AJP - Renal AJP: Advances in Physiology Education
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol 282: F943-F952, 2002. First published August 8, 2001; doi:10.1152/ajprenal.0108.2001
0363-6127/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
282/5/F943    most recent
0108.2001v1
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 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 Web of Science (7)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cussac, D.
Right arrow Articles by Paris, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cussac, D.
Right arrow Articles by Paris, H.
Vol. 282, Issue 5, F943-F952, May 2002

alpha 2B-Adrenergic receptors activate MAPK and modulate proliferation of primary cultured proximal tubule cells

Daniel Cussac1, Stéphane Schaak1, Céline Gales2, Christodoulos Flordellis3, Colette Denis1, and Hervé Paris1

Institut National de la Santé et de la Recherche Médicale 1 Unit 388 and 2 Unit 531, Institut L. Bugnard, Centre Hospitalier Universitaire Rangueil, 31403 Toulouse Cedex 4, France; and 3 Department of Pharmacology, School of Medicine, University of Patras, 26110 Rio Patras, Greece

In the rat proximal tubule, the alpha 2B-adrenergic receptor (alpha 2B-AR) enhances Na+ reabsorption by increasing the activity of Na+/H+ exchanger isoform NHE3. The mechanisms involved are unclear, and inhibition of cAMP production remains controversial. In this study, we reinvestigated alpha 2B-AR signaling pathways using rat proximal tubule cells (PTC) in primary culture and LLC-PK1 cells permanently transfected with the RNG gene (rat nonglycosylated alpha 2-AR). Binding experiments indicated that PTC express substantial amounts of alpha 2B-AR (130 fmol/mg protein), and only RNG transcripts were detected. In both cell types, the alpha 2B-AR is coupled to G protein, and its stimulation by dexmedetomidine, but not by UK-14304, provoked a significant inhibition of the accumulation of cAMP induced by forskolin or parathyroid hormone. Exposure to alpha 2-agonists increased arachidonic acid release and caused extracellular signal-regulated kinase (ERK)1/2 phosphorylation, which correlated with enhanced mitogen-activated protein kinse (MAPK) activity and nuclear translocation. MAPK phosphorylation was blunted by pertussis toxin but not by protein kinase C desensitization, and it coincided with transient phosphorylation of Shc. Finally, treatment with UK-14304 accelerated cell growth. Further studies will be necessary to clarify the precise mechanism of MAPK activation, but the present data suggest that alpha 2B-AR may play a positive role during tubular regeneration.

kidney; mitogen-activated protein kinase


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
D. Cussac, S. Schaak, C. Denis, and H. Paris
alpha 2B-Adrenergic Receptor Activates MAPK via a Pathway Involving Arachidonic Acid Metabolism, Matrix Metalloproteinases, and Epidermal Growth Factor Receptor Transactivation
J. Biol. Chem., May 24, 2002; 277(22): 19882 - 19888.
[Abstract] [Full Text] [PDF]




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