Intracellular Ca2+ transients in HT29 cells induced by hypotonic cell swelling

1993 ◽  
Vol 423 (3-4) ◽  
pp. 274-279 ◽  
Author(s):  
R. Nitschke ◽  
J. Leipziger ◽  
R. Greger
Keyword(s):  
Cell Swelling ◽  
Ht29 Cells ◽  
Hypotonic Cell Swelling

Small-conductance Cl? channels in HT29 cells: activation by Ca2+, hypotonic cell swelling and 8-Br-cGMP

1992 ◽  
Vol 421 (2-3) ◽  
pp. 238-246 ◽  
Author(s):  
K. Kunzelmann ◽  
R. Kubitz ◽  
M. Grolik ◽  
R. Warth ◽  
R. Greger
Keyword(s):  
Cell Swelling ◽  
Ht29 Cells ◽  
Cl Channels ◽  
Hypotonic Cell Swelling ◽  
Small Conductance

Forskolin and PMA pretreatment of HT29 cells alters their chloride conductance induced by cAMP, Ca2+ and hypotonic cell swelling

1994 ◽  
Vol 428 (1) ◽  
pp. 76-83 ◽  
Author(s):  
K. Kunzelmann ◽  
N. Allert ◽  
R. Kubitz ◽  
W. V. Breuer ◽  
Z. I. Cabantchik ◽  
...  
Keyword(s):  
Chloride Conductance ◽  
Cell Swelling ◽  
Ht29 Cells ◽  
Hypotonic Cell Swelling

Ca2+ uptake in GH3 cells during hypotonic swelling: the sensory role of stretch-activated ion channels

1996 ◽  
Vol 270 (6) ◽  
pp. C1790-C1798 ◽  
Author(s):  
Y. Chen ◽  
S. M. Simasko ◽  
J. Niggel ◽  
W. J. Sigurdson ◽  
F. Sachs
Keyword(s):  
Volume Regulation ◽  
Cell Swelling ◽  
Gh3 Cells ◽  
Membrane Tension ◽  
Hypotonic Cell Swelling ◽  
Stretch Activated Channels ◽  
Ca2 Channels ◽  
Hypotonic Swelling ◽  
Volume Decrease

Hypotonic cell swelling triggers an increase in intracellular Ca2+ concentration that is deemed responsible for the subsequent regulated volume decrease in many cells. To understand the mechanisms underlying this increase, we have studied the Ca2+ sources that contribute to hypotonic cell swelling-induced Ca2+ increase (HICI) in GH3 cells. Fura 2 fluorescence of cell populations revealed that extracellular, but not intracellular, stores of Ca2+ were required. HICI was abolished by nifedipine, a blocker of L-type Ca2+ channels, and Gd3+, a nonspecific blocker of stretch-activated channels (SACs), suggesting two components for the Ca2+ membrane pathway: L-type Ca2+ channels and SACs. Using HICI as an assay, we found that venom from the spider Grammostola spatulata could block HICI without blocking L-type Ca2+ channels. The venom did, however, block SAC activity. This suggests that Ca(2+)-permeable SACs, rather than L-type Ca2+ channels, are the sensing elements for HICI. These results support the model for volume regulation in which SACs, activated by an increase of the membrane tension during hypotonic cell swelling, trigger HICI, leading to a volume decrease.

scholarly journals Functional interaction of the K-Cl cotransporter (KCC1) with the Na-K-Cl cotransporter in HEK-293 cells

1999 ◽  
Vol 276 (2) ◽  
pp. C328-C336 ◽  
Author(s):  
Christopher M. Gillen ◽  
Bliss Forbush
Keyword(s):  
Cell Swelling ◽  
Primary Role ◽  
Functional Interaction ◽  
Hek 293 ◽  
Hek 293 Cells ◽  
Hek Cells ◽  
293 Cells ◽  
Hypotonic Cell Swelling ◽  
The Relationship ◽  
Fold Activation

We have studied the regulation of the K-Cl cotransporter KCC1 and its functional interaction with the Na-K-Cl cotransporter. K-Cl cotransporter activity was substantially activated in HEK-293 cells overexpressing KCC1 (KCC1-HEK) by hypotonic cell swelling, 50 mM external K, and pretreatment with N-ethylmaleimide (NEM). Bumetanide inhibited 86Rb efflux in KCC1-HEK cells after cell swelling [inhibition constant ( K i) ∼190 μM] and pretreatment with NEM ( K i ∼60 μM). Thus regulation of KCC1 is consistent with properties of the red cell K-Cl cotransporter. To investigate functional interactions between K-Cl and Na-K-Cl cotransporters, we studied the relationship between Na-K-Cl cotransporter activation and intracellular Cl concentration ([Cl]i). Without stimulation, KCC1-HEK cells had greater Na-K-Cl cotransporter activity than controls. Endogenous Na-K-Cl cotransporter of KCC1-HEK cells was activated <2-fold by low-Cl hypotonic prestimulation, compared with 10-fold activation in HEK-293 cells and >20-fold activation in cells overexpressing the Na-K-Cl cotransporter (NKCC1-HEK). KCC1-HEK cells had lower resting [Cl]i than HEK-293 cells; cell volume was not different among cell lines. We found a steep relationship between [Cl]i and Na-K-Cl cotransport activity within the physiological range, supporting a primary role for [Cl]iin activation of Na-K-Cl cotransport and in apical-basolateral cross talk in ion-transporting epithelia.

scholarly journals Cholesterol Depletion Facilitates Recovery from Hypotonic Cell Swelling in CHO Cells

2011 ◽  
Vol 28 (6) ◽  
pp. 1247-1254 ◽  
Author(s):  
Gregory B. Kowalsky ◽  
Derek Beam ◽  
Myung J. Oh ◽  
Frederick Sachs ◽  
Susan Z. Hua ◽  
...  
Keyword(s):  
Cho Cells ◽  
Cell Swelling ◽  
Cholesterol Depletion ◽  
Hypotonic Cell Swelling

scholarly journals Cholesterol Depletion Facilitates Recovery from Hypotonic Cell Swelling of CHO

2010 ◽  
Vol 98 (3) ◽  
pp. 318a
Author(s):  
Gregory Kowalsky ◽  
Derek Beam ◽  
Frederick Sachs ◽  
Susan Hua ◽  
Irena Levitan
Keyword(s):  
Cell Swelling ◽  
Cholesterol Depletion ◽  
Hypotonic Cell Swelling

Preferential potentiation by hypotonic cell swelling of muscarinic cation current in guinea pig ileum

1997 ◽  
Vol 272 (1) ◽  
pp. C240-C253 ◽  
Author(s):  
Y. Waniishi ◽  
R. Inoue ◽  
Y. Ito
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Muscarinic Receptor ◽  
Time Course ◽  
Cell Swelling ◽  
Patch Clamp Technique ◽  
Cationic Current ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Hypotonic Cell Swelling

The effects of hypotonic cell swelling (HCS) on muscarinic receptor-activated cationic current in guinea pig ileal smooth muscle were investigated by the whole cell patch-clamp technique. With nystatin-perforated recording, reduced external tonicity from 312 to 262 mosM caused cell swelling but hardly affected the membrane currents activated by depolarization, such as outward-rectifying K and voltage-dependent Ca currents. In contrast, the inward current evoked by carbachol at -60 mV was greatly increased (approximately 50%) by the same extent of hypotonicity. This effect is likely to occur through potentiation of nonselective cation channels coupled to the muscarinic receptor (mNSCCs) and probably does not involve elevated intracellular Ca2+ concentration ([Ca2+]i), since neither removal of external Ca2+ nor [Ca2+]i buffering with 10 mM 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid significantly affected the results. Furthermore, the time course and degree of this potentiation closely matched those of video-microscopically monitored HCS. These results support the view that mechanosensitive modulation may be a powerful mechanism to regulate mNSCCs activity in gut smooth muscle, together with membrane potential and [Ca2+]i.

Membrane Reserves and Hypotonic Cell Swelling

2006 ◽  
Vol 214 (1-2) ◽  
pp. 43-56 ◽  
Author(s):  
Nicolas Groulx ◽  
Francis Boudreault ◽  
Sergei N. Orlov ◽  
Ryszard Grygorczyk
Keyword(s):  
Cell Swelling ◽  
Hypotonic Cell Swelling

scholarly journals Involvement of microtubules in the swelling-induced stimulation of transcellular taurocholate transport in perfused rat liver

1993 ◽  
Vol 291 (2) ◽  
pp. 355-360 ◽  
Author(s):  
D Häussinger ◽  
N Saha ◽  
C Hallbrucker ◽  
F Lang ◽  
W Gerok
Keyword(s):  
Inhibitory Effect ◽  
Pentose Phosphate ◽  
Cell Swelling ◽  
Stimulatory Action ◽  
Bile Acid Transporter ◽  
14Co2 Production ◽  
Hypotonic Cell Swelling ◽  
Taurocholate Transport ◽  
Dependent Mechanism ◽  
Stimulation Of

An increase of the hepatocellular hydratation state, induced by hypotonic exposure, amino acids or tauroursodeoxycholate, was shown to increase within minutes the Vmax of transcellular taurocholate transport and excretion into bile [Häussinger, Hallbrucker, Saha, Lang and Gerok (1992) Biochem. J. 288, 681-689]. This stimulatory effect of cell swelling on taurocholate excretion into bile is abolished in the presence of colchicine (5 microM). On the other hand, colchicine did not affect the stimulatory action of hypotonic cell swelling on 14CO2 production from [1-14C]glycine or [1-14C]glucose. Likewise, volume regulatory K+ fluxes following anisotonic exposure were not influenced in the presence of colchicine. Lumicolchicine (5 microM), a stereoisomer of colchicine without an inhibitory effect on microtubules, did not abolish the stimulation of taurocholate excretion into bile following hypo-osmotic exposure. Hypertonic cell shrinkage decreased taurocholate excretion into bile by about 35%; this effect was fully reversible upon normotonic re-exposure. With colchicine pretreatment, however, the hypertonicity-induced inhibition of taurocholate excretion was blunted and was no longer reversible upon normotonic re-exposure. The results suggest that stimulation of taurocholate excretion into bile in response to cell swelling involves a colchicine-sensitive, probably microtubule-dependent, mechanism, but not the stimulation of other cell-volume-sensitive pathways such as glycine oxidation or the pentose-phosphate shunt. It is hypothesized that the swelling-induced stimulation of taurocholate excretion into bile is due to a microtubule-dependent insertion of bile acid transporter molecules into the canalicular membrane.

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