Cell cycle-dependent activity of the volume- and Ca2+-activated anion currents in Ehrlich lettre ascites cells

✍ Scribed by Thomas Kjær Klausen; Andreas Bergdahl; Charlotte Hougaard; Palle Christophersen; Stine F. Pedersen; Else K. Hoffmann

• Publisher: John Wiley and Sons
• Year: 2006
• Tongue: English
• Weight: 402 KB
• Volume: 210
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.20918

✦ Synopsis

Abstract

Recent evidence implicates the volume‐regulated anion current (VRAC) and other anion currents in control or modulation of cell cycle progression; however, the precise involvement of anion channels in this process is unclear. Here, Cl^−^ currents in Ehrlich Lettre Ascites (ELA) cells were monitored during cell cycle progression, under three conditions: (i) after osmotic swelling (i.e., VRAC), (ii) after an increase in the free intracellular Ca^2+^ concentration (i.e., the Ca^2+^‐activated Cl^−^ current, CaCC), and (iii) under steady‐state isotonic conditions. The maximal swelling‐activated VRAC current decreased in G1 and increased in early S phase, compared to that in G0. The isotonic steady‐state current, which seems to be predominantly VRAC, also decreased in G1, and increased again in early S phase, to a level similar to that in G0. In contrast, the maximal CaCC current (500 nM free Ca^2+^ in the pipette), was unaltered from G0 to G1, but decreased in early S phase. A novel high‐affinity anion channel inhibitor, the acidic di‐aryl‐urea NS3728, which inhibited both VRAC and CaCC, attenuated ELA cell growth, suggesting a possible mechanistic link between cell cycle progression and cell cycle‐dependent changes in the capacity for conductive Cl^−^ transport. It is suggested that in ELA cells, entrance into the S phase requires an increase in VRAC activity and/or an increased potential for regulatory volume decrease (RVD), and at the same time a decrease in CaCC magnitude. J. Cell. Physiol. 210: 831–842, 2007. © 2006 Wiley‐Liss, Inc.