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At least 667 records · Page 37Linked to original sources
PubMed1987

The transport of reactive intermediates in a co-cultivation system: the role of intercellular communication.

The transport of reactive intermediates through gap junctions was studied in a co-cultivation system consisting of primary chick-embryo liver cells and V79 Chinese hamster cells. The formation of gap junctions was studied by measurement of the incorporation of [3H]hypoxanthine in HGPRT deficient V79 mutant cells after co-cultivation with the hepatocytes. Under control conditions the heterologous gap junctions allowed for the transfer of [3H]hypoxanthine resulting in an average value of 13 grains/cell. Addition of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA), inhibited this transfer in a dose related way to background values. The transfer of reactive intermediates was measured as the number of sister chromatid exchanges (SCEs) induced in the V79 cells. For both compounds tested, benzo[a]pyrene and dimethylnitrosamine, transport of reactive intermediates through gap junctions was observed. When the inhibitory effects of TPA were investigated at different time points after start of the co-cultivation, inhibition was measurable after 6 h and increased to a maximal inhibition of 50%, observed after 24 h. No effect of TPA was observed on the number of SCEs. When the metabolic cooperation deficient V79 mutant cell line MC--27, was used the effects were completely comparable to those of TPA for both compounds. The lower mutagenic effects in the MC--27 cells cannot be attributed to a lower intrinsic sensitivity for mutagens of these cells.

Animals↗
PubMed1984

Relationship between intercellular communication and radiosensitivity of human tumor xenografts.

Micro-electrode techniques permit the detection of electrical coupling between adjacent cells if they are connected by intercellular junctions (gap junctions). This technique was applied to four human tumors xenografted onto nude mice. In three of the tumors, which showed a 'contact resistance' after irradiation in vivo, electrical coupling could be established. No coupling was found in the other tumor, which did not exhibit contact resistance. These results are similar to those obtained recently with cultured spheroids of mammalian cell lines in which only the electrically coupled cell types developed contact resistance to ionizing radiation.

Adenocarcinoma↗
PubMed1989

[Studies on the gap junctional intercellular communication (GJIC) of human stomach carcinoma cells in comparison with normal cells and the effect of the tumor promoter, TPA].

This work was conducted by using a rapid and simple technique, scrape-loading and dye transfer (SLDT) to study GJIC of human stomach carcinoma MGC-803 cells in comparison with normal WB rat liver cells, Chinese hamster V79 cells and a primary culture of chicken embryonic myoblasts. Cells were plated and grown overnight to confluency in 35 mm plastic dishes in appropriate media. Monolayered cells, after rinsing in PBS, were immersed in the mixed 0.05% Lucifer Yellow (MW 457.2) and 0.05% Rhodamine-Dextran (MW. 10,000) in PBS. Scrape loading was performed by utilization of a sharp knife. Cells were incubated in dye solution for an additional 3 min. at room temperature before rinsing with PBS and observation under fluorescent microscope. Cells competent in GJIC showed transfer of Lucifer Yellow from the injured border to interior cells while the high MW. Rhodamine-Dextran dye stayed in situ in the loaded cells. Cells incompetent in GJIC did not show dye transfer; both Lucifer Yellow and Rhodamine-Dtranex were retained in the original loaded cells of the injured border. The background cell monolayer away from the scrape line was dark indicating that none of the dye molecules could permeate through cell membrane in the conditions described. It was found that human stomach carcinoma MGC-803 cells lack GJIC; Chinese hamster V79 cells showed modest GJIC; WB rat liver cells and chick myoblasts showed marked GJIC. The tumor promoter, TPA(1-100 ng/ml), inhibits GJIC of the normal cells efficiently. An inhibitor of calmodulin, Trifluoperazine (TFP) (5-20 microM), evidently increased the GJIC of stomach carcinoma MGC-803 cells. Noteworthy is that TFP in the dosage range used in SLDT experiments showed inhibitory effect on cell growth and DNA synthesis of MGC-803 cells documented in parallel experiments. These results indicate that the lack of GJIC in MGC-803 cells correlates with their uncontrolled cell proliferation; the improvement of GJIC correlates with the inhibition of tumor cell proliferation. TPA inhibition of GJIC in normal cells in this work confirmed previous reports. Interestingly, it was found that when V79 cells were treated with TFP and then shifted to medium containing both TFP and TPA, GJIC was blocked. It is likely that TPA overcomes the effect of TFP on GJIC of MGC-803 cells. These results provide further evidence for the role of GJIC in carcinogenesis, specially the tumor promotion phase.

Adenocarcinoma↗
PubMed1994

The nitric oxide-cyclic GMP signal transduction system for intracellular and intercellular communication.

From our work and that of others, it is now quite apparent that the NO-cGMP system can function as an intracellular or intercellular signal transduction system (Murad et al., 1988, 1990; Murad, 1989a,b; Ishii et al., 1989, 1991). If a specific cell possesses both NO synthase and an isoform of guanylyl cyclase that is activatable with NO, then cGMP levels in that cell can be regulated by agents that alter NO synthase activity and NO formation (Fig. 1). NO, or a complex of NO which is liberated from the producing or donor cell, can also activate guanylyl cyclase in a neighboring or perhaps a distant cell to increase cGMP synthesis. In the latter scenario, NO or its carrier complex behaves as a paracrine substance, autacoid, or hormone. Interestingly, the liberated extracellular NO can also feed back and increase cGMP synthesis in the cell of origin. This is best demonstrated by the inhibitory effects of hemoglobin on agonist-induced cGMP accumulation in homogeneous cell culture systems where the hormone or agonist effects on cGMP are mediated by NO. Presumably, hemoglobin would not be permeable and could only trap or scavenge extracellular NO to account for its ability to decrease hormonally induced cGMP increases in homogeneous cell populations. There is no direct evidence that NO can act as an endocrine substance to increase cGMP synthesis in a distant target cell population. However, complexes or carrier states of NO that would liberate NO at a distant site could most certainly be viewed as endocrinological agents (hormones or autocoids). We suspect that appropriately designed experiments in the future will also support this role for NO as an endocrinological agent that can also function at a distance similar to classical hormones. Indeed, we believe that NO should be added to the list of agents that can function as a neurotransmitter, paracrine substance, and autacoid or hormone. It can also be viewed as an intracellular, as well as intercellular, messenger. To date, no substance has played such a diverse role in intracellular and intercellular signal transduction. Thus, NO appears to be a unique and simple molecule with diverse functions in signal transduction.

Amino Acid Oxidoreductases↗
PubMed1984

Intercellular communication and the control of growth: XII. Alteration of junctional permeability by simian virus 40. Roles of the large and small T antigens.

We studied the action of temperature-sensitive mutant simian virus 40--a transformation-inducing DNA virus--on the junctional permeability to mono-, di- and triglutamate in rat embryo-, pancreas islet (epithelial)-, and 10T1/2 cell cultures. Junctional permeability was reduced (reversibly) in the transformed state. To dissect the genetics of this alteration, we used two kinds of mutant virus DNA. One kind had a temperature-sensitive mutation on the A gene, rendering the large T antigen (the gene product) thermolabile (T+ in equilibrium T-). The other had a deletion on the F gene, in addition, abolishing (permanently) the expression of the little t addition (t-). The junctional alteration occurred in the condition T+ t+, but not in the conditions T- t+, T+ t- or T- t-. Both antigens, thus, are necessary for this junctional alteration--a genetic requirement identical to that for decontrol of growth (but distinct from that of the cytoskeletal alteration).

Animals↗
PubMed1983

Intercellular communication in the supporting cells of the organ of Corti.

We have directly tested the concept that the supporting cells of the organ of Corti are functionally coupled through gap junctions. In vitro and in vivo preparations were evaluated. Electrical measurements clearly show that the cells are coupled ionically. Voltage drops measured in neighboring cells in response to intracellular current injections indicate that current spread decays rapidly. Despite the existence of electrical coupling, fluorescent dye injection studies revealed no dye spread into adjacent cells, other than a few instances which were clearly artifactual. However, it is possible that dye spread is very slow and that dye in adjacent cells is diluted below visual detectability. In any case, dye coupling is remarkably poor compared to other electrically coupled tissues. The role of coupling in the supporting cells may be nutritive, considering the avascular nature of Corti's organ.

Animals↗
PubMed2005

[Gap junctions--major structures promoting intercellular communication].

Gap junctions provide humoral and electric communication between the cells, thus contributing to their morpho-functional cooperation. Gap junction is formed by multiple intercellular channels, each of them being made by two closed hemichannels--connexons, that are oligomeric transmembrane proteins built by 6 subunits, belonging to connexin family. Permeability and electric conductivity of gap junction channels is determined by molecular peculiarities of connexins, their capacity for phosphorilation and by some extra- and intracellular factors. According to the current data, gap junctions in both cell cultures and tissues are dynamic structures with a short half-life period. Main mechanisms responsible for gap junction assembly and destruction have been discovered. These mechanisms were shown to depend upon peculiarities of differential genome activity and to be controlled by extra- and intracellular factors. The data on the gap junctions in the nervous system, heart and epidermis are presented.

Animals↗