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Am J Physiol Cell Physiol 281: C1978-C1990, 2001;
0363-6143/01 $5.00
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Vol. 281, Issue 6, C1978-C1990, December 2001

Role of JNK in hypertonic activation of Clminus -dependent Na+/H+ exchange in Xenopus oocytes

Greg G. Goss1, Lianwei Jiang2,3, David H. Vandorpe2,3, Dawn Kieller1, Marina N. Chernova2,3, Marilyn Robertson1, and Seth L. Alper2,3,4

1 Department of Biological Science, University of Alberta, Edmonton, Alberta, Canada T6G 2E9, 2 Molecular Medicine and Renal Units, Beth Israel Deaconess Medical Center, Boston; and Departments of 3 Medicine and 4 Cell Biology, Harvard Medical School, Boston, Massachusetts 02215

In the course of studying the hypertonicity-activated ion transporters in Xenopus oocytes, we found that activation of endogenous oocyte Na+/H+ exchange activity (xoNHE) by hypertonic shrinkage required Cl-, with an EC50 for bath [Cl-] of ~3 mM. This requirement for chloride was not supported by several nonhalide anions and was not shared by xoNHE activated by acid loading. Hypertonicity-activated xoNHE exhibited an unusual rank order of inhibitory potency among amiloride derivatives and was blocked by Cl- transport inhibitors. Chelation of intracellular Ca2+ by injection of EGTA blocked hypertonic activation of xoNHE, although many inhibitors of Ca2+-related signaling pathways were without inhibitory effect. Hypertonicity activated oocyte extracellular signal-regulated kinase 1/2 (ERK1/2), but inhibitors of neither ERK1/2 nor p38 prevented hypertonic activation of xoNHE. However, hypertonicity also stimulated a Cl--dependent increase in c-Jun NH2-terminal kinase (JNK) activity. Inhibition of JNK activity prevented hypertonic activation of xoNHE but not activation by acid loading. We conclude that hypertonic activation of Na+/H+ exchange in Xenopus oocytes requires Cl- and is mediated by activation of JNK.

Na+/H+ exchange; c-Jun NH2-terminal kinase; extracellular signal-regulated kinase; p38; transport; SP600125; U-0126


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