Department of Cell Physiology, National Institute for Physiological Sciences; and Core Research for Evolutional Science and Technology of Japan Science and Technology Corporation, Okazaki 444-8585, Japan
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ABSTRACT |
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Parallel activation of
Ca2+-dependent K+ channels and volume-sensitive
Cl channels is known to be responsible for KCl efflux
during regulatory volume decrease (RVD) in human epithelial Intestine
407 cells. The present study was performed to identify the
K+ channel type. RT-PCR demonstrated mRNA expression of
Ca2+-activated, intermediate conductance K+
(IK), but not small conductance K+ (SK1) or large
conductance K+ (BK) channels in this cell line. Whole cell
recordings showed that ionomycin or hypotonic stress activated inwardly
rectifying K+ currents that were reversibly blocked by IK
channel blockers [clotrimazole (CLT) and charybdotoxin] but not by SK
and BK channel blockers (apamin and iberiotoxin). Inside-out recordings
revealed the existence of CLT-sensitive single K+-channel
activity, which exhibited an intermediate unitary conductance (30 pS at
100 mV). The channel was activated by cytosolic Ca2+ in
inside-out patches and by a hypotonic challenge in cell-attached patches. The RVD was suppressed by CLT, but not by apamin or
iberiotoxin. Thus we conclude that the IK channel is involved in the
RVD process in these human epithelial cells.
Ca2+-activated K+ channel; patch clamp; clotrimazole; osmotic swelling
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INTRODUCTION |
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CELL VOLUME REGULATION
is an essential function for animal cells because osmotic
perturbation is coupled to a variety of physiological and pathological
processes, such as cell proliferation, cell differentiation, and
apoptosis (23, 37). Under hypoosmotic conditions,
a regulatory volume decrease (RVD) is accomplished by efflux of
K+, Cl, and organic osmolytes, which results
in the extrusion of osmotically obliged water in a variety of cell
types (15, 35, 36).
Osmotic cell swelling has been reported to be associated with the activation of different types of K+ channels, including Ca2+-activated K+ channels (5, 21, 27, 39, 50, 52, 57, 58), stretch-activated K+ channels (8, 31, 42, 54), Ca2+- and stretch-activated K+ channels (20, 38), voltage-gated K+ channels (1, 6, 9, 43, 46), MinK channels (3, 28), and two-pore (2P) domain TASK channels (33). Summarizing previous observations, Pasantes-Morales and Morales-Mulia (40) recently suggested that the RVD in most types of epithelial cells involves Ca2+-dependent K+ channels, whereas that in nonepithelial cells involves Ca2+-independent K+ channels.
Ca2+-activated K+ channels are ubiquitously
distributed in mammalian cells, and these channels play important roles
in many different cell functions. On the basis of their
electrophysiological characteristics, three major classes of
Ca2+-activated K+ channels have been described
(24): voltage-dependent, large-conductance K+
channels (BK or hSlo for its -subunit); voltage-independent, small-conductance K+ channels (SK); and inwardly
rectifying, intermediate-conductance K+ channels (IK). It
is well known that the BK, IK, and SK channel proteins are products of
three different genes (10, 56). Although there is ample
evidence that the RVD process involves Ca2+-activated
K+ channels in Intestine 407 cells (13, 14),
it is not known which type of Ca2+-activated K+
channel protein is involved. Thus, in the present study, we had the aim
of determining the molecular identity of this volume-regulatory K+ channel.
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MATERIALS AND METHODS |
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Cell culture. A human epithelial cell line, Intestine 407, was cultured in monolayer in Fischer's medium supplemented with 10% newborn bovine serum, as described previously (13). For patch-clamp and volume measurements, cells were detached from the plastic substrate and suspended, as described previously (22). After cell culture was suspended with agitation, the cells were placed in a chamber (0.3 ml) and, after they had attached to the glass bottom, perfused with bath solution at about 3 ml/min by gravity feed from reservoirs. Cells used for some cell-attached recordings were first loaded with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) by preincubation with 50 µM BAPTA-AM for 15 min at 37°C.
RT-PCR.
Poly(A)+ RNA was extracted from Intestine 407 cells by
using the Direct mRNA purification kit with magnetic porous glass (MPG; CPG, Lincoln Park, NJ). Briefly, the cells were detached from culture
flasks and homogenized in a buffer containing LiDs and ethylene
glycol-bis(-aminoethyl
ether)-N,N,N',N'-tetraacetic acid (EGTA). Poly(A)+ RNA was extracted with MPG-bound
oligo(dT)25s. The isolated poly(A)+ RNA was
reverse transcribed by using the SuperScript preamplification system
(Invitrogen, Carlsbad, CA). The resultant first strand cDNA was used
for PCR. Primers were designed and synthesized according to the
published sequences of cDNA encoding human SK1 (hSK1), human IK
(hIK) (18), and human BK
-subunit (hSlo)
(51), as summarized in Table
1. As a positive control, we also
amplified mRNA of glyceraldehyde-3-phosphate dehydrogenase (GAPDH)
using the primers listed in Table 1.
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Cell volume measurements. Cell volume was measured at room temperature (22-26°C) or 37°C by an electronic sizing technique with a Coulter-type cell size analyzer (CDA-500; Sysmex, Kobe, Japan), as previously described (13). The mean volume of the cell population was calculated from the cell volume distribution after the machine was calibrated with latex beads of known volume.
Isotonic (310 mosmol/kgH2O) or hypotonic (200 mosmol/kgH2O) solution consisted of (in mM) 95 NaCl, 4.5 KCl, 1 MgCl2, 1 CaCl2, 110 or 0 mannitol, and 5 N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)/NaOH (pH 7.3).Patch-clamp experiments.
Whole cell and single-channel recordings were performed at room
temperature. Pipettes were pulled from borosilicate glass capillaries
with a micropipette puller (P-2000; Sutter Instruments, Novato, CA).
The electrode had a resistance of 1.8-2.5 M for whole cell
recordings and of around 7 M
for single-channel recordings when
filled with pipette solution. Data were acquired using an EPC-9
amplifier and Pulse software (HEKA Electroniks, Lambrecht, Germany).
Current signals were low-pass filtered at 2.9 and 1.0 kHz using a
four-pole Bessel filter and digitized at 10 and 4 kHz, in whole cell
and single-channel recordings, respectively. Sampled data were analyzed
by an original software application called PulseMate and Origin 6.1 (Origin Lab, Northampton, MA). In most experiments, a grounded Ag-AgCl
pellet electrode was placed in the perfusion solution. When
Cl
-free bath solution was used, a 3 M KCl-agar bridge was used.
Chemicals. EGTA, BAPTA, BAPTA-AM, and Na-gluconate were purchased from Wako Pure Chemical Industries (Osaka, Japan), and clofilium was from Research Biochemicals (Natick, MA). All other reagents were obtained from Sigma-Aldrich Japan (Tokyo, Japan). Stock solutions of 5 mM CLT, 50 mM NPPB, and 1 mM ionomycin were prepared in dimethyl sulfoxide (DMSO). Tetraethylammonium (TEA), charybdotoxin (ChTX), iberiotoxin, and apamin were directly added to the appropriate solution before use.
Statistical analysis. Data are presented as means ± SE of n observations. Statistical differences in data were evaluated by one-dimensional ANOVA and Scheffé's post hoc multiple comparison tests. Data were considered to be significant at P < 0.01.
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RESULTS |
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Molecular expression of IK channels.
RT-PCR was performed on RNA isolated from Intestine 407 cells to
examine the expression of five types of Ca2+-activated
K+ channels. As shown in Fig.
1 (lanes 2 and 4),
DNA fragments of expected size at 241 and 457 bp were amplified by
hIK-specific primers (Table 1, pairs 1 and 2)
from reverse transcribed cDNA. The nucleotide sequence of these PCR
products was completely identical to the corresponding sequence in the
hIK channel (18). However, no PCR product was amplified
when reverse transcriptase was omitted from the reaction (Fig. 1,
lanes 3 and 5).
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Functional expression of IK channels.
When Intestine 407 cells were dialyzed with low-Cl
pipette solution and exposed to Cl
-free bath solution
containing a Cl
channel blocker, NPPB (50 µM), addition
of ionomycin (1 µM) increased whole cell currents, as observed
previously (17). As shown in Fig.
2A, the ionomycin-activated
current exhibited slight inward rectification. Time-dependent
activation was observed at large positive potentials (upper
inset). When the extracellular K+ concentration
([K+]o) was increased, the reversal potential
(Erev) shifted in the positive direction. The
Erev shift per 10-fold increase in
[K+]o was 53 mV (lower inset),
indicating high selectivity of K+
(PNa/PK < 0.01). A
wide spectrum K+ channel blocker (24, 56), TEA
(20 mM), partially suppressed the currents (Fig. 2Ba). The
current was largely abolished by 200 nM CLT (Fig. 2Bb),
which is a blocker specific to IK (53). The
ionomycin-activated current was also sensitive to 20 nM ChTX (Fig.
2Bc), which is known to block not only BK channels
(32) but also IK channels (11, 45). The
Erev values for TEA-, CLT-, and ChTX-sensitive
currents were
80.6 ± 5.3,
82.8 ± 4.2, and
83.6 ± 3.0 mV (n = 6), respectively, and these values are
close to that of the equilibrium potential for K+ (
90
mV). In contrast, the ionomycin-activated current was insensitive to
100 nM apamin (Fig. 2Bd) and 100 nM iberiotoxin (data not
shown, n = 3), blockers that are specific to SK and BK
(24, 56), respectively.
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Swelling-induced activation of IK channels.
A hypotonic challenge reversibly induced increases in cell size and
membrane currents in Intestine 407 cells under whole cell clamp in
which low-Cl pipette solution and Cl
-free
bath solution containing 50 µM NPPB were used (Fig.
4A). The profile of the
swelling-induced current (Fig. 4Aa) and the I-V relation
(Fig. 4Ac) were similar to those of ionomycin-induced current (Fig. 2A). The swelling-induced current was very
sensitive to CLT (200 nM; Fig. 4Ab). The
Erev for CLT-sensitive current was
84.3 ± 7.2 mV (Fig. 4Ac). When intracellular Ca2+
was chelated with 5 mM BAPTA introduced to the pipette solution, a
hypotonic challenge induced cell swelling but activated whole cell
currents very little, as shown in Fig. 4B.
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Involvement of IK channel in the RVD process.
After Intestine 407 cells were exposed to hypotonic solution at room
temperature, the mean cell volume promptly increased and then gradually
recovered (Fig. 6), as observed
previously (13). The RVD was inhibited by the application
of 200 nM CLT (Fig. 6A). However, application of SK and BK
channel blockers, apamin (100 nM) and iberiotoxin (100 nM), failed to
significantly affect the RVD (Fig. 6A). Also, the RVD was
not inhibited by another K+ channel blocker, clofilium (100 µM; Fig. 6B), which is known to block both KCNQ (MinK)
(2) and KCNK5 (TASK) channels (33). CLT
sensitivity and clofilium insensitivity of the RVD that were essentially the same were observed at 37°C (data not shown,
n = 6 each). In light of these data, we conclude that
the K+ channel type involved in the RVD of Intestine 407 cells is the CLT-sensitive IK channel.
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DISCUSSION |
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A number of types of K+ channels have been demonstrated to be involved in K+ efflux during volume regulation after osmotic swelling (40). In human epithelial Intestine 407 cells, we previously concluded that the volume-regulatory K+ channel is classified into a Ca2+-activated one, based on the following observations: the RVD was inhibited by chelation of cytosolic Ca2+ and by application of a K+ channel blocker Ba2+ (13), osmotic cell swelling brought about activation of Ca2+-dependent K+ conductance under voltage-clamp (13), and swelling-induced K+ conductance activation was associated with an increase in the cytosolic free Ca2+ concentration measured with Ca2+-selective microelectrodes (14). The present study provided five lines of evidence that the identity of this channel is an hIK channel (16, 18): 1) RT-PCR demonstrated exclusive expression of hIK mRNA (Fig. 1), 2) whole cell K+ currents activated by ionomycin exhibited weak voltage dependence and were sensitive to the IK channel blockers CLT and ChTX (Fig. 2), 3) single K+-channel events induced by an increase in cytosolic Ca2+ exhibited slight inward rectification with an intermediate unitary conductance and were sensitive to CLT (Fig. 3), 4) swelling-induced whole cell and single-channel currents were both inhibited by the presence of CLT and by cytosolic Ca2+ chelation (Figs. 4 and 5), and 5) the RVD was inhibited by CLT (Fig. 6A).
Maxi-K+ or BK channels, which exhibit striking voltage
dependence (24), have been found to be activated during
osmotic swelling in a number of other cell types (4, 7, 19, 44,
49). In human osteoblast-like C1 cells, BK channels, together
with IK channels, were shown to be involved in the RVD
(58). In Intestine 407 cells, however, a BK channel
blocker, iberiotoxin, failed to inhibit the RVD and
Ca2+-activated whole cell K+ currents. Also,
swelling- or Ca2+-activated K+ channel events
exhibited weak voltage dependence and never exhibited Maxi unitary
conductance. Moreover, mRNA of the BK channel -subunit hSlo was
never detected by RT-PCR. Involvement of apamin-sensitive SK channels
in the RVD of Intestine 407 cells could also be excluded by the
observation that there was no RT-PCR signal for SK1 and that the RVD
and the Ca2+-activated whole cell K+ currents
were not sensitive to apamin.
Recently, Niemeyer et al. (33) provided clear evidence for the involvement of the TASK-2 type of 2P domain K+ channels in the RVD of Ehrlich ascites tumor cells. It is known that 2P domain K+ channels are independent of cytosolic Ca2+ and are insensitive to Ba2+ (41). Thus, in Intestine 407 cells, TASK-2 channels may not play a role in the RVD, which was found to be dependent on cytosolic Ca2+ (13, 14) and sensitive to Ba2+ (13). In the present study, in fact, the RVD of Intestine 407 cells was found to be totally insensitive to clofilium (Fig. 6B), which is known to block TASK-2 (33). Clofilium insensitivity may also rule out the involvement of the MinK channel, which is sensitive to this class III antiarrhythmic drug (2).
The involvement of IK channels in the RVD process has been reported in mouse erythroid cells (32), human T lymphocytes (21), and human tracheal cells (25). Vázquez et al. (55) reported that CFTR expression is a prerequisite to swelling-induced IK channel activation in tracheal cells. However, the present study provided an example of the involvement of IK channel activation in Intestine 407 cells, which do not express CFTR (12). In Intestine 407 cells, IK channels could be activated by a cytosolic Ca2+ rise due to swelling, as well as due to stimulation of phospholipase C-linked P2Y2 receptor by ATP released from swollen cells (37).
The RVD mechanism is of essential importance to some cell types, such as enterocytes, in which the swelling-inducing osmotic gradient across the cell membrane is produced by active solute uptake (29, 34, 47). K+ channel activation may play an important role in volume regulation during Na+-coupled absorption of organic solutes in small intestine, as Ba2+-sensitive K+ conductance activation was observed in Necturus small intestinal enterocytes during exposure to galactose (25, 26). Single-channel recordings demonstrated that L-alanine application activated Ca2+-dependent K+ channels with an intermediate unitary conductance in Necturus enterocytes (48). In guinea pig jejunum enterocytes, the RVD that takes place after osmotic swelling due to Na+-coupled solute absorption was found to be inhibited by ChTX (29, 30). Our results suggest that IK channels play, at least in part, a volume-regulatory role in small intestinal epithelial cells during Na2+-dependent organic solute absorption in vivo.
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ACKNOWLEDGEMENTS |
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We are grateful to R.Z. Sabirov for discussion, to K. Shigemoto, S. Tanaka, and E.L. Lee for technical assistance, and to T. Okayasu for secretarial assistance.
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FOOTNOTES |
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Address for reprint requests and other correspondence: Y. Okada, Dept. of Cell Physiology, National Institute for Physiological Sciences, Myodaiji-cho, Okazaki 444-8585, Japan (E-mail: okada{at}nips.ac.jp).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
First published September 11, 2002;10.1152/ajpcell.00132.2002
Received 20 March 2002; accepted in final form 4 September 2002.
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