Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride channels

Research output: Contribution to journalJournal articlepeer-review

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Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride channels. / Poulsen, Kristian Arild; Andersen, E C; Hansen, C F; Klausen, Thomas Kjær; Hougaard, Charlotte; Lambert, I H; Hoffmann, Else Kay.

In: American Journal of Physiology: Cell Physiology, Vol. 298, No. 1, 2010, p. C14-25.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Poulsen, KA, Andersen, EC, Hansen, CF, Klausen, TK, Hougaard, C, Lambert, IH & Hoffmann, EK 2010, 'Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride channels', American Journal of Physiology: Cell Physiology, vol. 298, no. 1, pp. C14-25. https://doi.org/10.1152/ajpcell.00654.2008

APA

Poulsen, K. A., Andersen, E. C., Hansen, C. F., Klausen, T. K., Hougaard, C., Lambert, I. H., & Hoffmann, E. K. (2010). Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride channels. American Journal of Physiology: Cell Physiology, 298(1), C14-25. https://doi.org/10.1152/ajpcell.00654.2008

Vancouver

Poulsen KA, Andersen EC, Hansen CF, Klausen TK, Hougaard C, Lambert IH et al. Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride channels. American Journal of Physiology: Cell Physiology. 2010;298(1):C14-25. https://doi.org/10.1152/ajpcell.00654.2008

Author

Poulsen, Kristian Arild ; Andersen, E C ; Hansen, C F ; Klausen, Thomas Kjær ; Hougaard, Charlotte ; Lambert, I H ; Hoffmann, Else Kay. / Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride channels. In: American Journal of Physiology: Cell Physiology. 2010 ; Vol. 298, No. 1. pp. C14-25.

Bibtex

@article{7442d80017c811df8ed1000ea68e967b,
title = "Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride channels",
abstract = "Changes in cell volume and ion gradients across the plasma membrane play a pivotal role in the initiation of apoptosis. Here we explore the kinetics of apoptotic volume decrease (AVD) and ion content dynamics in wild-type (WT) and multidrug-resistant (MDR) Ehrlich ascites tumor cells (EATC). In WT EATC, induction of apoptosis with cisplatin (5 muM) leads to three distinctive AVD stages: an early AVD(1) (4-12 h), associated with a 30% cell water loss; a transition stage AVD(T) ( approximately 12 to 32 h), where cell volume is partly recovered; and a secondary AVD(2) (past 32 h), where cell volume was further reduced. AVD(1) and AVD(2) were coupled to net loss of Cl(-), K(+), Na(+), and amino acids (ninhydrin-positive substances), whereas during AVD(T), Na(+) and Cl(-) were accumulated. MDR EATC was resistant to cisplatin, showing increased viability and less caspase 3 activation. Compared with WT EATC, MDR EATC underwent a less pronounced AVD(1,) an augmented AVD(T), and a delay in induction of AVD(2). Changes in AVD were associated with inhibition of Cl(-) loss during AVD(1), augmented NaCl uptake during AVD(T), and a delay of Cl(-) loss during AVD(2). Application of the anion channel inhibitor NS3728 inhibited AVD and completely abolished the differences in AVD, ionic movements, and caspase 3 activation between WT and MDR EATC. Finally, the maximal capacity of volume-regulated anion channel was found to be strongly repressed in MDR EATC. Together, these data suggest that impairment of AVD, primarily via modulation of NaCl movements, contribute to protection against apoptosis in MDR EATC.",
author = "Poulsen, {Kristian Arild} and Andersen, {E C} and Hansen, {C F} and Klausen, {Thomas Kj{\ae}r} and Charlotte Hougaard and Lambert, {I H} and Hoffmann, {Else Kay}",
note = "Keywords: Animals; Apoptosis; Carrier Proteins; Cell Cycle; Cell Size; Chloride Channels; Cisplatin; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Homeostasis; Humans; Neoplasms; P-Glycoprotein",
year = "2010",
doi = "10.1152/ajpcell.00654.2008",
language = "English",
volume = "298",
pages = "C14--25",
journal = "American Journal of Physiology: Cell Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "1",

}

RIS

TY - JOUR

T1 - Deregulation of apoptotic volume decrease and ionic movements in multidrug-resistant tumor cells: role of chloride channels

AU - Poulsen, Kristian Arild

AU - Andersen, E C

AU - Hansen, C F

AU - Klausen, Thomas Kjær

AU - Hougaard, Charlotte

AU - Lambert, I H

AU - Hoffmann, Else Kay

N1 - Keywords: Animals; Apoptosis; Carrier Proteins; Cell Cycle; Cell Size; Chloride Channels; Cisplatin; Drug Resistance, Multiple; Drug Resistance, Neoplasm; Homeostasis; Humans; Neoplasms; P-Glycoprotein

PY - 2010

Y1 - 2010

N2 - Changes in cell volume and ion gradients across the plasma membrane play a pivotal role in the initiation of apoptosis. Here we explore the kinetics of apoptotic volume decrease (AVD) and ion content dynamics in wild-type (WT) and multidrug-resistant (MDR) Ehrlich ascites tumor cells (EATC). In WT EATC, induction of apoptosis with cisplatin (5 muM) leads to three distinctive AVD stages: an early AVD(1) (4-12 h), associated with a 30% cell water loss; a transition stage AVD(T) ( approximately 12 to 32 h), where cell volume is partly recovered; and a secondary AVD(2) (past 32 h), where cell volume was further reduced. AVD(1) and AVD(2) were coupled to net loss of Cl(-), K(+), Na(+), and amino acids (ninhydrin-positive substances), whereas during AVD(T), Na(+) and Cl(-) were accumulated. MDR EATC was resistant to cisplatin, showing increased viability and less caspase 3 activation. Compared with WT EATC, MDR EATC underwent a less pronounced AVD(1,) an augmented AVD(T), and a delay in induction of AVD(2). Changes in AVD were associated with inhibition of Cl(-) loss during AVD(1), augmented NaCl uptake during AVD(T), and a delay of Cl(-) loss during AVD(2). Application of the anion channel inhibitor NS3728 inhibited AVD and completely abolished the differences in AVD, ionic movements, and caspase 3 activation between WT and MDR EATC. Finally, the maximal capacity of volume-regulated anion channel was found to be strongly repressed in MDR EATC. Together, these data suggest that impairment of AVD, primarily via modulation of NaCl movements, contribute to protection against apoptosis in MDR EATC.

AB - Changes in cell volume and ion gradients across the plasma membrane play a pivotal role in the initiation of apoptosis. Here we explore the kinetics of apoptotic volume decrease (AVD) and ion content dynamics in wild-type (WT) and multidrug-resistant (MDR) Ehrlich ascites tumor cells (EATC). In WT EATC, induction of apoptosis with cisplatin (5 muM) leads to three distinctive AVD stages: an early AVD(1) (4-12 h), associated with a 30% cell water loss; a transition stage AVD(T) ( approximately 12 to 32 h), where cell volume is partly recovered; and a secondary AVD(2) (past 32 h), where cell volume was further reduced. AVD(1) and AVD(2) were coupled to net loss of Cl(-), K(+), Na(+), and amino acids (ninhydrin-positive substances), whereas during AVD(T), Na(+) and Cl(-) were accumulated. MDR EATC was resistant to cisplatin, showing increased viability and less caspase 3 activation. Compared with WT EATC, MDR EATC underwent a less pronounced AVD(1,) an augmented AVD(T), and a delay in induction of AVD(2). Changes in AVD were associated with inhibition of Cl(-) loss during AVD(1), augmented NaCl uptake during AVD(T), and a delay of Cl(-) loss during AVD(2). Application of the anion channel inhibitor NS3728 inhibited AVD and completely abolished the differences in AVD, ionic movements, and caspase 3 activation between WT and MDR EATC. Finally, the maximal capacity of volume-regulated anion channel was found to be strongly repressed in MDR EATC. Together, these data suggest that impairment of AVD, primarily via modulation of NaCl movements, contribute to protection against apoptosis in MDR EATC.

U2 - 10.1152/ajpcell.00654.2008

DO - 10.1152/ajpcell.00654.2008

M3 - Journal article

C2 - 19846756

VL - 298

SP - C14-25

JO - American Journal of Physiology: Cell Physiology

JF - American Journal of Physiology: Cell Physiology

SN - 0363-6143

IS - 1

ER -

ID: 17583480