Epidermal growth factor- and stress-induced loss of gap junctional communication is mediated by ERK-1/ERK-2 but not ERK-5 in rat liver epithelial cells

2007 ◽  
Vol 364 (2) ◽  
pp. 313-317 ◽  
Author(s):  
Kotb Abdelmohsen ◽  
Elisabeth Sauerbier ◽  
Niloofar Ale-Agha ◽  
Juliane Beier ◽  
Philippe Walter ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Rat Liver ◽  
Gap Junctional Communication ◽  
Liver Epithelial Cells ◽  
Junctional Communication ◽  
Epidermal Growth ◽  
Rat Liver Epithelial Cells ◽  
Gap Junctional

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.

The epidermal growth factor-induced migration of rat liver epithelial cells is associated with a transient inhibition of DNA synthesis

1991 ◽  
Vol 100 (2) ◽  
pp. 349-355
Author(s):  
P. Geimer ◽  
E.G. Bade
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Epithelial Cells ◽  
Dna Synthesis ◽  
Rat Liver ◽  
S Phase ◽  
Liver Epithelial Cells ◽  
Epidermal Growth ◽  
Rat Liver Epithelial Cells ◽  
Inhibition Of Dna Synthesis

Epidermal growth factor (EGF) is a potent mitogen for most cultured cells and has previously been shown to induce the migration of rat liver epithelial cells. We have now demonstrated that under migration-inducing conditions EGF does not stimulate cell proliferation, but causes instead a transient inhibition of DNA synthesis. Analysis at the single-cell level by [3H]thymidine autoradiography indicated that in 40–50% of the EGF-treated cell population the entry into S phase is delayed. The simultaneous demonstration of migration tracks by laminin immunofluorescence revealed that the transient inhibition of DNA synthesis is not restricted to the migratory cells. The effect is also observed with the stationary subpopulation and appears, therefore, to be independent of the induction of migration. The independence of both processes was further supported by showing that induction of migration by EGF proceeds undisturbed in cells blocked in S phase by aphidicolin. These results indicated that for rat liver epithelial cells the induction of migration by EGF has priority over cell proliferation. The data also emphasize the need for a time-course analysis when studying factors that stimulate or inhibit DNA synthesis or cell proliferation.

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