Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (41)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Ren, P.
Right arrow Articles by Ruch, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ren, P.
Right arrow Articles by Ruch, R. J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis, Vol 19, 169-175, Copyright © 1998 by Oxford University Press

ARTICLES

Inhibition of gap junctional intercellular communication by tumor promoters in connexin43 and connexin32-expressing liver cells: cell specificity and role of protein kinase C

P Ren, PP Mehta and RJ Ruch
Department of Pathology, Medical College of Ohio, Toledo 43699, USA.

In this study, we investigated whether the tumor promoters, 12-O- tetradecanoylphorbol-13-acetate (TPA), phenobarbital (PB), and 1,1- bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), inhibited gap junctional intercellular communication (GJIC) in a cell-specific or connexin-specific manner and whether protein kinase C was involved. To do this, we used highly communicating WB-F344 rat liver epithelial cells, which express connexin43 as their predominant gap junction protein, WB-aB1 cells, which are a GJIC-incompetent mutant line of WB- F344 cells and that express connexin43, WB-a/32-10 cells, which are a highly communicating derivative of WB-aB1 cells generated by stable transduction with a connexin32 retroviral expression vector, and primary cultured rat hepatocytes, which express conexin32 predominantly. Treatment of WB-F344 and WB-a/32-10 cells, but not hepatocytes, with TPA inhibited GJIC (assayed by Lucifer Yellow dye microinjection). This inhibition involved protein kinase C because (i) inhibition was prevented by co-treatment of the cells with a specific protein kinase C inhibitor, bis-indolylmaleimide, and (ii) treatment with TPA for 24 h had no effect on dye-coupling in agreement with the downregulation of protein kinase C. TPA also caused the internalization of Cx43-containing gap junctions and the formation of a hyperphosphorylated form of Cx43, Cx43-P3, in WB-F344 cells only, but TPA had no effect on Cx32-containing gap junctions or protein mobility. In contrast, PB inhibited GJIC only in hepatocytes and DDT inhibited GJIC in all three types of cells; bis-indolylmaleimide did not block the effects of either agent. These results indicate that the inhibitory actions of TPA and PB on GJIC are cell-specific rather than connexin- specific and that TPA inhibits connexin43 and connexin32-mediated GJIC through a protein kinase C-dependent mechanism.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Toxicol SciHome page
M. Machala, L. Blaha, J. Vondracek, J. E. Trosko, J. Scott, and B. L. Upham
Inhibition of Gap Junctional Intercellular Communication by Noncoplanar Polychlorinated Biphenyls: Inhibitory Potencies and Screening for Potential Mode(s) of Action
Toxicol. Sci., November 1, 2003; 76(1): 102 - 111.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
E. Leithe, V. Cruciani, T. Sanner, S.-O. Mikalsen, and E. Rivedal
Recovery of gap junctional intercellular communication after phorbol ester treatment requires proteasomal degradation of protein kinase C
Carcinogenesis, July 1, 2003; 24(7): 1239 - 1245.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
K. A. Warner, M. J. Fernstrom, and R. J. Ruch
Inhibition of Mouse Hepatocyte Gap Junctional Intercellular Communication by Phenobarbital Correlates with Strain-Specific Hepatocarcinogenesis
Toxicol. Sci., February 1, 2003; 71(2): 190 - 197.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
L. Blaha, P. Kapplova, J. Vondracek, B. Upham, and M. Machala
Inhibition of Gap-Junctional Intercellular Communication by Environmentally Occurring Polycyclic Aromatic Hydrocarbons
Toxicol. Sci., January 1, 2002; 65(1): 43 - 51.
[Abstract] [Full Text] [PDF]

Home page
 CarcinogenesisHome page
E. Rivedal and H. Opsahl
Role of PKC and MAP kinase in EGF- and TPA-induced connexin43 phosphorylation and inhibition of gap junction intercellular communication in rat liver epithelial cells
Carcinogenesis, September 1, 2001; 22(9): 1543 - 1550.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
S.-H. Jeong, S. S. M. Habeebu, and C. D. Klaassen
Cadmium Decreases Gap Junctional Intercellular Communication in Mouse Liver
Toxicol. Sci., September 1, 2000; 57(1): 156 - 166.
[Abstract] [Full Text] [PDF]

Home page
 Toxicol SciHome page
F. J. Elcock, E. Deag, R. A. Roberts, and J. K. Chipman
Nafenopin Causes Protein Kinase C-Mediated Serine Phosphorylation and Loss of Function of Connexin 32 Protein in Rat Hepatocytes without Aberrant Expression or Localization
Toxicol. Sci., July 1, 2000; 56(1): 86 - 94.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.