Cell Volume-Regulated Cation Channels

1998 ◽  
pp. 8-20 ◽  
Author(s):  
F. Wehner
Keyword(s):  
Cell Volume ◽  
Cation Channels

scholarly journals Enhanced susceptibility to suicidal death of erythrocytes from transgenic mice overexpressing erythropoietin

2007 ◽  
Vol 293 (3) ◽  
pp. R1127-R1134 ◽  
Author(s):  
Michael Föller ◽  
Ravi S. Kasinathan ◽  
Saisudha Koka ◽  
Stephan M. Huber ◽  
Beat Schuler ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Transgenic Mice ◽  
Cell Volume ◽  
Cation Channels ◽  
Forward Scatter ◽  
Membrane Asymmetry ◽  
Phosphatidylserine Exposure ◽  
Suicidal Death ◽  
Osmotic Lysis ◽  
The Difference

Eryptosis, a suicidal death of mature erythrocytes, is characterized by decrease of cell volume, cell membrane blebbing, and breakdown of cell membrane asymmetry with phosphatidylserine exposure at the cell surface. Triggers of eryptosis include increased cytosolic Ca2+ activity, which could result from activation of Ca2+-permeable cation channels. Ca2+ triggers phosphatidylserine exposure and activates Ca2+-sensitive K+ channels, leading to cellular K+ loss and cell shrinkage. The cation channels and thus eryptosis are stimulated by Cl− removal and inhibited by erythropoietin. The present experiments explored eryptosis in transgenic mice overexpressing erythropoietin (tg6). Erythrocytes were drawn from tg6 mice and their wild-type littermates (WT). Phosphatidylserine exposure was estimated from annexin binding and cell volume from forward scatter in fluorescence-activated cell sorting (FACS) analysis. The percentage of annexin binding was significantly larger and forward scatter significantly smaller in tg6 than in WT erythrocytes. Transgenic erythrocytes were significantly more resistant to osmotic lysis than WT erythrocytes. Cl− removal and exposure to the Ca2+ ionophore ionomycin (1 μM) increased annexin binding and decreased forward scatter, effects larger in tg6 than in WT erythrocytes. The K+ ionophore valinomycin (10 nM) triggered eryptosis in both tg6 and WT erythrocytes and abrogated differences between genotypes. An increase of extracellular K+ concentration to 125 mM blunted the difference between tg6 and WT erythrocytes. Fluo-3 fluorescence reflecting cytosolic Ca2+ activity was larger in tg6 than in WT erythrocytes. In conclusion, circulating erythrocytes from tg6 mice are sensitized to triggers of eryptosis but more resistant to osmotic lysis, properties at least partially due to enhanced Ca2+ entry and increased K+ channel activity.

scholarly journals Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 2: Functional and Molecular Properties of ASOR/PAC Channels and Their Roles in Cell Volume Dysregulation and Acidotoxic Cell Death

2021 ◽  
Vol 9 ◽  
Author(s):  
Yasunobu Okada ◽  
Kaori Sato-Numata ◽  
Ravshan Z. Sabirov ◽  
Tomohiro Numata
Keyword(s):  
Cell Death ◽  
Cell Volume ◽  
Apoptotic Cell ◽  
Cell Volume Regulation ◽  
Anion Channel ◽  
Cell Swelling ◽  
Dimensional Structure ◽  
Cation Channels ◽  
Anion Channels ◽  
Animal Cells

For survival and functions of animal cells, cell volume regulation (CVR) is essential. Major hallmarks of necrotic and apoptotic cell death are persistent cell swelling and shrinkage, and thus they are termed the necrotic volume increase (NVI) and the apoptotic volume decrease (AVD), respectively. A number of ubiquitously expressed anion and cation channels play essential roles not only in CVR but also in cell death induction. This series of review articles address the question how cell death is induced or protected with using ubiquitously expressed ion channels such as swelling-activated anion channels, acid-activated anion channels, and several types of TRP cation channels including TRPM2 and TRPM7. In the Part 1, we described the roles of swelling-activated VSOR/VRAC anion channels. Here, the Part 2 focuses on the roles of the acid-sensitive outwardly rectifying (ASOR) anion channel, also called the proton-activated chloride (PAC) anion channel, which is activated by extracellular protons in a manner sharply dependent on ambient temperature. First, we summarize phenotypical properties, the molecular identity, and the three-dimensional structure of ASOR/PAC. Second, we highlight the unique roles of ASOR/PAC in CVR dysfunction and in the induction of or protection from acidotoxic cell death under acidosis and ischemic conditions.

Effect of isosmotic removal of extracellular Na+ on cell volume and membrane potential in muscle cells

1994 ◽  
Vol 267 (3) ◽  
pp. C759-C767 ◽  
Author(s):  
C. Pena-Rasgado ◽  
J. C. Summers ◽  
K. D. McGruder ◽  
J. DeSantiago ◽  
H. Rasgado-Flores
Keyword(s):  
Membrane Potential ◽  
Membrane Permeability ◽  
Cell Volume ◽  
Muscle Cells ◽  
Membrane Depolarization ◽  
Cation Channels ◽  
Volume Loss ◽  
Barnacle Muscle ◽  
Nonselective Cation Channels

Isosmotic removal of extracellular Na+ (Nao) is a frequently performed manipulation. With the use of isolated voltage-clamped barnacle muscle cells, the effect of this manipulation on isosmotic cell volume was studied. Replacement of Nao by tris(hydroxymethyl)aminomethane produced membrane depolarization (approximately 20 mV) and cell volume loss (approximately 14%). The membrane depolarization was verapamil insensitive but depended on extracellular Ca2+ (Cao) and was probably due to activation of intracellular Ca2+ (Cai)-dependent nonselective cation channels. The cell volume loss did not require membrane depolarization but depended on Cao. This was probably due to an increase in Cai, mediated by activation of Ca2+ influx via Na+/Ca2+ exchange. Nao replacement by Li+ also promoted membrane depolarization (approximately 20 mV) and cell volume loss (20%). Both effects were reduced (approximately 73%) but were not abolished by Cao removal. Under this condition, the remaining membrane depolarization was probably due to a higher membrane permeability of Li+ over Na+. The remaining cell volume loss was due to membrane depolarization, which probably induced Ca2+ release from intracellular stores.

scholarly journals Cell Death Induction and Protection by Activation of Ubiquitously Expressed Anion/Cation Channels. Part 1: Roles of VSOR/VRAC in Cell Volume Regulation, Release of Double-Edged Signals and Apoptotic/Necrotic Cell Death

2021 ◽  
Vol 8 ◽  
Author(s):  
Yasunobu Okada ◽  
Ravshan Z. Sabirov ◽  
Kaori Sato-Numata ◽  
Tomohiro Numata
Keyword(s):  
Cell Death ◽  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Cation Channels ◽  
Necrotic Cell Death ◽  
Anion Channels ◽  
Necrotic Cell ◽  
Regulated Necrosis

Cell volume regulation (CVR) is essential for survival and functions of animal cells. Actually, normotonic cell shrinkage and swelling are coupled to apoptotic and necrotic cell death and thus called the apoptotic volume decrease (AVD) and the necrotic volume increase (NVI), respectively. A number of ubiquitously expressed anion and cation channels are involved not only in CVD but also in cell death induction. This series of review articles address the question how cell death is induced or protected with using ubiquitously expressed ion channels such as swelling-activated anion channels, acid-activated anion channels and several types of TRP cation channels including TRPM2 and TRPM7. The Part 1 focuses on the roles of the volume-sensitive outwardly rectifying anion channels (VSOR), also called the volume-regulated anion channel (VRAC), which is activated by cell swelling or reactive oxygen species (ROS) in a manner dependent on intracellular ATP. First we describe phenotypical properties, the molecular identity, and physical pore dimensions of VSOR/VRAC. Second, we highlight the roles of VSOR/VRAC in the release of organic signaling molecules, such as glutamate, glutathione, ATP and cGAMP, that play roles as double-edged swords in cell survival. Third, we discuss how VSOR/VRAC is involved in CVR and cell volume dysregulation as well as in the induction of or protection from apoptosis, necrosis and regulated necrosis under pathophysiological conditions.

Cation channels, cell volume and the death of an erythrocyte

2003 ◽  
Vol 447 (2) ◽  
pp. 121-125 ◽  
Author(s):  
Florian Lang ◽  
Karl S. Lang ◽  
Thomas Wieder ◽  
Svetlana Myssina ◽  
Christina Birka ◽  
...  
Keyword(s):  
Cell Volume ◽  
Cation Channels

Cation channels of the TRPC family contribute to development of nephropathy and retinopathy in the STZ model

2015 ◽  
Vol 10 (S 01) ◽  
Author(s):  
M Freichel ◽  
D Schumacher ◽  
C Matka ◽  
I Mathar ◽  
U Kriebs ◽  
...  
Keyword(s):  
Cation Channels

Contribution of large bacteria to bacterial biomass in a deep freshwater lake (Lake Biwa, Japan)

2020 ◽  
Vol 85 ◽  
pp. 131-139
Author(s):  
S Shen ◽  
Y Shimizu
Keyword(s):  
Cell Volume ◽  
Bacterial Cell ◽  
Lake Biwa ◽  
Bacterial Biomass ◽  
Spatial Variations ◽  
Freshwater Lake ◽  
Heterotrophic Nanoflagellates ◽  
Bacterial Productivity ◽  
Transmission Electron ◽  
Seasonal And Spatial Variations

Despite the importance of bacterial cell volume in microbial ecology in aquatic environments, literature regarding the effects of seasonal and spatial variations on bacterial cell volume remains scarce. We used transmission electron microscopy to examine seasonal and spatial variations in bacterial cell size for 18 mo in 2 layers (epilimnion 0.5 m and hypolimnion 60 m) of Lake Biwa, Japan, a large and deep freshwater lake. During the stratified period, we found that the bacterial cell volume in the hypolimnion ranged from 0.017 to 0.12 µm3 (median), whereas that in the epilimnion was less variable (0.016 to 0.033 µm3, median) and much lower than that in the hypolimnion. Additionally, in the hypolimnion, cell volume during the stratified period was greater than that during the mixing period (up to 5.7-fold). These differences in cell volume resulted in comparable bacterial biomass in the hypolimnion and epilimnion, despite the fact that there was lower bacterial abundance in the hypolimnion than in the epilimnion. We also found that the biomass of larger bacteria, which are not likely to be grazed by heterotrophic nanoflagellates, increased in the hypolimnion during the stratified period. Our data suggest that estimation of carbon flux (e.g. bacterial productivity) needs to be interpreted cautiously when cell volume is used as a constant parametric value. In deep freshwater lakes, a difference in cell volume with seasonal and spatial variation may largely affect estimations.

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