Regulation of the volume-sensitive taurine efflux pathway in NIH3T3 mouse fibroblasts.

Abstract

Osmotically swollen NIH3T3 fibroblasts regulate their cell volume towards their initial value just like most mammalian cells1. This back regulation, designated regulatory volume decrease (RVD), is the result of loss of KCl and organic osmolytes1,2. It is estimated that the loss of cellular amino acids constitutes 20% of the total loss of osmolytes following exposure to a medium with half osmolarity2. The swelling-induced K+ efflux is partly via a K+ selective pathway and partly via a K+, Cl- cotransporter1,3, whereas the swelling-induced Cl- efflux is Ca2+ independent and via a non-selective anion pathway, that exhibits moderate outward rectification as well as time dependent inactivation1,3. Taurine is an important organic osmolyte in NIH3T3 cells and the swelling-induced taurine release from NIH3T3 cells is Na+-independent and mediated via a leak pathway that accepts a variety of neutral amino acids2. The volume-sensitive organic osmolyte channel (VSOAC), that accepts Cl- as well as a broad range of organic osmolytes, has been proposed as the volume-sensitive taurine efflux pathway in mammalian cells4. However, the time courses for the swelling-induced taurine efflux and Cl- efflux in NIH3T3 cells differ with respect to the time point for maximal activation and time point for inactivation2. Furthermore, the swelling-induced Cl- loss and the swelling-induced taurine loss from NIH3T3 cells diverge with respect to their sensitivity to anion channel blockers2, kinase inhibitors3 and expression of constitutive Rho3.KeywordsFocal Adhesion KinaseNIH3T3 CellProtein Tyrosine PhosphataseRegulatory Volume DecreaseEhrlich Ascites Tumor CellThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.