibroblast interactions such as N-cadherin, Mel-CAM, and zonula occludens protein-1 (ZO-1); (3) loss of anchorage to the basement membrane because of an altered expression of the extracellular-matrix binding integrin family. In the current review, we describe the alterations in cell-cell adhesion and communication associated with melanoma development and progression, and discuss how a greater understanding of these processes may aid the future therapy of this disease.

Cadherins↗