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At least 127 records · Page 7Linked to original sources
PubMed1996

Participation of gap-junctional cell communication on the adaptive response in human cells induced by low dose of X-rays.

To investigate the radioadaptive response of normal cells to low-dose radiation, we irradiated human embryonic (HE) cells and HeLa cells with low-dose X-rays and examined the changes in sensitivity to subsequent high-dose X-irradiation using the trypan blue dye-exclusion test. When HE cells were irradiated by 200 cGy, the growth ratio of the living cells 5 days after the irradiation decreased to 37% of that of the cells which received no X-irradiation. When the cells received a conditioning irradiation of 10-20 cGy 4 h before the irradiation of 200 cGy, the relative growth ratios increased significantly to 45-53%, and a peak was reached at a conditioning dose of 13 cGy to the cells. This conditioning effect was not observed in LeLa cells. When the HE cells were suspended in a Ca2+ ion-free medium or TPA added to the medium while receiving the conditioning irradiation of 13 cGy, the effect of the conditioning dose was not observed. This indicates that normal cells show an adaptive response to low-dose radiation and become more radioresistant. These results suggest that gap junctional intercellular communication may play a role in radioadaptive responses in human cells.

Adaptation, Physiological↗
PubMed2003

Further studies on the effect of intracellular angiotensins on heart cell communication: on the role of endogenous angiotensin II.

The influence of intracellular angiotensin I (Ang I) and angiotensin II (Ang II) on the process of cell communication was investigated in isolated cell pairs from the failing heart of cardiomyopathic hamsters at 2 and at 6 months of age. Measurements of junctional conductance were performed on weekly coupled ventricular cells (4-5.3 nS) using two separated voltage clamp circuits. The results indicated that at 2 months of age, when no signs of heart failure are detected, the angiotensin converting enzyme (ACE) activity is low and similar to controls (0.26 nmol/mg/min). Here the intracellular dialysis of angiotensin I (10(-8) M) caused a decline of junctional conductance of 33+/-3.6% (n=35) (P<0.05) within 10 min while the administration of the same concentration of Ang I elicited cell uncoupling in cell pairs of 6-month-old cardiomyopathic hamsters in which the ACE activity was enhanced (0.41+/-0.05 nmol/mg/min) (P<0.05). Intracellular administration of angiotensin II in cell pairs of 2-month-old hamsters caused a decline of junctional conductance of only 25+/-4.5% (n=35) (P<0.05) compared to cell uncoupling in 6-month-old cardiomyopathic hamsters. Intracellular losartan(10(-8) M) reduced the effect of intracellular Ang II by 68+/-3.5% (n=28) on 2-month-old hamsters and abolished the effect of the peptide on 6-month-old hamsters. To investigate the influence of endogenous angiotensin II on the regulation of cell coupling, enalapril maleate (10(-8) M) or enalaprilat (10(-9) M) was used. The results indicated that at 2 months of age, no change in cell coupling was elicited by the ACE inhibitor while at 6 months of age, there was an increment of cell coupling of 72+/-6.2% (P<0.05). Similar results were found with intracellular losartan (10(-8) M). These results support the view that endogenous angiotensin II is involved in the regulation of cell communication at an advanced stage of heart failure when the ACE activity is enhanced and the cardiac renin angiotensin system (RAS) is activated.

Angiotensin II↗
PubMed2004

Drosophila genetic variants that change cell size and rate of proliferation affect cell communication and hence patterning.

We explore in this paper the role of genetic variants that affect cell size and proliferation in the determination of organ size. We use genetic mosaics of loss or gain of function in six different loci, which promotes smaller or larger than normal cells, associated to either smaller or larger than normal territories. These variants have autonomous effects on patterning and growth in mutant territories. However, there is no correlation between cell size or rate of proliferation on the size of the mutant territory. In addition, these mosaics show non-autonomous effects on surrounding wildtype cells, consisting always in a reduction in number of non-mutant cells. In all mutant conditions the final size (and shape) of the wing is different than normal. The phenotypes of the same variants include higher density of chaetae in the notum. These autonomous and non-autonomous effects suggest that the control of size in the wing is the result of local cell communication defining canonic distances between cells in a positional-values landscape.

Animals↗
PubMed1980

Structure of the junction between communicating cells.

An 18-A resolution map of the 'gap junction' has been obtained by electron microscopy. The protein oligomer in the junctional membranes, the 'connexon', is a cyclinder composed of six subunits which are titled around its axis. Analysis of two different subunit configurations suggests how the connexon might regulate the passage of small molecules between cell interiors.

Animals↗
PubMedDate not supplied

Correction of cell-cell communication defect by introduction of a protein kinase into mutant cells.

The cell-to-cell permeability of the junctions of various cultured mammalian cell types depends on the concentration of intracellular cyclic AMP [( cAMP]i). The permeability rises when the cells are supplied with exogenous cyclic AMP or when their cyclic AMP synthesis is stimulated with choleragen or hormones; it falls when [cAMP]i is lowered by application of serum or due to increase in cell density. The rise and fall in permeability take several hours to develop (the rise is protein synthesis-dependent) and they occur concurrently with the rise and fall in the number of intramembrane particles of the gap junctions, which probably embody the cell-to-cell channels. Is this permeability regulation mediated by phosphorylating protein kinase? In many eukaryotes, the cyclic AMP receptor is a protein kinase consisting of a pair of regulatory subunits and a pair of catalytic subunits. The latter dissociate from the holoenzyme as the cyclic AMP binds to the regulatory subunits and, in this dissociated form, catalyse the phosphorylation of the target. The regulatory subunit occurs in two isoenzyme forms, I and II. The catalytic subunit seems invariant; subunits from different isoenzymes can substitute for each other. We show here that a mutant cell lacking the isoenzyme I is deficient in permeable junctions, and that this junctional defect is corrected when the mutant is supplied with exogenous catalytic subunit.

Animals↗
PubMed2005

Artificial cell-cell communication in yeast Saccharomyces cerevisiae using signaling elements from Arabidopsis thaliana.

The construction of synthetic cell-cell communication networks can improve our quantitative understanding of naturally occurring signaling pathways and enhance our capabilities to engineer coordinated cellular behavior in cell populations. Towards accomplishing these goals in eukaryotes, we developed and analyzed two artificial cell-cell communication systems in yeast. We integrated Arabidopsis thaliana signal synthesis and receptor components with yeast endogenous protein phosphorylation elements and new response promoters. In the first system, engineered yeast 'sender' cells synthesize the plant hormone cytokinin, which diffuses into the environment and activates a hybrid exogenous/endogenous phosphorylation signaling pathway in nearby engineered yeast 'receiver' cells. For the second system, the sender network was integrated into the receivers under positive-feedback regulation, resulting in population density-dependent gene expression (that is, quorum sensing). The combined experimental work and mathematical modeling of the systems presented here can benefit various biotechnology applications for yeast and higher level eukaryotes, including fermentation processes, biomaterial fabrication and tissue engineering.

Alkyl and Aryl Transferases↗
PubMed2004

Hypertension attenuates cell-to-cell communication in hamster retractor muscle feed arteries.

This study examined whether hypertension attenuated cell-to-cell communication in skeletal muscle resistance arteries. Briefly, arteries feeding the retractor muscle of normotensive and hypertensive hamsters were cannulated, pressurized, and superfused with a physiological saline solution. Cell-to-cell communication was functionally assessed by application of vasoactive stimuli (via micropipette) to a small portion of a feed artery while diameter at sites distal to the point of agent application was monitored. In keeping with past observations, discrete application of a smooth muscle depolarizing agent (phenylephrine or KCl) elicited a localized vasoconstriction that conducted poorly along feed arteries from normotensive hamsters. In contrast, acetylcholine, an agent known to hyperpolarize endothelial cells, elicited a vasodilation in normotensive feed arteries that conducted with little decay. Whereas smooth muscle depolarizing agents continued to elicit a localized response, conduction of endothelium-dependent vasodilation was attenuated in hypertensive hamsters. This decrease occurred in the absence of changes in vessel reactivity to intravascular pressure or to global application of phenylephrine, U-46619, or acetylcholine. We propose, on the basis of these physiological observations, quantitative mRNA measurements of connexins 37, 40, 43, and 45, and analysis of the literature, that an increase in endothelial-to-endothelial or smooth muscle-to-endothelial coupling resistance is likely responsible for hypertension-induced impairment in vascular communication. We hypothesize that this attenuation could contribute to the rise in total peripheral resistance characteristically observed in hypertension.

Animals↗
PubMed1976

Studies on cell communication with enucleated human fibroblasts.

Metabolic cooperation, the correction of the mutant phenotype in cells deficient in hypoxanthine phosphoribosyltransferase (HPRT-) by intimate contact with normal cells (HPRT+), represents a form of cell communication that is easily studied with radioautography. In the present study it was found that the formation of cell junctions needed for communication does not require protein synthesis nor is it under the immediate control of the cell nucleus. Enucleated normal cells efficiently communicate with HPRT- mutant cells. The effectiveness of enucleated cells as donors in metabolic cooperation provides evidence that it is the transfer of small molecules, nucleotide, or nucleotide derivatives that is responsible for correction of the mutant phenotype. Karyoplasts (nuclei with small amounts of cytoplasm surrounded by a plasma membrane) are unable to efficiently communicate with intact cells. The utilization of [3H]hypoxanthine by communicating mixtures of HPRT+ and HPRT- human cells is not significantly different than in the normal cells alone. Metabolic cooperation, as studied involves a redistribution of purine-containing compounds among communicating cells.

Adenine↗
PubMed1985

Modes of cell:cell communication in the immune system.

Different cell types in the immune system appear to mediate their effects by markedly different means. B lymphocytes couple information for specificity with information for function in a single long-range molecule, antibody. Major histocompatibility complex (MHC)-restricted T cells, which we have analyzed in detail, appear to recognize antigen only on the surface of cells bearing the appropriate MHC gene product. This interaction provokes the T cell to release short-range, non-antigen-specific mediators (lymphokines) that preferentially act on the target cell bearing the antigen and stimulating the T cell. Regulatory T cells appear to make antigen-specific long-range molecules that, like antibody, combine specificity with information for function. However, unlike antibody molecules, these regulatory T cell products display recognition for particular target cells in the form of genetic restrictions. These behaviors are compared to strategies of cell:cell communication in the nervous system.

Animals↗
PubMed2002

Regulation of cell-to-cell communication in non-tumorigenic and malignant human prostate epithelial cells.

BACKGROUND: Gap-junction-mediated intercellular communication (GJIC) is required for normal development and tissue homeostasis. However, the role of GJIC in human prostate carcinogenesis and progression remains ill-defined. METHODS: The ability of hormones, anti-hormones, and the anti-hypertensive drug, forskolin, to restore GJIC in non-tumorigenic (RWPE-1 and PWR-1E) and malignant (RWPE-2, LNCaP, DU-145) human prostate epithelial cell lines, was examined by Scrape-Loading/Dye Transfer (SL/DT) and Fluorescence Recovery After Photobleaching (FRAP) methods using an Ultima laser cytometer. RESULTS: Results from both assays show that PWR-1E, RWPE-2, LNCaP, and DU-145 cells have weak or absent GJIC activity. However, the non-tumorigenic RWPE-1 cells showed restoration of some GJIC (nearly 10%) after 1 hr in the FRAP assay. Forskolin and estrone, which increase intracellular cAMP levels, induced a significant and consistent increase (2.8- and 4.4-fold, respectively) in cell-to-cell communication only in the non-tumorigenic RWPE-1 cells. Furthermore, estrone induced a two-fold increase in connexin 43 (Cx43) and a 30% decrease in Cx32 expression, while forskolin caused a 50% reduction in Cx32 with no effect on Cx43 expression in RWPE-1 cells. CONCLUSIONS: These data suggest that agents that increase Cx43:Cx32 ratio may be used to restore GJIC in junctionally-deficient, non-tumorigenic immortalized cells, thus providing insights into potential mechanisms responsible for the multistep carcinogenesis in the human prostate.

Cell Communication↗
PubMed2002

Mast cells induce upregulation of P-selectin and intercellular adhesion molecule 1 on carotid endothelial cells in a new in vitro model of mast cell to endothelial cell communication.

It is suggested that mast cells contribute to cell recruitment in inflammation through the upregulation of endothelial adhesion molecules. P-selectin and intercellular adhesion molecule(ICAM)-1 are two key adhesion molecules that have been associated indirectly with mast cell activity. The canine C2 mastocytoma cell line and primary cultures of canine carotid endothelial cells were used to establish a new in vitro model to help study the interaction between mast cells and endothelial cells. Carotid endothelial cells were incubated with mast cell mediators to uncover their effect on endothelial ICAM-1 and P-selectin expression. To assess the relative contributions of tumour necrosis factor (TNF)-alpha and histamine to such effect, an H1 antihistamine and a TNF-alpha blocking antibody were used. Prior to activation by mast cell mediators, P-selectin was expressed only within the cytoplasm, and ICAM-1 was constitutively expressed on the surface of the canine carotid endothelial cells. Both adhesion molecules were enhanced significantly and strongly upon mast cell activation at various time points. Unstored TNF-alpha was fully responsible for ICAM-1 upregulation. P-selectin was up-regulated by both preformed and newly synthesized mast cell mediators, but neither histamine nor TNF-alpha accounted for such an effect. Therefore,a new model is proposed in which the pro-inflammatory effect of mast cells on endothelial cells can be studied in vitro. In this model, it has been demonstrated that only TNF-alpha accounts for the overexpression of ICAM-1 induced by mast cells, and that mast cells up-regulate P-selectin expression through a histamine-independent mechanism.

Animals↗
PubMed2006

Involvement of protein kinases in self-organization of the rhythm of protein synthesis by direct cell-cell communication.

Primary cultures of rat hepatocytes grown on slides were studied in serum-free medium. Ultradian protein synthesis rhythm was used as a marker of synchronization of individual oscillations, resulting in the formation of a common rhythm of the cell population, i.e. cell-cell self-organization. Dense synchronous and sparse non-synchronous cultures were used to estimate effect of protein kinase activity on the kinetics of protein synthesis. Treatment of dense cultures with the inhibitors H7 (40 microM) or H8 (25 microM) resulted in a loss of the protein synthesis rhythm, a suppression of the cell-cell self-organization. Stimulation of protein kinase activity with either 0.5 or 1.0 microM phorbol 12-miristate-13-acetate (PMA) or 10 microM forskolin caused the appearance of the synthetic rhythm in non-synchronous sparse cultures under otherwise normal conditions. Inhibition of protein kinase activity with H7 resulted in signal factors, such as gangliosides and phenylephrine, failing to initiate this rhythm in sparse cultures. Activation of protein kinase activity with PMA shifted the phase pattern of the protein synthesis rhythm. Thus, according to our previous and the new data, protein kinase activity and consequently protein phosphorylation is the crucial step of sequence of processes resulting in synchronization during self-organization of cells in producing a common rhythm in the population. The general pathway can be presented as follows: signaling of gangliosides or other calcium agonists-->efflux of calcium ion from intracellular stores, with elevation of calcium concentration in the cytoplasm-->activation of protein kinases-->protein phosphorylation-->synchronization of individual oscillations in protein synthesis rates-->induction of a common rhythm throughout this population. The data have been discussed concerning similarity of the direct cell-cell communication and the cell self-organization in cultures and in organism.

Animals↗
PubMed1991

Potassium transfer assay for cell communication: effects of phorbol esters, retinoic acid, and furosemide.

Using a mass culture assay for the contact-dependent transfer of potassium among cells with intrinsic differences in ability to concentrate it, we have investigated the ability of several drugs to influence this form of cell communication. We concentrated on 12-O-tetradecanoylphorbol-13-acetate (TPA), which is known to interfere with gap junction-mediated communication and ion transport in several other systems, and compared its effects with those of its inactive derivative, 4-O-methyl-TPA. We found that the communication between mouse BALB/c 3T3 cells and human diploid fibroblasts was reduced in the presence of TPA but not O-methyl-TPA and that this inhibition was not obscured by small but measurable influences of TPA on steady-state content and transport of 86Rb+. We confirmed these findings using an autoradiographic assay for transfer of uridine derivatives among cells in contact. We also showed that retinoic acid had no effect on communication in the ion transfer assay but that furosemide, an inhibitor of Na(+)-K(+)-2Cl- cotransport, stimulated ion transfer dramatically both in the presence and absence of TPA. These results indicate both the promise and the limitations of the potassium transfer assay for identifying potential modulators of gap junction-mediated cell communication.

3T3 Cells↗
PubMed2001

The role of connexin-mediated cell-cell communication in breast cancer metastasis.

Gap junctional intercellular communication (GJIC) is a form of cell-cell communication mediating the exchange of small molecules between neighboring cells. Gap junctions (GJs) are formed by connexins (Cxs), and are subject to tight and dynamic regulation. They are involved in the cell cycle, differentiation, and cell signaling. The loss of Cxs and GJs is a hallmark of carcinogenesis, while their induction in cancer cells leads to a reversal of the cancer phenotype, induction of differentiation, and regulation of cell growth. On the basis of the observations about Cx loss in breast cancer, this review examines Cxs' involvement in breast cancer metastasis. Previous work indicates that Cx expression is inversely correlated to metastatic potential. This is probably because of the loss of cooperation between neighboring cells, leading to cell heterogeneity and cell dissociation in the tumor. The possible involvement of Cx activity during metastasis will be discussed.

Breast Neoplasms↗
PubMed2005

Cell-to-cell communication via plasmodesmata during Arabidopsis embryogenesis.

In Arabidopsis embryogenesis, positional information establishes the overall body plan and lineage-dependent cell fate specifies local patterning. Position-dependent gene expression and responses to the plant hormone auxin are also crucial. Recently, another mechanism that delivers positional information has been uncovered. This pathway utilizes cell-to-cell communication via plasmodesmata. Plasmodesmata span the walls between neighboring plant cells. Groups of cells that allow intercellular transport of biotic and abiotic tracers form symplastic domains of shared communication. Initially, cells of the embryo form one symplast. As development proceeds, symplastic sub-domains that correspond to the major morphological regions of the plant (i.e. shoot apex, cotyledons, hypocotyl, and root) are formed. These sub-domains further resolve into tissue-specific domains of communication (such as protodermal and vascular regions). Cell-to-cell communication via plasmodesmata between embryonic and maternal tissues ceases as development proceeds.

Arabidopsis↗