scholarly journals Development of a Photoswitchable Lithium-Sensitive Probe to Analyze Nonselective Cation Channel Activity in Migrating Cancer Cells

2019 ◽  
Vol 95 (5) ◽  
pp. 573-583 ◽  
Author(s):  
Jinxin V. Pei ◽  
Sabrina Heng ◽  
Michael L. De Ieso ◽  
Georgina Sylvia ◽  
Mohamad Kourghi ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Cation Channel ◽  
Nonselective Cation Channel ◽  
Channel Activity

Ca(2+)-activated nonselective cation channel in apical membrane of vestibular dark cells

1992 ◽  
Vol 262 (6) ◽  
pp. C1423-C1429 ◽  
Author(s):  
D. C. Marcus ◽  
S. Takeuchi ◽  
P. Wangemann
Keyword(s):  
Single Channel ◽  
Apical Membrane ◽  
Cation Channel ◽  
Nonselective Cation Channel ◽  
Channel Activity ◽  
Dark Cells ◽  
Linear Current ◽  
Current Voltage ◽  
K Secretion ◽  
Vestibular Dark Cells

Patch-clamp recordings were made on cell-attached and excised apical membrane from dark cells of the semicircular canal of the gerbil. These cells are thought to secrete K+ and absorb Na+ from the luminal fluid (endolymph). Single-channel events were identified as being equally conductive (27.6 +/- 0.4 pS; n = 48) for K+, Na+, Rb+, Li+, and Cs+ and 1.4 times more permeable to NH4+ but not permeable to Cl-, Ca2+, Ba2+, nor to N-methyl-D-glucamine. The channels displayed linear current-voltage relations that passed nearly through the origin (intercept: -2.6 +/- 0.5 mV; n = 48) when conductive monovalent cations were present on both sides of the membrane in equal concentrations. Channel activity required the presence of Ca2+ at the cytosolic face; there was no activity at less than or equal to 10(-7) M Ca2+ and full activity at greater than or equal to 10(-5) M Ca2+. Cell-attached recordings had a mean reversal voltage of -36.4 +/- 7.9 mV (n = 7), which was interpreted to reflect the intracellular potential of dark cells under the present conditions. We have identified a nonselective cation channel in the apical membrane of vestibular dark cells that might participate in K+ secretion or Na+ absorption under stimulated conditions, but the density appears to be insufficient to fully account for the transepithelial K+ flux.

Calcium-Sensing Receptor Stimulation Induces Nonselective Cation Channel Activation in Breast Cancer Cells

2006 ◽  
Vol 211 (2) ◽  
pp. 127-137 ◽  
Author(s):  
Yassine El Hiani ◽  
Ahmed Ahidouch ◽  
Morad Roudbaraki ◽  
Stéphanie Guenin ◽  
Gérard Brûlé ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cation Channel ◽  
Nonselective Cation Channel ◽  
Calcium Sensing Receptor ◽  
Receptor Stimulation ◽  
Channel Activation ◽  
Calcium Sensing

scholarly journals Loss of primary cilia increases polycystin-2 and TRPV4 and the appearance of a nonselective cation channel in the mouse cortical collecting duct

2019 ◽  
Vol 317 (3) ◽  
pp. F632-F637 ◽  
Author(s):  
Takamitsu Saigusa ◽  
Qiang Yue ◽  
Marlene A. Bunni ◽  
P. Darwin Bell ◽  
Douglas C. Eaton
Keyword(s):  
Collecting Duct ◽  
Cation Channel ◽  
Conditional Knockout ◽  
Nonselective Cation Channel ◽  
Channel Activity ◽  
Open Probability ◽  
Duct Cells ◽  
Collecting Ducts ◽  
Collecting Duct Cells

Flow-related bending of cilia results in Ca2+ influx through a polycystin-1 (Pkd1) and polycystin-2 (Pkd2) complex, both of which are members of the transient receptor potential (TRP) family (TRPP1 and TRPP2, respectively). Deletion of this complex as well as cilia result in polycystic kidney disease. The Ca2+ influx pathway has been previously characterized in immortalized collecting duct cells without cilia and found to be a 23-pS channel that was a multimere of TRPP2 and TRPV4. The purpose of the present study was to determine if this TRPP2 and TRPV4 multimere exists in vivo. Apical channel activity was measured using the patch-clamp technique from isolated split-open cortical collecting ducts from adult conditional knockout mice with ( Ift88flox/flox) or without ( Ift88−/−) cilia. Single tubules were isolated for measurements of mRNA for Pkd1, Pkd2, Trpv4, and epithelial Na+ channel subunits. The predominant channel activity from Ift88flox/flox mice was from epithelial Na+ channel [5-pS Na+-selective channels with long mean open times (475.7 ± 83.26 ms) and open probability > 0.2]. With the loss of cilia, the predominant conductance was a 23-pS nonselective cation channel (reversal potential near 0) with a short mean open time (72 ± 17 ms), open probability < 0.08, and a characteristic flickery opening. Loss of cilia increased mRNA levels for Pkd2 and Trpv4 from single isolated cortical collecting ducts. In conclusion, 23-pS channels exist in vivo, and activity of this channel is elevated with loss of cilia, consistent with previous finding of an elevated-unregulated Ca2+-permeable pathway at the apical membrane of collecting duct cells that lack cilia.

A mechanogated nonselective cation channel in proximal tubule that is ATP sensitive

2002 ◽  
Vol 283 (1) ◽  
pp. F93-F104 ◽  
Author(s):  
Craig G. Hurwitz ◽  
Vivian Y. Hu ◽  
Alan S. Segal
Keyword(s):  
Proximal Tubule ◽  
Basolateral Membrane ◽  
Cation Channel ◽  
Transepithelial Transport ◽  
Single Channels ◽  
Epithelial Polarity ◽  
Nonselective Cation Channel ◽  
Channel Activity ◽  
Entry Pathway ◽  
Hypotonic Swelling

Ion channels that are gated in response to membrane deformation or “stretch” are empirically designated stretch-activated channels. Here we describe a stretch-activated nonselective cation channel in the basolateral membrane (BLM) of the proximal tubule (PT) that is nucleotide sensitive. Single channels were studied in cell-intact and cell-free patches from the BLM of PT cells that maintain their epithelial polarity. The limiting inward Cs+ conductance is ∼28 pS, and channel activity persists after excision into a Ca2+- and ATP-free bath. The stretch-dose response is sigmoidal, with half-maximal activation of about −19 mmHg at −40 mV, and the channel is activated by depolarization. The inward conductance sequence is: NH[Formula: see text] ∼ Cs+ ∼ Rb+> K+ ∼ Na+ ∼ Li+ > Ca2+ ∼ Ba2+> N-methyl-d-glucamine ∼ tetraethylammonium. The venom of the common Chilean tarantula, Grammostola spatulata, completely blocks channel activity in cell-attached patches. Hypotonic swelling reversibly activates the channel. Intracellular ATP concentration ([ATP]i) reversibly blocks the channel (inhibitory constant ∼0.48 mM), suggesting that channel function is coupled to the metabolic state of the cell. We conclude that this channel may function as a Ca2+ entry pathway and/or be involved in regulation of cell volume. We speculate this channel may be important when [ATP]i is depleted, as occurs during periods of increased transepithelial transport or with ischemic injury.

IK1 channel activity contributes to cisplatin sensitivity of human epidermoid cancer cells

2008 ◽  
Vol 294 (6) ◽  
pp. C1398-C1406 ◽  
Author(s):  
Elbert L. Lee ◽  
Yuichi Hasegawa ◽  
Takahiro Shimizu ◽  
Yasunobu Okada
Keyword(s):  
Cancer Cells ◽  
Cellular Response ◽  
Physiological Role ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Dominant Negative ◽  
Cation Channels ◽  
Channel Activity ◽  
Kb Cells ◽  
Induced Apoptosis

Cisplatin, a platinum-based drug, is an important weapon against many types of cancer. It induces apoptosis by forming adducts with DNA, although many aspects of its mechanism of action remain to be clarified. Previously, we found a role for the volume-sensitive, outwardly rectifying Cl− channel in cisplatin-induced apoptosis. To investigate the possibility that cation channels also have a role in the cellular response to cisplatin, we examined the activity of cation channels in cisplatin-sensitive KB-3-1 (KB) epidermoid cancer cells by the whole cell patch-clamp method. A cation channel in KB cells, activated by hypotonic stress, was identified as the Ca2+-activated, intermediate-conductance K+ (IK1) channel on the basis of its requirement for intracellular Ca2+, its blockage by the blockers clotrimazole and triarylmethane-34, and its suppression by a dominant-negative construct. Activity of this channel was not observed in KCP-4 cells, a cisplatin-resistant cell line derived from KB cells, and its molecular expression, observed by semiquantitative RT-PCR and immunostaining, appeared much reduced. Cell volume measurements confirmed a physiological role for the IK1 channel as a component of the volume-regulatory machinery in KB cells. A possible role of the IK1 channel in cisplatin-induced apoptosis was investigated. It was found that clotrimazole and triarylmethane-34 inhibited a cisplatin-induced decrease in cell viability and increase in caspase-3/7 activity, whereas 1-ethyl-2-benzimidazolinone, an activator of the channel, had the opposite effect. Thus IK1 channel activity appears to mediate, at least in part, the response of KB cells to cisplatin treatment.

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