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Articles in PresS, published online ahead of print August 14, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00245.2002
Submitted on May 28, 2002
Accepted on July 31, 2002
1 Cell Signalling, Universitat Pompeu Fabra, Barcelona, Spain
2 Clinical Sciences Centre, MRC, London, United Kingdom
* To whom correspondence should be addressed. E-mail: miguel.valverde{at}cexs.upf.es.
The cell regulatory volume decrease (RVD) response triggered by hypotonic solutions is mainly achieved by the coordinated activity of Cl- and K+ channels. We now describe the molecular nature of the K+ channels involved in the RVD response of the human bronchial epithelial cell line 16HBE14o-. These cells, under isotonic conditions, present a potassium current consistent with the activity of Maxi K+ channels, confirmed by RT-PCR and western-blot. Single-channel and whole-cell Maxi K+ currents were readily and reversibly activated following the exposure of HBE cells to a 28% hypotonic solution. Both Maxi K+ current activation and RVD response showed calcium dependency, inhibition by TEA, Ba2+, iberiotoxin and the cationic channel blocker Gd3+ but were insensitive to clofilium, clotrimazole and apamin. The presence of the recently cloned swelling-activated, Gd3+-sensitive cation channels (TRPV4, also known as OTRPC4, TRP12 or VR-OAC) was detected by RT-PCR in HBE cells. This channel, TRPV4, which senses changes in volume, might provide the pathway for Ca2+ influx under hypotonic solutions, and consequently, the activation of Maxi K+ channels.
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