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J. Biol. Chem., Vol. 275, Issue 45, 34849-34852, November 10, 2000

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ACCELERATED PUBLICATION
Contribution of the IsK (MinK) Potassium Channel Subunit to Regulatory Volume Decrease in Murine Tracheal Epithelial Cells^*

Hagar Lock and Miguel A. Valverde

From the Cell Signalling Unit, Department of Experimental Sciences, Universitat Pompeu Fabra, C/Dr. Aiguader 80, 08003 Barcelona, Spain

The cell volume regulatory response following hypotonic shocks is often achieved by the coordinated activation of K⁺ and Cl channels. In this study, we investigate the identity of the K⁺ and Cl channels that mediate the regulatory volume decrease (RVD) in ciliated epithelial cells from murine trachea. RVD was inhibited by tamoxifen and 1,9-dideoxyforskolin, two agents that block swelling-activated Cl channels. These data suggest that swelling-activated Cl channels play an important role in cell volume regulation in murine tracheal epithelial cells. Ba²⁺ and apamin, inhibitors of K⁺ channels, were without effect on RVD, while tetraethylammoniun had little effect on RVD. In contrast, clofilium, an inhibitor of the KvLQT/IsK potassium channel complex potently inhibited RVD, suggesting a role for the KvLQT/IsK channel complex in cell volume regulation by tracheal epithelial cells. To investigate further the role of KvLQT/IsK channels in RVD, we used IsK knock-out mice. When exposed to hypotonic solutions, tracheal cells from IsK(+/+) mice underwent RVD, whereas cells from IsK(/) failed to recover their normal size. These data suggest that the IsK potassium subunit plays an important role in RVD in murine tracheal epithelial cells.

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