Am J Physiol Cell Physiol Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 283: C1655-C1666, 2002. First published August 1, 2002; doi:10.1152/ajpcell.00041.2002
0363-6143/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
283/6/C1655    most recent
00041.2002v2
00041.2002v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (17)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kagawa, T.
Right arrow Articles by Arias, I. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kagawa, T.
Right arrow Articles by Arias, I. M.
Vol. 283, Issue 6, C1655-C1666, December 2002

Mechanism by which cAMP activates PI3-kinase and increases bile acid secretion in WIF-B9 cells

Tatehiro Kagawa, Lyuba Varticovski, Yoshimichi Sai, and Irwin M. Arias

Department of Physiology, Tufts University School of Medicine, Boston, Massachusetts 02111

Previous studies in rat bile canalicular membrane vesicles and WIF-B9 cells revealed that cAMP-induced trafficking of ATP-binding cassette (ABC) transporters to the canalicular membrane and their activation require phosphoinositide 3-kinase (PI3-K) products. In the present studies, canalicular secretion of fluorescein isothiocyanate-glycocholate in WIF-B9 cells was increased by cAMP and a decapeptide that enhances PI3-K activity; these effects were inhibited by wortmannin. To determine the mechanism(s) whereby cAMP activates PI3-K, we examined signal transduction pathways in WIF-B9 and COS-7 cells. cAMP activated PI3-K in both cell lines in a phosphotyrosine-independent manner. PI3-K activity increased in association with p110beta in both cell lines. The effect of cAMP was KT-5720 sensitive, suggesting involvement of protein kinase A. Expression of a dominant-negative beta -adrenergic receptor kinase COOH terminus (beta -ARKct), which blocks Gbeta gamma signaling, decreased PI3-K activation in both cell lines. cAMP increased GTP-bound Ras in COS-7 but not WIF-B9 cells. Expression of dominant-negative Ras abolished cAMP-mediated PI3-K, which suggests that the effect is downstream of Ras and Gbeta gamma . These data indicate that cAMP activates PI3-K in a cell type-specific manner and provide insight regarding mechanisms of PI3-K activation required for bile acid secretion.

bile secretion; heterotrimeric G protein; Gbeta gamma ; protein kinase A; Ras


This article has been cited by other articles:


Home page
 J. Virol.Home page
M. J. Farquhar, H. J. Harris, M. Diskar, S. Jones, C. J. Mee, S. U. Nielsen, C. L. Brimacombe, S. Molina, G. L. Toms, P. Maurel, et al.
Protein Kinase A-Dependent Step(s) in Hepatitis C Virus Entry and Infectivity
J. Virol., September 1, 2008; 82(17): 8797 - 8811.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
T. Kagawa, N. Watanabe, K. Mochizuki, A. Numari, Y. Ikeno, J. Itoh, H. Tanaka, I. M. Arias, and T. Mine
Phenotypic differences in PFIC2 and BRIC2 correlate with protein stability of mutant Bsep and impaired taurocholate secretion in MDCK II cells
Am J Physiol Gastrointest Liver Physiol, January 1, 2008; 294(1): G58 - G67.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
K. Mochizuki, T. Kagawa, A. Numari, M. J. Harris, J. Itoh, N. Watanabe, T. Mine, and I. M. Arias
Two N-linked glycans are required to maintain the transport activity of the bile salt export pump (ABCB11) in MDCK II cells
Am J Physiol Gastrointest Liver Physiol, March 1, 2007; 292(3): G818 - G828.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
S. Glaser, D. Alvaro, H. Francis, Y. Ueno, L. Marucci, A. Benedetti, S. D. Morrow, M. Marzioni, M. G. Mancino, J. L. Phinizy, et al.
Adrenergic receptor agonists prevent bile duct injury induced by adrenergic denervation by increased cAMP levels and activation of Akt
Am J Physiol Gastrointest Liver Physiol, April 1, 2006; 290(4): G813 - G826.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
S. L. Jones and Y. Sharief
Asymmetrical protein kinase A activity establishes neutrophil cytoskeletal polarity and enables chemotaxis
J. Leukoc. Biol., July 1, 2005; 78(1): 248 - 258.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
K. A. Cullen, J. McCool, M. S. Anwer, and C. R. L. Webster
Activation of cAMP-guanine exchange factor confers PKA-independent protection from hepatocyte apoptosis
Am J Physiol Gastrointest Liver Physiol, August 1, 2004; 287(2): G334 - G343.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
S. Misra, L. Varticovski, and I. M. Arias
Mechanisms by which cAMP increases bile acid secretion in rat liver and canalicular membrane vesicles
Am J Physiol Gastrointest Liver Physiol, July 7, 2003; 285(2): G316 - G324.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online