Reduced cell-cell communication between mitotic and nonmitotic coupled cells

Stein, Lisa S.; Boonstra, J; Burghardt, Robert C.

doi:10.1016/0014-4827(92)90141-t

Cited by 69 publications

(39 citation statements)

References 19 publications

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“…Cx43 phosphorylated at S368 was most abundant relative to total Cx43 during S and G2/M. This result is consistent with previous reports where gap junctional communication was shut-down during mitosis (Stein et al, 1992;Xie et al, 1997) and phosphorylation at S368 had been shown to reduce communication . Here, we found that G 0 cells contain very little p368 and that S368 is increasingly phosphorylated as cells approach and progress through S phase.…”

Section: Tpa-induced Phosphorylation Of S368 Occurs On Both Intracellsupporting

confidence: 92%

“…structures reassemble and communication is gradually restored as cells proceed through G1 (Stein et al, 1992;Xie et al, 1997). Cx43 is phosphorylated at multiple serine residues in vivo (Berthoud et al, 1992;Brissette et al, 1991;Crow et al, 1990;Kadle et al, 1991;Laird et al, 1991;Musil et al, 1990), and upon phosphorylation, Cx43 migration in polyacrylamide gel electrophoresis (SDS-PAGE) is reduced.…”

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confidence: 99%

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Connexin43 phosphorylation at S368 is acute during S and G2/M and in response to protein kinase C activation

Solan

Fry

TenBroek

et al. 2003

Journal of Cell Science

125

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Phorbol esters such as 12-O-tetradeconylphorbol-13-acetate (TPA)activate protein kinase C, increase Connexin43 (Cx43) phosphorylation, and decrease cell-cell communication via gap junctions in many cell types. Previous work has implicated protein kinase C (PKC) in the direct phosphorylation of Cx43 at S368, which results in a change in single channel behavior that contributes to a decrease in intercellular communication. We have examined Cx43 phosphorylation in several cell lines with an antibody specific for phosphorylated S368. We show that this antibody detects Cx43 only when it is phosphorylated at S368 and, consistent with previous results, TPA treatment causes a dramatic increase in phosphorylation at S368. However, in some cell types, the increased phosphorylation at S368 did not cause a detectable shift in migration as compared with the nonphosphorylated Cx43. Immunofluorescence showed increased S368 immunolabeling in cytoplasmic and plasma membrane structures in response to TPA. Immunoblot analysis of synchronized cells showed increased phosphorylation at S368 during S and G2/M phases of the cell cycle. S-phase cells contained more total Cx43 but assembled fewer functional gap junctional channels than G0-phase cells. Since M-phase cells also communicate poorly and contain few assembled gap junctions, phosphorylation at S368 appears to be negatively correlated with gap junction assembly. Thus, both gap junctional communication and S368 phosphorylation change during S phase and G2/M, implying that phosphorylation at S368 might play a role in key cell-cycle events.

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Section: Tpa-induced Phosphorylation Of S368 Occurs On Both Intracellsupporting

confidence: 92%

mentioning

confidence: 99%

Connexin43 phosphorylation at S368 is acute during S and G2/M and in response to protein kinase C activation

Solan

Fry

TenBroek

et al. 2003

Journal of Cell Science

125

View full text Add to dashboard Cite

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“…Because laser cytometry with the ACAS 570 can be performed on anchored cells, there are unique opportunities to examine a variety of responses by individual cells over time (see, e.g., 3,28). The potential for diffusion of intracellular GSH between individual contacting ROSE-199 and ras-R199 was examined.…”

Section: Analysis Of Gsh Content In Cocultured Cellsmentioning

confidence: 99%

Kinetic analysis of glutathione in anchored cells with monochlorobimane

1995

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A method for the measurement of intracellular glutathione content and glutathione S-transferase activity with monochlorobimane in adherent cells is described. The method involves the kinetic analysis of monochlorobimane conjugation to glutathione over a relatively short period of time. This permits extrapolation over time for determination of equilibrium fluorescence intensity (relative glutathione level) ftom scan intensity data that follows first-order kinetics, minimizing problems commonly associated with the use of monochlorobimane. By using measured fluorescence intensity values from glutathione standards, a suspension calibration curve was generated and, subsequently, was used to determine the photomultiplier tube saturation rate. A theoretical intracellular calibration curve was then generated to quantify glutathione content in cells. This method was also applied to study the changes in glutathione in a variety of rodent and human cell lines and in selected cocultures of cells exhibiting similar or different glutathione levels. Comparison of the glutathione levels obtained with monochlorobimane and a standard colorimetric method (GSH-400) indicated good correlation between the two methods. These studies support the use of laser cytometry for measuring intracellular glutathione with monochlorobimane as well as changes in glutathione occurring in cells that establish physical contacts with other cells. Laser cytometric analysis of glutathione in anchored cells also provides opportunities to monitor individual cellular responses to a variety of experimental manipulations, such as responses to various toxic insults or the protective effects of gap junction-mediated intercellular communication. o 1995 wiley-Liss, I~C .

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“…8,9) Reduction of GJIC is suggested to be associated with the process of mitosis. 25) Thus, modulation of carcinogenesis by GJIC is considered to be important, especially in the promotion phase. genesis, together with an inverse correlation of the expression with hepatocellular proliferation, suggesting that Cx 32 expression has an important role in the hepatocarcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

Suppressive Effect of Irsogladine Maleate on Diethylnitrosamine‐initiated and Phenobarbital‐promoted Hepatocarcinogenesis in Male F344 Rats

Sugie¹,

Okamoto²,

Ueda³

et al. 1998

Japanese Journal of Cancer Research

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Modifying effects of irsogladine maleate (IRG) on diethylnitrosamine (DEN)-induced hepatocarcinogenesis were examined in male F344 rats. Six-week-old rats were divided into 8 groups. Groups 1 through 4 were given a single i.p. injection of DEN (200 mg/kg body weight) at the start of the experiment, whereas groups 5 through 8 received a single i.p. injection of saline as the vehicle treatment. Groups 1 and 8 were kept on the basal diet and distilled water throughout the experiment (36 weeks). Groups 2 and 7 were exposed to 500 ppm phenobarbital (PB) in the drinking water, starting one week after the carcinogen or vehicle treatment. Groups 3 and 5 were fed the diet mixed with 125 ppm IRG from one week after DEN or vehicle treatment. Groups 4 and 6 were given 125 ppm IRG-containing diet and drinking water with 500 ppm PB after the carcinogen or vehicle treatment. Liver neoplasms developed in groups 1 (1/15 rats, 7%) and 2 (14/14 rats, 100%). However, no liver tumors were found in rats of groups 3 through 8. Incidence and average number of liver neoplasms in group 4 (0/14 rats, 0%) were less than those in group 2 (P< < < <0.0001).The number of glutathione S-transferase placental form (GST-P)-positive liver cell foci in group 3 or 4 was significantly smaller than that in the appropriate control (P< < < <0.01, P< < < <0.001, respectively).The average and unit areas of these foci in group 4 were also significantly smaller than those in group 2 (P< < < <0.001, P< < < <0.05, respectively). These results suggest that IRG could be a chemopreventive agent for rat liver carcinogenesis.

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Reduced cell-cell communication between mitotic and nonmitotic coupled cells

Cited by 69 publications

References 19 publications

Connexin43 phosphorylation at S368 is acute during S and G2/M and in response to protein kinase C activation

Connexin43 phosphorylation at S368 is acute during S and G2/M and in response to protein kinase C activation

Kinetic analysis of glutathione in anchored cells with monochlorobimane

Suppressive Effect of Irsogladine Maleate on Diethylnitrosamine‐initiated and Phenobarbital‐promoted Hepatocarcinogenesis in Male F344 Rats

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