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Ionic mechanisms of regulatory volume increase (RVI) in the human hepatoma cell-line HepG2

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons98736

Wehner,  Frank
Abt. II: Systemische Zellbiologie, Max Planck Institute of Molecular Physiology, Max Planck Society;

Lawonn,  Peter
Max Planck Institute of Molecular Physiology, Max Planck Society;

Tinel,  Hanna
Max Planck Institute of Molecular Physiology, Max Planck Society;

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Wehner, F., Lawonn, P., & Tinel, H. (2002). Ionic mechanisms of regulatory volume increase (RVI) in the human hepatoma cell-line HepG2. Pflügers Archiv - European Journal of Physiology, 443(5-6): 1, pp. 779-790. Retrieved from http://dx.doi.org/10.1007/s00424-001-0765-x.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0014-0ED4-E
Abstract
We studied the effects of hypertonic stress on ion transport and cell volume regulation (regulatory volume increase; RVI) in the human tumor cell-line HepG2. Ion conductances were monitored in intracellular current-clamp measurements with rapid ion-substitutions and in whole-cell patch-clamp recordings; intracellular pH buffering capacity and activation of Na+/H+ antiport were determined fluorometrically; the rates of Na+-K(+)2Cl- symport and Na+/K+-ATPase were quantified on the basis of time-dependent and furosemide- or ouabain- sensitive Rb-86(+) uptake, respectively; changes in cell volume were recorded by means of confocal laser-scanning microscopy. It was found that hypertonic conditions led to the activation of a cation conductance that was inhibited by Gd3+, flufenamate as well as amiloride, but not by benzamil or ethyl-isopropyl- amiloride (EIPA). Most likely, this cation conductance was non- selective for Na+ over K+. Hypertonic stress did not change K+ conductance, whereas possible changes in Cl- conductance remain ambiguous. The contribution of Na+/H+ antiport to the RVI process appeared to be minor. Under hypertonic conditions an approximately 3.5-fold stimulation of NaK+-2Cl- symport was observed but this transporter did not significantly contribute to the overall RVI process. Hypertonic stress did not increase the activity of Na+/K(+)ATPase, which even under isotonic conditions appeared to be working at its limit. It is concluded that the main mechanism in the RVI of HepG2 cells is the activation of a novel non-selective cation conductance. In contrast, there is little if any contribution of K+ conductance, Na+/H+ antiport, Na+-K+-2Cl- symport, and Na+/K+- ATPase to this process.