Retinoic acid modulates gap junctional intercellular communication in hepatocytes and hepatoma cells

Gap junctional communication permits the direct exchange of small molecules and ions and has been implicated in tissue homeostasis/metabolite exchange. The lack of gap junctional intercellular communication (GJIC) plays important roles in the promotion and progression of carcinogenesis. In the prese...

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Bibliographic Details
Published in:Cellular and molecular life sciences : CMLS 2002-10, Vol.59 (10), p.1758-1765
Main Authors: Ara, C, Massimi, M, Devirgiliis Conti, L
Format: Article
Language:English
Subjects:
Animals
Carcinogenesis
Carcinoma, Hepatocellular - pathology
Cell Communication - drug effects
Cell Communication - physiology
Cell Differentiation
Cell Division - drug effects
Cellular biology
Female
Gap Junctions - drug effects
Gap Junctions - physiology
Gene expression
Genotype & phenotype
Gestational Age
Hepatocytes - cytology
Hepatocytes - drug effects
Humans
Liver
Liver - cytology
Liver - drug effects
Liver - embryology
Liver Neoplasms
Metabolites
Molecular weight
Phosphorylation
Phosphoserine - metabolism
Pregnancy
Rats
Rats, Wistar
Tretinoin - pharmacology
Tumor Cells, Cultured
Tumors
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Summary:Gap junctional communication permits the direct exchange of small molecules and ions and has been implicated in tissue homeostasis/metabolite exchange. The lack of gap junctional intercellular communication (GJIC) plays important roles in the promotion and progression of carcinogenesis. In the present study, we demonstrate that treatment of human hepatoma Hep G2 cells with retinoic acid (RA) results in increased amounts and phosphorylation of connexins, their stabilisation in plasma membrane plaques and enhanced GJIC. In cultured fetal hepatocytes, which represent a non-transformed, proliferating and incompletely differentiated liver system, the effects of RA are limited to the establishment of connexin in areas of cell-cell contact and the improvement of GJIC. This suggests that modulation of cell-cell channel communication by RA occurs differently in these two experimental models: while RA is able to revert cell transformation in Hep G2 cells, in fetal hepatocytes it may induce the expression of a more differentiated phenotype.
ISSN:1420-682X
1420-9071
DOI:10.1007/PL00012503