Ion Transport in MDCK Cells

1985 ◽  
pp. 37-50 ◽  
Author(s):  
S. Fernández-Castelo ◽  
J. J. Bolívar ◽  
R. López-Vancell ◽  
G. Beaty ◽  
M. Cereijido
Keyword(s):  
Ion Transport ◽  
Mdck Cells

Hyperosmotic and isosmotic shrinkage differentially affect protein phosphorylation and ion transport

2012 ◽  
Vol 90 (2) ◽  
pp. 209-217 ◽  
Author(s):  
Svetlana V. Koltsova ◽  
Olga A. Akimova ◽  
Sergei V. Kotelevtsev ◽  
Ryszard Grygorczyk ◽  
Sergei N. Orlov
Keyword(s):  
Ion Transport ◽  
Protein Phosphorylation ◽  
Cell Volume ◽  
Mdck Cells ◽  
Rat Aorta ◽  
Cellular Functions ◽  
Hypertonic Medium ◽  
Mitogen Activated Protein ◽  
Volume Decrease ◽  
In Cells

In the present work, we compared the outcome of hyperosmotic and isosmotic shrinkage on ion transport and protein phosphorylation in C11-MDCK cells resembling intercalated cells from collecting ducts and in vascular smooth muscle cells (VSMC) from the rat aorta. Hyperosmotic shrinkage was triggered by cell exposure to hypertonic medium, whereas isosmotic shrinkage was evoked by cell transfer from an hypoosmotic to an isosmotic environment. Despite a similar cell volume decrease of 40%–50%, the consequences of hyperosmotic and isosmotic shrinkage on cellular functions were sharply different. In C11-MDCK and VSMC, hyperosmotic shrinkage completely inhibited Na+,K+-ATPase and Na+,Pi cotransport. In contrast, in both types of cells isosmotic shrinkage slightly increased rather than suppressed Na+,K+-ATPase and did not change Na+,Pi cotransport. In C11-MDCK cells, phosphorylation of JNK1/2 and Erk1/2 mitogen-activated protein kinases was augmented in hyperosmotically shrunken cells by ∼7- and 2-fold, respectively, but was not affected in cells subjected to isosmotic shrinkage. These results demonstrate that the data obtained in cells subjected to hyperosmotic shrinkage cannot be considered as sufficient proof implicating cell volume perturbations in the regulation of cellular functions under isosmotic conditions.

Transfection Alters Ion Transport in MDCK Cells

1996 ◽  
Vol 149 (1) ◽  
pp. 49-55 ◽  
Author(s):  
D.M. Kaji *, † , J. Bates ◽  
J.D. Goyzueta *, † , K. Prasadan ◽  
H. Yu ◽  
S. Kumar
Keyword(s):  
Ion Transport ◽  
Mdck Cells

Vasopressin stimulates DNA synthesis and ion transport in quiescent epithelial cells

1985 ◽  
Vol 249 (3) ◽  
pp. C267-C270 ◽  
Author(s):  
V. M. Reznik ◽  
R. J. Shapiro ◽  
S. A. Mendoza
Keyword(s):  
Epithelial Cells ◽  
Dna Synthesis ◽  
Ion Transport ◽  
Growth Regulation ◽  
Mdck Cells ◽  
Subsequent Increase ◽  
Low Concentrations ◽  
Pump Activity ◽  
Monovalent Ion ◽  
Na Uptake

The mitogenic effect of vasopressin was studied in subconfluent quiescent renal epithelial cells (MDCK). Vasopressin stimulated DNA synthesis in the presence of low concentrations of serum. Vasopressin increased the entry of Na into the cells and increased ouabain-sensitive 86Rb uptake, a measure of Na-K pump activity. Because the activity of the Na-K pump in MDCK cells is steeply dependent on intracellular Na, it is likely that stimulation of the Na-K pump by vasopressin was mediated by the increase in Na entry into the cells. Thus both serum and vasopressin stimulate Na uptake and Na-K pump activity in quiescent MDCK cells with a subsequent increase in DNA synthesis. It is concluded that growth regulation in epithelial cells may be mediated in part by changes in monovalent ion transport.

scholarly journals Mechanism of NaCl transport-stimulated prostaglandin formation in MDCK cells

1987 ◽  
Vol 252 (3) ◽  
pp. C307-C314 ◽  
Author(s):  
A. Kurtz ◽  
J. Pfeilschifter ◽  
K. Malmstrom ◽  
R. D. Woodson ◽  
C. Bauer
Keyword(s):  
Arachidonic Acid ◽  
Ion Transport ◽  
Membrane Lipids ◽  
Chloride Transport ◽  
Mdck Cells ◽  
Lactate Production ◽  
Nacl Transport ◽  
Free Arachidonic Acid ◽  
Lactate Formation ◽  
Stimulation Of

Recently we have found that stimulation of NaCl transport in high-resistance MDCK cells enhances their prostaglandin formation. In the present study, we investigated the mechanisms by which prostaglandin formation could be linked to the ion transport in these cells. We found that stimulation of transport caused a transient stimulation of prostaglandin formation lasting 5–10 min. The rise in prostaglandin formation was paralleled by a rise of free intracellular arachidonic acid. Analysis of membrane lipids revealed that the rise of free arachidonic acid was paralleled by a loss of arachidonic acid from polyphosphoinositides. We failed to obtain indications for the stimulation of calcium-dependent phospholipase A2. However, we did obtain evidence that the incorporation of arachidonic acid into phospholipids was diminished during stimulation of ion transport, indicating a decreased rate of reesterification. Despite the fact that there was no significant fall in total cellular ATP on stimulation of ion transport, we found a high and transient rise of lactate production of the cells on stimulation of the ion transport indicating an alteration of the ADP/ATP ratio. Moreover, prostaglandin formation and lactate formation were linearly correlated in this situation. When glucose utilization was inhibited by mannoheptulose, the rise in lactate formation was abolished, whereas that of PG formation was unaltered, indicating that lactate formation and prostaglandin formation were not causally linked on stimulation of ion transport. Our results suggest that an increase in the rate of sodium chloride transport by MDCK cells stimulates formation by an inhibition of reesterification of free arachidonic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Ion transport and signalling in human labial glands

1999 ◽  
Vol 44 ◽  
pp. S15-S19 ◽  
Author(s):  
R Turner
Keyword(s):  
Ion Transport ◽  
Labial Glands

Characterization of acetylcholine-induced ion transport in human duodenum

2001 ◽  
Vol 120 (5) ◽  
pp. A532-A532
Author(s):  
R LARSEN ◽  
M HANSEN ◽  
N BINSLEV ◽  
A MERTZNIELSEN
Keyword(s):  
Ion Transport
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