HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/C390    most recent 00104.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lambert, I. H. Search for Related Content PubMed PubMed Citation Articles by Lambert, I. H.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Activation and inactivation of the volume-sensitive taurine leak pathway in NIH3T3 fibroblasts and Ehrlich Lettre ascites cells

Department of Molecular Biology, University of Copenhagen, Copenhagen, Denmark

Submitted 15 March 2007 ; accepted in final form 29 April 2007

Hypotonic exposure provokes the mobilization of arachidonic acid, production of ROS, and a transient increase in taurine release in Ehrlich Lettre cells. The taurine release is potentiated by H₂O₂ and the tyrosine phosphatase inhibitor vanadate and reduced by the phospholipase A₂ (PLA₂) inhibitors bromoenol lactone (BEL) and manoalide, the 5-lipoxygenase (5-LO) inhibitor ETH-615139, the NADPH oxidase inhibitor diphenyl iodonium (DPI), and antioxidants. Thus, swelling-induced taurine efflux in Ehrlich Lettre cells involves Ca²⁺-independent (iPLA₂)/secretory PLA₂ (sPLA₂) plus 5-LO activity and modulation by ROS. Vanadate and H₂O₂ stimulate arachidonic acid mobilization and vanadate potentiates ROS production in Ehrlich Lettre cells and NIH3T3 fibroblasts under hypotonic conditions. However, vanadate-induced potentiation of the volume-sensitive taurine efflux is, in both cell types, impaired in the presence of BEL and DPI and following restoration of the cell volume. Thus, potentiation of the volume-sensitive taurine efflux pathway following inhibition of tyrosine phosphatase activity reflects increased arachidonic acid mobilization and ROS production for downstream signaling. Vanadate delays the inactivation of volume-sensitive taurine efflux in NIH3T3 cells, and this delay is impaired in the presence of DPI. Vanadate has no effect on the inactivation of swelling-induced taurine efflux in Ehrlich Lettre cells. It is suggested that increased tyrosine phosphorylation of regulatory components of NADPH oxidase leads to increased ROS production and a subsequent delay in inactivation of the volume-sensitive taurine efflux pathway and that NADPH oxidase or antioxidative capacity differ between NIH3T3 and Ehrlich Lettre cells.

organic osmolytes; reactive oxygen species; vanadate; H₂O₂; tyrosine phosphatases; arachidonic acid mobilization

This article has been cited by other articles:

				I. H. Lambert, T. K. Klausen, A. Bergdahl, C. Hougaard, and E. K. Hoffmann ROS activate KCl cotransport in nonadherent Ehrlich ascites cells but K+ and Cl- channels in adherent Ehrlich Lettre and NIH3T3 cells Am J Physiol Cell Physiol, July 1, 2009; 297(1): C198 - C206. [Abstract] [Full Text] [PDF]

				E. K. Hoffmann, I. H. Lambert, and S. F. Pedersen Physiology of Cell Volume Regulation in Vertebrates Physiol Rev, January 1, 2009; 89(1): 193 - 277. [Abstract] [Full Text] [PDF]

				M. B. Friis, K. G. Vorum, and I. H. Lambert Volume-sensitive NADPH oxidase activity and taurine efflux in NIH3T3 mouse fibroblasts Am J Physiol Cell Physiol, June 1, 2008; 294(6): C1552 - C1565. [Abstract] [Full Text] [PDF]