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1 Unitat de Senyalització Cellular, Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, 08003 Barcelona, Spain; and 2 Medical Research Council Clinical Sciences Centre, Imperial College, London W12 0NN, United Kingdom
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 (HBE) cell line 16HBE14o
.
These cells, under isotonic conditions, present a K+
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, for the activation of maxi K+ channels.
cell volume regulation; calcium; potassium channels; KCNMA1; airways; 16HBE14o; TRPV4
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