Skip Navigation

This Article
Right arrow Full Text (PDF)
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 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 (22)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Kwiatkowski, A. P.
Right arrow Articles by Klaunig, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kwiatkowski, A. P.
Right arrow Articles by Klaunig, J. E.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1994 Oxford University Press

research-article

Comparison of glucocorticoid-mediated changes in the expression and function of rat hepatocyte gap junctional proteins

Ann P. Kwiatkowski, Thomas K. Baker and James E. Klaunig 1

Department of Pharmacology and Toxicology, Division of Toxicology, Indiana University School of Medicine 1001 Walnut St, MF003, Indianapolis, IN 46202, USA

1To whom correspondence should be addressed

Gap junctional intercellular communication (GJIC) is often modulated by chemical carcinogens and during carcinogenesis, in part, through changes in gap junction mRNA levels. However, the mechanisms by which gap junction mRNA levels are altered in either normal or cancer cells are largely unknown. Since glucocorticoids are potent modulators of gene expression and stability, we have investigated the effects of these hormones on GJIC and gap junction mRNA expression in rat hepatocytes cultured in three different media. Addition of dexamethasone to cultures of rat hepatocytes resulted in a maintenance of GJIC and both major liver gap junctional mRNAs, connexin (Cx)26 and Cx32, at levels above those in hepatocytes cultured in glucocorticoid-free media. In addition, hepatocytes cultured without dexamethasone for 24 h could be induced to communicate and increase Cx mRNA levels by the addition of dexamethasone to their medium. These media-independent changes in GJIC and gap junction mRNA levels by dexamethasone warrant further investigations into their mechanisms of action and the potential therapeutic value of glucocorticoids in the treatment of cancer.


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
 Arch OphthalmolHome page
D. Dierks, B. Lei, K. Zhang, and D. P. Hainsworth
Effects of Intravitreous Injection of Preserved and Nonpreserved Triamcinolone in Rabbit Retina--Reply
Arch Ophthalmol, November 1, 2006; 124(11): 1666 - 1668.
[Full Text] [PDF]

Home page
 Cancer Res.Home page
M. Mesnil and H. Yamasaki
Bystander Effect in Herpes Simplex Virus-Thymidine Kinase/Ganciclovir Cancer Gene Therapy: Role of Gap-junctional Intercellular Communication1
Cancer Res., August 1, 2000; 60(15): 3989 - 3999.
[Abstract] [Full Text]

Home page
 International Journal of ToxicologyHome page
J. E. A. Leakey, J. E. Seng, C. R. Barnas, V. M. Baker, and R. W. Hart
A Mechanistic Basis for the Beneficial Effects of Caloric Restriction On Longevity and Disease: Consequences for the Interpretation of Rodent Toxicity Studies
International Journal of Toxicology, January 1, 1998; 17(2_suppl): 5 - 56.
[Abstract] [PDF]

Home page
 J. Cell Sci.Home page
T Kojima, T Mitaka, Y Shibata, and Y Mochizuki
Induction and regulation of connexin26 by glucagon in primary cultures of adult rat hepatocytes
J. Cell Sci., January 8, 1995; 108(8): 2771 - 2780.
[Abstract] [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.