Enhancement of Ca2+ Influx and Ciliary Beating by Membrane Hyperpolarization due to ATP-Sensitive K+ Channel Opening in Mouse Airway Epithelial Cells

2013 ◽  
Vol 347 (1) ◽  
pp. 145-153 ◽  
Author(s):  
Teruya Ohba ◽  
Eiji Sawada ◽  
Yoshiaki Suzuki ◽  
Hisao Yamamura ◽  
Susumu Ohya ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
K Channel ◽  
Airway Epithelial ◽  
Membrane Hyperpolarization ◽  
Ciliary Beating ◽  
Channel Opening

scholarly journals Ciliary Beating Recovery in Deficient Human Airway Epithelial Cells after Lentivirus Ex Vivo Gene Therapy

PLoS Genetics ◽  
2009 ◽  
Vol 5 (3) ◽  
pp. e1000422 ◽  
Author(s):  
Brigitte Chhin ◽  
Didier Negre ◽  
Olivier Merrot ◽  
Jacqueline Pham ◽  
Yves Tourneur ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Epithelial Cells ◽  
Ex Vivo ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Ciliary Beating ◽  
Human Airway ◽  
Ex Vivo Gene Therapy ◽  
Human Airway Epithelial Cells

Basolateral K+ channels in airway epithelia. II. Role in Cl- secretion and evidence for two types of K+ channel

1990 ◽  
Vol 258 (6) ◽  
pp. L343-L348 ◽  
Author(s):  
J. D. McCann ◽  
M. J. Welsh
Keyword(s):  
Epithelial Cells ◽  
Time Course ◽  
Basolateral Membrane ◽  
Airway Epithelial Cells ◽  
K Channel ◽  
Airway Epithelial ◽  
K Channels ◽  
Cl Secretion ◽  
Transient Component ◽  
Permeable Supports

We previously described a Ca2(+)-activated K+ channel (KCLIC) in airway epithelial cells [J. D. McCann, J. Matsuda, M. Garcia, G. Kaczorowski, and M. J. Welsh. Am. J. Physiol 258 (Lung Cell. Mol. Physiol. 2): L334-L342, 1990]. To determine whether the KCLIC channel is a basolateral membrane channel and to understand its role in Cl- secretion, we studied airway epithelial cells grown on permeable supports. When cells were stimulated with A23187, charybdotoxin (ChTX) inhibited Cl- secretion and 86Rb efflux at the same concentrations, indicating that the KCLIC channel is required for Ca2(+)-stimulated Cl- secretion. We also investigated the function of K+ channels in adenosine 3',5'-cyclic monophosphate-stimulated secretion. Addition of isoproterenol caused a biphasic increase in Cl- secretion; the time course of the transient component correlated with the time course of the isoproterenol-induced increase in Ca2+ concentration [( Ca2+]c). ChTX inhibited the transient component, but not the prolonged component of secretion; Ba2+ inhibited the sustained component. These results suggest that when cells are grown on permeable supports isoproterenol-induced secretion depends on activation of two types of K+ channel: the KCLIC channel that is stimulated initially and a ChTX-insensitive K+ channel that is stimulated during sustained secretion. This conclusion was supported by measurement of 86Rb efflux from cell monolayers

Stretch-activated channels in airway epithelial cells

1993 ◽  
Vol 265 (5) ◽  
pp. C1306-C1318 ◽  
Author(s):  
Y. K. Kim ◽  
E. R. Dirksen ◽  
M. J. Sanderson
Keyword(s):  
Epithelial Cells ◽  
Basolateral Membrane ◽  
Reversal Potential ◽  
Airway Epithelial Cells ◽  
K Channel ◽  
Resting Membrane Potential ◽  
Airway Epithelial ◽  
Open Probability ◽  
Open States ◽  
Slow Time Constant

Two type of stretch-activated (SA) ion channels were identified in the basolateral membrane of isolated rabbit airway epithelial cells by patch-clamp techniques. Pressure activation and deactivation of one channel, which had a conductance of 29 pS, occurred after a delay of approximately 20-30 s. The open probability of this delayed stretch-activated (DSA) channel was increased from < 0.01 to 0.45 at 50 mmHg of suction. The reversal potential of the DSA channel, calculated from the pipette potential at which membrane currents reversed [-31.3 +/- 3.6 (SD) mV] and the resting membrane potential (-27.8 +/- 3.3 mV) was +3.5 +/- 3.3 mV. None of the equilibrium potentials of the ions used were similar to the calculated reversal potential of the DSA channel, suggesting that this channel is nonselective for cations. The DSA channel gating behavior was characterized by bursts of rapid transitions between open and closed states. The distribution of the open and closed times revealed that this gating behavior could be fitted with two open states and two closed states. Only the slow time constant of the closed state was decreased by suction. The second SA channel was selective for K+ and had a conductance of 65 pS but a long delay was not associated with the pressure sensitivity of this channel. The open probability of the K(+)-selective SA channel was increased from < 0.01 to 0.30 by 50 mmHg of suction. The K(+)-selective SA channel was distinct from the well-characterized basolateral K+ channel.

scholarly journals Expression of intermediate-conductance, Ca2+-activated K+ channel (KCNN4) in H441 human distal airway epithelial cells

2006 ◽  
Vol 291 (5) ◽  
pp. L957-L965 ◽  
Author(s):  
S. M. Wilson ◽  
S. G. Brown ◽  
N. McTavish ◽  
R. P. McNeill ◽  
E. M. Husband ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Membrane Conductance ◽  
Airway Epithelial Cells ◽  
K Channel ◽  
Channel Blockers ◽  
Resting Cells ◽  
Airway Epithelial ◽  
Distal Airway

Electrophysiological studies of H441 human distal airway epithelial cells showed that thapsigargin caused a Ca2+-dependent increase in membrane conductance ( GTot) and hyperpolarization of membrane potential ( Vm). These effects reflected a rapid rise in cellular K+ conductance ( GK) and a slow fall in amiloride-sensitive Na+ conductance ( GNa). The increase in GTot was antagonized by Ba2+, a nonselective K+ channel blocker, and abolished by clotrimazole, a KCNN4 inhibitor, but unaffected by other selective K+ channel blockers. Moreover, 1-ethyl-2-benzimidazolinone (1-EBIO), which is known to activate KCNN4, increased GK with no effect on GNa. RT-PCR-based analyses confirmed expression of mRNA encoding KCNN4 and suggested that two related K+ channels (KCNN1 and KCNMA1) were absent. Subsequent studies showed that 1-EBIO stimulates Na+ transport in polarized monolayers without affecting intracellular Ca2+ concentration ([Ca2+]i), suggesting that the activity of KCNN4 might influence the rate of Na+ absorption by contributing to GK. Transient expression of KCNN4 cloned from H441 cells conferred a Ca2+- and 1-EBIO-sensitive K+ conductance on Chinese hamster ovary cells, but this channel was inactive when [Ca2+]i was <0.2 μM. Subsequent studies of amiloride-treated H441 cells showed that clotrimazole had no effect on Vm despite clear depolarizations in response to increased extracellular K+ concentration ([K+]o). These findings thus indicate that KCNN4 does not contribute to Vm in unstimulated cells. The present data thus establish that H441 cells express KCNN4 and highlight the importance of GK to the control of Na+ absorption, but, because KCNN4 is quiescent in resting cells, this channel cannot contribute to resting GK or influence basal Na+ absorption.

scholarly journals Calmodulin-Dependent Regulation of Overexpressed but Not Endogenous TMEM16A Expressed in Airway Epithelial Cells

Membranes ◽  
2021 ◽  
Vol 11 (9) ◽  
pp. 723
Author(s):  
Khaoula Talbi ◽  
Jiraporn Ousingsawat ◽  
Raquel Centeio ◽  
Rainer Schreiber ◽  
Karl Kunzelmann
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelial Cells ◽  
Hek293 Cells ◽  
K Channel ◽  
Airway Epithelial ◽  
Colonic Epithelial Cells ◽  
Cl Channel ◽  
Endogenous Expression ◽  
Regulatory Properties ◽  
Limit Evidence

Regulation of the Ca2+-activated Cl− channel TMEM16A by Ca2+/calmodulin (CAM) is discussed controversially. In the present study, we compared regulation of TMEM16A by Ca2+/calmodulin (holo-CAM), CAM-dependent kinase (CAMKII), and CAM-dependent phosphatase calcineurin in TMEM16A-overexpressing HEK293 cells and TMEM16A expressed endogenously in airway and colonic epithelial cells. The activator of the Ca2+/CAM-regulated K+ channel KCNN4, 1-EBIO, activated TMEM16A in overexpressing cells, but not in cells with endogenous expression of TMEM16A. Evidence is provided that CAM-interaction with TMEM16A modulates the Ca2+ sensitivity of the Cl− channel. Enhanced Ca2+ sensitivity of overexpressed TMEM16A explains its activity at basal (non-elevated) intracellular Ca2+ levels. The present results correspond well to a recent report that demonstrates a Ca2+-unbound form of CAM (apo-CAM) that is pre-associated with TMEM16A and mediates a Ca2+-dependent sensitization of activation (and inactivation). However, when using activators or inhibitors for holo-CAM, CAMKII, or calcineurin, we were unable to detect a significant impact of CAM, and limit evidence for regulation by CAM-dependent regulatory proteins on receptor-mediated activation of endogenous TMEM16A in airway or colonic epithelial cells. We propose that regulatory properties of TMEM16A and and other members of the TMEM16 family as detected in overexpression studies, should be validated for endogenous TMEM16A and physiological stimuli such as activation of phospholipase C (PLC)-coupled receptors.

Differentiation of human pluripotent stem cells into airway epithelial cells

Pneumologie ◽  
2015 ◽  
Vol 69 (07) ◽  
Author(s):  
S Ulrich ◽  
S Weinreich ◽  
R Haller ◽  
S Menke ◽  
R Olmer ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
Pluripotent Stem Cells ◽  
Airway Epithelial Cells ◽  
Human Pluripotent Stem Cells ◽  
Airway Epithelial
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