Infection of rat liver epithelial cells with v-Ha-ras: Correlation between oncogene expression, gap junctional communication, and tumorigenicity

1990 ◽  
Vol 3 (2) ◽  
pp. 54-67 ◽  
Author(s):  
Adriaan W. De Feijter ◽  
Jean S. Ray ◽  
Chris M. Weghorst ◽  
James E. Klaunig ◽  
Jay I. Goodman ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Rat Liver ◽  
Gap Junctional Communication ◽  
Liver Epithelial Cells ◽  
Oncogene Expression ◽  
Junctional Communication ◽  
Rat Liver Epithelial Cells ◽  
Gap Junctional

Effect of angiotensin II and ethanol on the expression of connexin 43 in WB rat liver epithelial cells

2001 ◽  
Vol 357 (3) ◽  
pp. 769-777 ◽  
Author(s):  
Shaila BOKKALA ◽  
Helena M. REIS ◽  
Emanuel RUBIN ◽  
Suresh K. JOSEPH
Keyword(s):  
Angiotensin Ii ◽  
Epithelial Cells ◽  
Rat Liver ◽  
Connexin 43 ◽  
Ang Ii ◽  
Cx43 Expression ◽  
Gap Junctional Communication ◽  
Junctional Communication ◽  
Rat Liver Epithelial Cells ◽  
Gap Junctional

The turnover of connexin 43 (Cx43) is very rapid in many cells and involves both the lysosomal and proteasomal protease pathways. Here we show that Ca2+-mobilizing agonists such as angiotensin II (Ang II) can up-regulate the expression of Cx43 in WB rat liver epithelial cells. Vasopressin had the same effect in A7R5 smooth-muscle cells. The effect of Ang II was not prevented by pretreatment with proteasomal or lysosomal inhibitors and was associated with an enhanced biosynthesis of Cx43 as measured by metabolic labelling experiments. The accumulation of Cx43 occurred in intracellular compartments and at the cell surface, as determined by confocal immunofluorescence studies and by immunoblotting of fractions soluble and insoluble in Triton X-100. Chronic treatment of WB cells with ethanol inhibited Cx43 expression; this was associated with decreased biosynthesis of Cx43. Neither treatment with Ang II nor treatment with ethanol altered the levels of Cx43 mRNA. Incubation of WB cells with Ang II did not alter gap-junctional communication as judged by a dye-coupling assay. However, treatment with ethanol markedly decreased gap-junctional communication and this effect was diminished in Ang-II-treated cells, demonstrating that gap-junctional communication is linked to the level of Cx43 expression. We conclude that Cx43 biosynthesis is regulated by Ca2+-mobilizing agonists and ethanol in WB cells. The changes in Cx43 expression might have a role in modifying the conduction of metabolites and second messengers between cells.

Doxorubicin induces EGF receptor-dependent downregulation of gap junctional intercellular communication in rat liver epithelial cells

2005 ◽  
Vol 386 (3) ◽  
pp. 217-223 ◽  
Author(s):  
Kotb Abdelmohsen ◽  
Claudia von Montfort ◽  
Dominik Stuhlmann ◽  
P. Arne Gerber ◽  
Ulrich K.M. Decking ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Rat Liver ◽  
Intercellular Communication ◽  
Connexin 43 ◽  
Egf Receptor ◽  
Gap Junctional Intercellular Communication ◽  
Erk Activation ◽  
Liver Epithelial Cells ◽  
Rat Liver Epithelial Cells ◽  
Gap Junctional

Abstract Exposure of rat liver epithelial cells to doxorubicin, an anthraquinone derivative widely employed in cancer chemotherapy, led to a dose-dependent decrease in gap junctional intercellular communication (GJC). Gap junctions are clusters of inter-cellular channels consisting of connexins, the major connexin in the cells used being connexin-43 (Cx43). Doxorubicin-induced loss of GJC was mediated by activation of extracellular signal-regulated kinase (ERK)-1 and ERK-2, as demonstrated using inhibitors of ERK activation. Furthermore, activation of the epidermal growth factor (EGF) receptor by doxorubicin was responsible for ERK activation and the subsequent attenuation of GJC. Inhibition of GJC, however, was not by direct phosphorylation of Cx43 by ERK-1/2, whereas menadione, a 1,4-naphthoquinone derivative that was previously demonstrated to activate the same EGF receptor-dependent pathway as doxorubicin, resulting in downregulation of GJC, caused strong phos-phorylation of Cx43 at serines 279 and 282. Thus, ERK-dependent downregulation of GJC upon exposure to quinones may occur both by direct phosphorylation of Cx43 and in a phosphorylation-independent manner.

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