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Article ; Online: Ion channels and transporters in the development of drug resistance in cancer cells.

Hoffmann, Else K / Lambert, Ian H

Philosophical transactions of the Royal Society of London. Series B, Biological sciences

2014 Volume 369, Issue 1638, Page(s) 20130109

Abstract: Multi-drug resistance (MDR) to chemotherapy is the major challenge in the treatment of cancer. MDR can develop by numerous mechanisms including decreased drug uptake, increased drug efflux and the failure to undergo drug-induced apoptosis. Evasion of ... ...

Abstract	Multi-drug resistance (MDR) to chemotherapy is the major challenge in the treatment of cancer. MDR can develop by numerous mechanisms including decreased drug uptake, increased drug efflux and the failure to undergo drug-induced apoptosis. Evasion of drug-induced apoptosis through modulation of ion transporters is the main focus of this paper and we demonstrate how pro-apoptotic ion channels are downregulated, while anti-apoptotic ion transporters are upregulated in MDR. We also discuss whether upregulation of ion transport proteins that are important for proliferation contribute to MDR. Finally, we discuss the possibility that the development of MDR involves sequential and localized upregulation of ion channels involved in proliferation and migration and a concomitant global and persistent downregulation of ion channels involved in apoptosis.
MeSH term(s)	Apoptosis/physiology ; Drug Resistance, Multiple/physiology ; Drug Resistance, Neoplasm/physiology ; Gene Expression Regulation, Neoplastic/physiology ; Humans ; Ion Channels/metabolism ; Ion Transport ; Models, Biological ; Neoplasms/metabolism ; Neoplasms/physiopathology
Chemical Substances	Ion Channels
Language	English
Publishing date	2014-02-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208382-6
ISSN	1471-2970 ; 0080-4622 ; 0264-3839 ; 0962-8436
ISSN (online)	1471-2970
ISSN	0080-4622 ; 0264-3839 ; 0962-8436
DOI	10.1098/rstb.2013.0109
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Article ; Online: Rebuttal from Florian Lang and Else K. Hoffmann.

Lang, Florian / Hoffmann, Else K

The Journal of physiology

2013 Volume 591, Issue 24, Page(s) 6127

MeSH term(s)	Animals ; Apoptosis ; Cell Size ; Humans
Language	English
Publishing date	2013-11-08
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2013.265231
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Article ; Online: CrossTalk proposal: Cell volume changes are an essential step in the cell death machinery.

Lang, Florian / Hoffmann, Else K

The Journal of physiology

2013 Volume 591, Issue 24, Page(s) 6119–6121

MeSH term(s)	Animals ; Apoptosis ; Cell Size ; Humans ; Ion Transport ; Osmosis
Language	English
Publishing date	2013-11-08
Publishing country	England
Document type	Journal Article
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/jphysiol.2013.258632
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Article ; Online: Role of ion transport in control of apoptotic cell death.

Lang, Florian / Hoffmann, Else K

Comprehensive Physiology

2012 Volume 2, Issue 3, Page(s) 2037–2061

Abstract: Cell shrinkage is a hallmark and contributes to signaling of apoptosis. Apoptotic cell shrinkage requires ion transport across the cell membrane involving K(+) channels, Cl(-) or anion channels, Na(+)/H(+) exchange, Na(+),K(+),Cl(-) cotransport, and Na(+) ...

Abstract	Cell shrinkage is a hallmark and contributes to signaling of apoptosis. Apoptotic cell shrinkage requires ion transport across the cell membrane involving K(+) channels, Cl(-) or anion channels, Na(+)/H(+) exchange, Na(+),K(+),Cl(-) cotransport, and Na(+)/K(+)ATPase. Activation of K(+) channels fosters K(+) exit with decrease of cytosolic K(+) concentration, activation of anion channels triggers exit of Cl(-), organic osmolytes, and HCO3(-). Cellular loss of K(+) and organic osmolytes as well as cytosolic acidification favor apoptosis. Ca(2+) entry through Ca(2+)-permeable cation channels may result in apoptosis by affecting mitochondrial integrity, stimulating proteinases, inducing cell shrinkage due to activation of Ca(2+)-sensitive K(+) channels, and triggering cell-membrane scrambling. Signaling involved in the modification of cell-volume regulatory ion transport during apoptosis include mitogen-activated kinases p38, JNK, ERK1/2, MEKK1, MKK4, the small G proteins Cdc42, and/or Rac and the transcription factor p53. Osmosensing involves integrin receptors, focal adhesion kinases, and tyrosine kinase receptors. Hyperosmotic shock leads to vesicular acidification followed by activation of acid sphingomyelinase, ceramide formation, release of reactive oxygen species, activation of the tyrosine kinase Yes with subsequent stimulation of CD95 trafficking to the cell membrane. Apoptosis is counteracted by mechanisms involved in regulatory volume increase (RVI), by organic osmolytes, by focal adhesion kinase, and by heat-shock proteins. Clearly, our knowledge on the interplay between cell-volume regulatory mechanisms and suicidal cell death is still far from complete and substantial additional experimental effort is needed to elucidate the role of cell-volume regulatory mechanisms in suicidal cell death.
MeSH term(s)	Animals ; Apoptosis ; Humans ; Ion Channels/metabolism ; Ion Pumps/metabolism ; Ion Transport ; MAP Kinase Signaling System ; Potassium/metabolism
Chemical Substances	Ion Channels ; Ion Pumps ; Potassium (RWP5GA015D)
Language	English
Publishing date	2012-07
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2040-4603
ISSN (online)	2040-4603
DOI	10.1002/cphy.c110046
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Article: Cell volume regulation in epithelial physiology and cancer.

Pedersen, Stine F / Hoffmann, Else K / Novak, Ivana

Frontiers in physiology

2013 Volume 4, Page(s) 233

Abstract: The physiological function of epithelia is transport of ions, nutrients, and fluid either in secretory or absorptive direction. All of these processes are closely related to cell volume changes, which are thus an integrated part of epithelial function. ... ...

Abstract	The physiological function of epithelia is transport of ions, nutrients, and fluid either in secretory or absorptive direction. All of these processes are closely related to cell volume changes, which are thus an integrated part of epithelial function. Transepithelial transport and cell volume regulation both rely on the spatially and temporally coordinated function of ion channels and transporters. In healthy epithelia, specific ion channels/transporters localize to the luminal and basolateral membranes, contributing to functional epithelial polarity. In pathophysiological processes such as cancer, transepithelial and cell volume regulatory ion transport are dys-regulated. Furthermore, epithelial architecture and coordinated ion transport function are lost, cell survival/death balance is altered, and new interactions with the stroma arise, all contributing to drug resistance. Since altered expression of ion transporters and channels is now recognized as one of the hallmarks of cancer, it is timely to consider this especially for epithelia. Epithelial cells are highly proliferative and epithelial cancers, carcinomas, account for about 90% of all cancers. In this review we will focus on ion transporters and channels with key physiological functions in epithelia and known roles in the development of cancer in these tissues. Their roles in cell survival, cell cycle progression, and development of drug resistance in epithelial cancers will be discussed.
Language	English
Publishing date	2013-08-30
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2013.00233
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Article: Effectors and signaling events activated by cell shrinkage in ehrlich ascites tumor cells: implications for cell proliferation and programmed cell death.

Hoffmann, Else K / Pedersen, Stine Falsig

Advances in experimental medicine and biology

2008 Volume 559, Page(s) 169–178

MeSH term(s)	Animals ; Apoptosis ; Carcinoma, Ehrlich Tumor/metabolism ; Carcinoma, Ehrlich Tumor/pathology ; Cell Proliferation ; Cell Size ; Lipid Metabolism ; Signal Transduction
Language	English
Publishing date	2008-04-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/0-387-23752-6_16
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Article ; Online: The Volume Activated Potassium Channel KCNK5 is Up-Regulated in Activated Human T Cells, but Volume Regulation is Impaired.

Kirkegaard, Signe S / Strøm, Pernille Dyhl / Gammeltoft, Steen / Hansen, Anker Jon / Hoffmann, Else K

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology

2016 Volume 38, Issue 3, Page(s) 883–892

Abstract: Background/aims: The potential role of the two-pore domain potassium channel KCNK5 (also known as TASK-2 and K(2P)5.1) in activated T cell physiology has only recently been described. So far KCNK5 has been described to be up-regulated in T cells in ... ...

Abstract	Background/aims: The potential role of the two-pore domain potassium channel KCNK5 (also known as TASK-2 and K(2P)5.1) in activated T cell physiology has only recently been described. So far KCNK5 has been described to be up-regulated in T cells in multiple sclerosis patients and to be implicated in the volume regulatory mechanism regulatory volume decrease (RVD) in T cells. Methods: We investigated the time-dependent expression pattern of KCNK5 in CD3/CD28 activated human T cells using qPCR and Western blotting and its role in RVD using a Coulter Counter. Results: KCNK5 is highly up-regulated in CD3/CD28 activated T cells both at mRNA (after 24 h) and protein level (72 and 144 h), but despite this up-regulation the RVD response is inhibited. Furthermore, the swelling-activated Cl- permeability in activated T cells is strongly decreased, and the RVD inhibition is predominantly due to the decreased Cl- permeability. Conclusion: The up-regulated KCNK5 in activated human T cells does not play a volume regulatory role, due to decreased Cl- permeability. We speculate that the KCNK5 up-regulation might play a role in hyperpolarization of the cell membrane leading to increased Ca2+ influx and proliferation of T cells.
MeSH term(s)	CD28 Antigens/metabolism ; CD3 Complex/pharmacology ; Calcium/metabolism ; Cell Size/drug effects ; Chlorine/metabolism ; Humans ; Intermediate-Conductance Calcium-Activated Potassium Channels/genetics ; Lymphocyte Activation ; Potassium Channels, Tandem Pore Domain/genetics ; Potassium Channels, Tandem Pore Domain/metabolism ; T-Lymphocytes/metabolism ; Up-Regulation
Chemical Substances	CD28 Antigens ; CD3 Complex ; Intermediate-Conductance Calcium-Activated Potassium Channels ; KCNK5 protein, human ; KCNN4 protein, human ; Potassium Channels, Tandem Pore Domain ; Chlorine (4R7X1O2820) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2016-02-25
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1067572-3
ISSN	1421-9778 ; 1015-8987
ISSN (online)	1421-9778
ISSN	1015-8987
DOI	10.1159/000443042
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Article: Shrinkage insensitivity of NKCC1 in myosin II-depleted cytoplasts from Ehrlich ascites tumor cells.

Hoffmann, Else K / Pedersen, Stine F

American journal of physiology. Cell physiology

2007 Volume 292, Issue 5, Page(s) C1854–66

Abstract: Protein phosphorylation/dephosphorylation and cytoskeletal reorganization regulate the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) during osmotic shrinkage; however, the mechanisms involved are unclear. We show that in cytoplasts, plasma membrane vesicles ... ...

Abstract	Protein phosphorylation/dephosphorylation and cytoskeletal reorganization regulate the Na(+)-K(+)-2Cl(-) cotransporter (NKCC1) during osmotic shrinkage; however, the mechanisms involved are unclear. We show that in cytoplasts, plasma membrane vesicles detached from Ehrlich ascites tumor cells (EATC) by cytochalasin treatment, NKCC1 activity evaluated as bumetanide-sensitive (86)Rb influx was increased compared with the basal level in intact cells yet could not be further increased by osmotic shrinkage. Accordingly, cytoplasts exhibited no regulatory volume increase after shrinkage. In cytoplasts, cortical F-actin organization was disrupted, and myosin II, which in shrunken EATC translocates to the cortical region, was absent. Moreover, NKCC1 activity was essentially insensitive to the myosin light chain kinase (MLCK) inhibitor ML-7, a potent blocker of shrinkage-induced NKCC1 activity in intact EATC. Cytoplast NKCC1 activity was potentiated by the Ser/Thr protein phosphatase inhibitor calyculin A, partially inhibited by the protein kinase A inhibitor H89, and blocked by the broad protein kinase inhibitor staurosporine. Cytoplasts exhibited increased protein levels of NKCC1, Ste20-related proline- and alanine-rich kinase (SPAK), and oxidative stress response kinase 1, yet they lacked the shrinkage-induced plasma membrane translocation of SPAK observed in intact cells. The basal phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) was increased in cytoplasts compared with intact cells, yet in contrast to the substantial activation in shrunken intact cells, p38 MAPK could not be further activated by shrinkage of the cytoplasts. Together these findings indicate that shrinkage activation of NKCC1 in EATC is dependent on the cortical F-actin network, myosin II, and MLCK.
MeSH term(s)	Actins/metabolism ; Animals ; Bumetanide/pharmacology ; Carcinoma, Ehrlich Tumor/metabolism ; Carcinoma, Ehrlich Tumor/pathology ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Cell Size ; Cell-Free System ; Cyclic AMP-Dependent Protein Kinase Type II ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Female ; Hypertonic Solutions ; Isoquinolines/pharmacology ; Mice ; Myosin Type II/deficiency ; Myosin Type II/metabolism ; Myosin-Light-Chain Kinase/metabolism ; Oxazoles/pharmacology ; Phosphoprotein Phosphatases/antagonists & inhibitors ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Protein Kinase Inhibitors/pharmacology ; Protein-Serine-Threonine Kinases/metabolism ; Rubidium Radioisotopes ; Sodium Potassium Chloride Symporter Inhibitors/pharmacology ; Sodium-Potassium-Chloride Symporters/metabolism ; Solute Carrier Family 12, Member 2 ; Staurosporine/pharmacology ; Sulfonamides/pharmacology ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Actins ; Hypertonic Solutions ; Isoquinolines ; Oxazoles ; Protein Kinase Inhibitors ; Rubidium Radioisotopes ; Slc12a2 protein, mouse ; Sodium Potassium Chloride Symporter Inhibitors ; Sodium-Potassium-Chloride Symporters ; Solute Carrier Family 12, Member 2 ; Sulfonamides ; Bumetanide (0Y2S3XUQ5H) ; calyculin A (7D07U14TK3) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Cyclic AMP-Dependent Protein Kinase Type II (EC 2.7.11.11) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11) ; Myosin-Light-Chain Kinase (EC 2.7.11.18) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Phosphoprotein Phosphatases (EC 3.1.3.16) ; Myosin Type II (EC 3.6.1.-) ; Staurosporine (H88EPA0A3N) ; N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide (M876330O56)
Language	English
Publishing date	2007-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00474.2006
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Article ; Online: Osmosensory mechanisms in cellular and systemic volume regulation.

Pedersen, Stine Falsig / Kapus, András / Hoffmann, Else K

Journal of the American Society of Nephrology : JASN

2011 Volume 22, Issue 9, Page(s) 1587–1597

Abstract: Perturbations of cellular and systemic osmolarity severely challenge the function of all organisms and are consequently regulated very tightly. Here we outline current evidence on how cells sense volume perturbations, with particular focus on mechanisms ... ...

Abstract	Perturbations of cellular and systemic osmolarity severely challenge the function of all organisms and are consequently regulated very tightly. Here we outline current evidence on how cells sense volume perturbations, with particular focus on mechanisms relevant to the kidneys and to extracellular osmolarity and whole body volume homeostasis. There are a variety of molecular signals that respond to perturbations in cell volume and osmosensors or volume sensors responding to these signals. The early signals of volume perturbation include integrins, the cytoskeleton, receptor tyrosine kinases, and transient receptor potential channels. We also present current evidence on the localization and function of central and peripheral systemic osmosensors and conclude with a brief look at the still limited evidence on pathophysiological conditions associated with deranged sensing of cell volume.
MeSH term(s)	Cell Size ; Homeostasis ; Kidney/cytology ; Kidney/physiology ; Macrophages/physiology ; Mechanotransduction, Cellular ; Osmolar Concentration
Language	English
Publishing date	2011-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2010121284
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Article ; Online: Sensors and signal transduction pathways in vertebrate cell volume regulation.

Hoffmann, Else K / Pedersen, Stine F

Contributions to nephrology

2006 Volume 152, Page(s) 54–104

Abstract: The ability to control cell volume is fundamental for proper cell function. This review highlights recent advances in the understanding of the complex sequences of events by which acute cell volume perturbation alters the activity of osmolyte transport ... ...

Abstract	The ability to control cell volume is fundamental for proper cell function. This review highlights recent advances in the understanding of the complex sequences of events by which acute cell volume perturbation alters the activity of osmolyte transport proteins in cells from vertebrate organisms. After cell swelling, the main effectors in the process of regulatory volume decrease are swelling-activated K(+) and Cl(-) channels, a taurine efflux pathway, and KCl cotransport. After cell shrinkage, the main effectors in the process of regulatory volume increase are Na(+)/H(+) exchange, Na(+), K(+), 2Cl(-) cotransport, and in some cells, shrinkageactivated Na(+) channels. All of these proteins are regulated in a unique manner by cell volume perturbations. The molecular identity of most, although not all, of these transport pathways is now known. Among other important advances, this has lead to the identification of transporter binding partners such as protein kinases and phosphatases, cytoskeletal elements and lipids. Considerable progress has also been made recently in understanding the upstream elements in volume sensing and volume-sensitive signal transduction, and salient features of these systems will be discussed. In contrast to the simple pathway of osmosensing in yeast, cells from vertebrate organisms appear to exhibit multiple volume sensing systems, the specific mechanism(s) activated being cell type- and stimulus-dependent. Candidate sensors include integrins and growth factor receptors, while other early events include regulation of Rho family GTP binding proteins, Ste20-related protein kinases, and phospholipases, as well as cytoskeletal reorganization, Transient Receptor Potential channel-mediated Ca(2+) influx, and generation of reactive oxygen species.
MeSH term(s)	Animals ; Biological Transport/physiology ; Calcium Channels/metabolism ; Cell Movement/physiology ; Cell Size ; Cell Survival ; Chloride Channels/metabolism ; Osmotic Pressure ; Reactive Oxygen Species/metabolism ; Signal Transduction/physiology ; Sodium-Potassium-Exchanging ATPase/metabolism ; Vertebrates/metabolism ; Vertebrates/physiology ; Water-Electrolyte Balance/physiology
Chemical Substances	Calcium Channels ; Chloride Channels ; Reactive Oxygen Species ; Sodium-Potassium-Exchanging ATPase (EC 3.6.3.9)
Language	English
Publishing date	2006-08-31
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1662-2782 ; 0302-5144
ISSN (online)	1662-2782
ISSN	0302-5144
DOI	10.1159/000096318
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