scholarly journals Cl − and K + channels and their role in primary brain tumour biology

2014 ◽  
Vol 369 (1638) ◽  
pp. 20130095 ◽  
Author(s):  
Kathryn L. Turner ◽  
Harald Sontheimer
Keyword(s):  
Ion Channels ◽  
Cell Volume ◽  
Surrounding Tissue ◽  
Volume Changes ◽  
Primary Brain Tumours ◽  
Primary Brain Tumour ◽  
Tumour Biology ◽  
M Phase ◽  
Volume Condensation ◽  
High Concentrations

Profound cell volume changes occur in primary brain tumours as they proliferate, invade surrounding tissue or undergo apoptosis. These volume changes are regulated by the flux of Cl − and K + ions and concomitant movement of water across the membrane, making ion channels pivotal to tumour biology. We discuss which specific Cl − and K + channels are involved in defined aspects of glioma biology and how these channels are regulated. Cl − is accumulated to unusually high concentrations in gliomas by the activity of the NKCC1 transporter and serves as an osmolyte and energetic driving force for volume changes. Cell volume condensation is required as cells enter M phase of the cell cycle and this pre-mitotic condensation is caused by channel-mediated ion efflux. Similarly, Cl − and K + channels dynamically regulate volume in invading glioma cells allowing them to adjust to small extracellular brain spaces. Finally, cell condensation is a hallmark of apoptosis and requires the concerted activation of Cl − and Ca 2+ -activated K + channels. Given the frequency of mutation and high importance of ion channels in tumour biology, the opportunity exists to target them for treatment.

scholarly journals A role for ion channels in glioma cell invasion

2005 ◽  
Vol 2 (1) ◽  
pp. 39-49 ◽  
Author(s):  
MICHAEL B. MCFERRIN ◽  
HARALD SONTHEIMER
Keyword(s):  
Ion Channels ◽  
Cell Volume ◽  
Progenitor Cells ◽  
Current Knowledge ◽  
Glioma Cells ◽  
Normal Brain ◽  
Volume Changes ◽  
Mature Brain ◽  
Raft Domains ◽  
Migratory Cells

Many cells, including neuronal and glial progenitor cells, stem cells and microglial cells, have the capacity to move through the extracellular spaces of the developing and mature brain. This is particularly pronounced in astrocyte-derived tumors, gliomas, which diffusely infiltrate the normal brain. Although a significant body of literature exists regarding signals that are involved in the guidance of cells and their processes, little attention has been paid to cell-shape and cell-volume changes of migratory cells. However, extracellular spaces in the brain are very narrow and represent a major obstacle that requires cells to dynamically regulate their volume. Recent studies in glioma cells show that this involves the secretion of Cl− and K+ with water. Pharmacological inhibition of Cl− channels impairs their ability to migrate and limits tumor progression in experimental tumor models. One Cl−-channel inhibitor, chlorotoxin, is currently in Phase II clinical trials to treat malignant glioma. This article reviews our current knowledge of cell-volume changes and the role of ion channels during the migration of glioma cells. It also discusses evidence that supports the importance of channel-mediated cell-volume changes in the migration of immature neurons and progenitor cells during development. New unpublished data is presented, which demonstrates that Cl− and K+ channels involved in cell shrinkage localize to lipid-raft domains on the invadipodia of glioma cells and that their presence might be regulated by trafficking of these proteins in and out of lipid rafts.

Signal Transduction and Cell Volume Regulation in Plant Leaflet Movements

Physiology ◽  
1996 ◽  
Vol 11 (3) ◽  
pp. 108-114 ◽  
Author(s):  
N Moran ◽  
YG Yueh ◽  
RC Crain
Keyword(s):  
Signal Transduction ◽  
Ion Channels ◽  
Ion Transport ◽  
Cell Volume ◽  
Volume Regulation ◽  
Biological Clock ◽  
Cell Volume Regulation ◽  
Volume Changes ◽  
Effect Of Light

Leaflet movements and underlying cell volume changes are visual indicators of ion transport in specialized cells of various plants. These cells are an attractive model to study regulation of plant ion transport. We focus on the effect of light, the biological clock, and mechanosensing on ion channels mediating cell volume regulation.

The Effects of Butyric Acid on the Differentiation, Proliferation, Apoptosis, and Autophagy of IPEC-J2 Cells

2020 ◽  
Vol 20 (4) ◽  
pp. 307-317
Author(s):  
Yuan Yang ◽  
Jin Huang ◽  
Jianzhong Li ◽  
Huansheng Yang ◽  
Yulong Yin
Keyword(s):  
Cell Viability ◽  
P38 Mapk ◽  
Butyric Acid ◽  
Cell Apoptosis ◽  
Mapk Pathway ◽  
Mrna Level ◽  
Dependent Manner ◽  
M Phase ◽  
High Concentrations ◽  
Underlying Mechanisms

Background: Butyric acid (BT), a short-chain fatty acid, is the preferred colonocyte energy source. The effects of BT on the differentiation, proliferation, and apoptosis of small intestinal epithelial cells of piglets and its underlying mechanisms have not been fully elucidated. Methods: In this study, it was found that 0.2-0.4 mM BT promoted the differentiation of procine jejunal epithelial (IPEC-J2) cells. BT at 0.5 mM or higher concentrations significantly impaired cell viability in a dose- and time-dependent manner. In addition, BT at high concentrations inhibited the IPEC-J2 cell proliferation and induced cell cycle arrest in the G2/M phase. Results: Our results demonstrated that BT triggered IPEC-J2 cell apoptosis via the caspase8-caspase3 pathway accompanied by excess reactive oxygen species (ROS) and TNF-α production. BT at high concentrations inhibited cell autophagy associated with increased lysosome formation. It was found that BT-reduced IPEC-J2 cell viability could be attenuated by p38 MAPK inhibitor SB202190. Moreover, SB202190 attenuated BT-increased p38 MAPK target DDIT3 mRNA level and V-ATPase mRNA level that were responsible for normal acidic lysosomes. Conclusion: In conclusion, 1) at 0.2-0.4 mM, BT promotes the differentiation of IPEC-J2 cells; 2) BT at 0.5 mM or higher concentrations induces cell apoptosis via the p38 MAPK pathway; 3) BT inhibits cells autophagy and promotes lysosome formation at high concentrations.

Liver cell hydration and integrin signaling

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Michele Bonus ◽  
Dieter Häussinger ◽  
Holger Gohlke
Keyword(s):  
Cell Volume ◽  
Liver Cell ◽  
Cell Function ◽  
The Other ◽  
Signaling Cascades ◽  
Integrin Signaling ◽  
Volume Changes ◽  
The One ◽  
And Oxidative Stress

Abstract Liver cell hydration (cell volume) is dynamic and can change within minutes under the influence of hormones, nutrients, and oxidative stress. Such volume changes were identified as a novel and important modulator of cell function. It provides an early example for the interaction between a physical parameter (cell volume) on the one hand and metabolism, transport, and gene expression on the other. Such events involve mechanotransduction (osmosensing) which triggers signaling cascades towards liver function (osmosignaling). This article reviews our own work on this topic with emphasis on the role of β1 integrins as (osmo-)mechanosensors in the liver, but also on their role in bile acid signaling.

Cell volume changes affect gluconeogenesis in the perfused liver of the catfishClarias batrachus

2004 ◽  
Vol 29 (3) ◽  
pp. 337-347 ◽  
Author(s):  
Carina Goswami ◽  
Shritapa Datta ◽  
Kuheli Biswas ◽  
Nirmalendu Saha
Keyword(s):  
Cell Volume ◽  
Perfused Liver ◽  
Volume Changes

scholarly journals Hydrogen, Bicarbonate, and Their Associated Exchangers in Cell Volume Regulation

2021 ◽  
Vol 9 ◽  
Author(s):  
Yizeng Li ◽  
Xiaohan Zhou ◽  
Sean X. Sun
Keyword(s):  
Ion Channels ◽  
Cell Volume ◽  
Volume Regulation ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Cell Function ◽  
Water Flux ◽  
Cell Volume Regulation ◽  
Sodium Potassium ◽  
Before And After

Cells lacking a stiff cell wall, e.g., mammalian cells, must actively regulate their volume to maintain proper cell function. On the time scale that protein production is negligible, water flow in and out of the cell determines the cell volume variation. Water flux follows hydraulic and osmotic gradients; the latter is generated by various ion channels, transporters, and pumps in the cell membrane. Compared to the widely studied roles of sodium, potassium, and chloride in cell volume regulation, the effects of proton and bicarbonate are less understood. In this work, we use mathematical models to analyze how proton and bicarbonate, combined with sodium, potassium, chloride, and buffer species, regulate cell volume upon inhibition of ion channels, transporters, and pumps. The model includes several common, widely expressed ion transporters and focuses on obtaining generic outcomes. Results show that the intracellular osmolarity remains almost constant before and after cell volume change. The steady-state cell volume does not depend on water permeability. In addition, to ensure the stability of cell volume and ion concentrations, cells need to develop redundant mechanisms to maintain homeostasis, i.e., multiple ion channels or transporters are involved in the flux of the same ion species. These results provide insights for molecular mechanisms of cell volume regulation with additional implications for water-driven cell migration.

scholarly journals Molecular mechanisms of regulation of fast-inactivating voltage-dependent transient outward K+current in mouse heart by cell volume changes

2005 ◽  
Vol 568 (2) ◽  
pp. 423-443 ◽  
Author(s):  
Guan-Lei Wang ◽  
Ge-Xin Wang ◽  
Shintaro Yamamoto ◽  
Linda Ye ◽  
Heather Baxter ◽  
...  
Keyword(s):  
Cell Volume ◽  
Molecular Mechanisms ◽  
Mouse Heart ◽  
Volume Changes ◽  
Voltage Dependent ◽  
K Current

Changes in vascular and extravascular volumes of eel muscle in response to catecholamines: the function of the caudal lymphatic heart

1982 ◽  
Vol 96 (1) ◽  
pp. 195-208
Author(s):  
P. S. Davie
Keyword(s):  
Vascular System ◽  
Volume Changes ◽  
Heart Frequency ◽  
Vascular Volume ◽  
Interstitial Volume ◽  
Resistance Vessels ◽  
Lymph Heart ◽  
Capillary Resistance ◽  
High Concentrations ◽  
Lymphatic Heart

1. Vascular volume changes in an isolated saline-perfused eel tail preparation in response to catecholamines were small (less than 2%) and are explicable in terms of changes in volume of pre-capillary resistance vessels. 2. Extravascular-extracellular (interstitial) volume increased less than 3% during infusion of adrenaline (AD) at concentrations of 1 × 10(−6) to 1 × 10(−3) M. Injection of doses of AD and noradrenaline (NA) between 1 nmol and 100 nmol caused maximum interstitial volume changes of less than 11%. 3. Isoprenaline caused only very small changes in vascular and interstitial volume. 4. Caudal lymph heart frequency increases when high concentrations (greater than 1 × 10(−6) M) and doses (greater than 1 nmol) of AD and NA were administered. 5. Caudal lymph heart frequency increases were significantly correlated with changes in outflow after vascular volume adjustments. One function of the caudal lymph heart is to return interstitial fluid to the vascular system.

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