AJP - Renal Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol 285: F336-F347, 2003. First published April 29, 2003; doi:10.1152/ajprenal.00003.2003
0363-6127/03 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
285/2/F336    most recent
00003.2003v1
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 (25)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bustamante, M.
Right arrow Articles by Féraille, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bustamante, M.
Right arrow Articles by Féraille, E.

Regulatory volume increase is associated with p38 kinase-dependent actin cytoskeleton remodeling in rat kidney MTAL

Mauro Bustamante,1 Frank Roger,1 Marie-Luce Bochaton-Piallat,2 Giulio Gabbiani,2 Pierre-Yves Martin,1 and Eric Féraille1

1Division de Néphrologie, Fondation pour Recherches Médicales, and 2Département de Pathologie, Centre Médical Universitaire, CH-1211 Genève 4, Switzerland

Submitted 7 January 2003 ; accepted in final form 22 April 2003

The kidney medulla is physiologically exposed to variations in extracellular osmolality. In response to hypertonic cell shrinkage, cells of the rat kidney medullary thick ascending limb of Henle's loop undergo p38 kinase-dependent regulatory volume increase (RVI). In the present study, we investigated the role of actin cytoskeleton reorganization in this process. Addition of hyperosmotic NaCl or sucrose, which activates MAP kinases and reduces cellular volume, induced a sustained actin polymerization occurring after 10 min and concurrently with RVI. In contrast, hyperosmotic urea, which does not modify MAP kinase activity and cellular volume, did not induce sustained actin polymerization. Fluorescence microscopy revealed that hyperosmotic NaCl and sucrose, but not urea, induced the redistribution of F-actin from a dense cortical ring to a diffuse network of actin bundles. Stabilization of actin filaments by jasplakinolide and inhibition of the generation of new actin filaments by swinholide A prevented RVI, whereas depolymerization of actin filaments by latrunculin B attenuated cell shrinkage and enhanced RVI. These actin-interfering drugs did not alter extracellular regulated kinase and p38 kinase activation under hypertonic conditions. Similar to swinholide A, inhibiting p38 kinase with SB-203580 abolished sustained actin polymerization, actin redistribution, and decreased RVI efficacy. We therefore propose that in rat kidney the medullary thick ascending limb of Henle's loop exposed to extracellular hypertonicity, p38 kinase activation induces depolymerization of the F-actin cortical ring and polymerization of a dense diffuse F-actin network that both contribute to increase RVI efficacy.

mitogen-activated protein kinase; osmolarity; kidney medulla; cell volume



Address for reprint requests and other correspondence: E. Féraille, Division de Néphrologie, Fondation pour Recherches Médicales, CH-1211 Genève 4, Switzerland (E-mail: Eric.Feraille{at}medecine.unige.ch).




This article has been cited by other articles:


Home page
Am. J. Physiol. Cell Physiol.Home page
U. Hasler
Controlled aquaporin-2 expression in the hypertonic environment
Am J Physiol Cell Physiol, April 1, 2009; 296(4): C641 - C653.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
A. C. P. Thirone, P. Speight, M. Zulys, O. D. Rotstein, K. Szaszi, S. F. Pedersen, and A. Kapus
Hyperosmotic stress induces Rho/Rho kinase/LIM kinase-mediated cofilin phosphorylation in tubular cells: key role in the osmotically triggered F-actin response
Am J Physiol Cell Physiol, March 1, 2009; 296(3): C463 - C475.
[Abstract] [Full Text] [PDF]


Home page
Physiol. Rev.Home page
M. B. Burg, J. D. Ferraris, and N. I. Dmitrieva
Cellular Response to Hyperosmotic Stresses
Physiol Rev, October 1, 2007; 87(4): 1441 - 1474.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Cell Physiol.Home page
K. B. E. Gagnon, R. England, and E. Delpire
Volume sensitivity of cation-Cl- cotransporters is modulated by the interaction of two kinases: Ste20-related proline-alanine-rich kinase and WNK4
Am J Physiol Cell Physiol, January 1, 2006; 290(1): C134 - C142.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2003 by the American Physiological Society.