A novel method for measuring dynamic changes in cell volume

2004 ◽  
Vol 96 (5) ◽  
pp. 1886-1893 ◽  
Author(s):  
Cristina E. Davis ◽  
Joshua J. Rychak ◽  
Bouvard Hosticka ◽  
Scott C. Davis ◽  
J. Edward John ◽  
...  
Keyword(s):  
Cell Volume ◽  
Cell Types ◽  
Glass Capillary ◽  
Adaptive Mechanisms ◽  
Large Populations ◽  
In Series ◽  
Osmolyte Transport ◽  
Novel Method ◽  
Coulter Counters ◽  
Pressure Changes

Many cell types regulate their volume in response to extracellular tonicity changes through a complex series of adaptive mechanisms. Several methods that are presently used to measure cell volume changes include Coulter counters, fluorescent techniques, electronic impedance, and video microscopy. Although these methods are widely used and accepted, there are limitations associated with each technique. This paper describes a new method to measure changes in cell volume based on the principle that fluid flow within a rigid system is well determined. For this study, cos-7 cells were plated to line the inner lumen of a glass capillary and stimulated to swell or shrink by altering the osmolarity of the perfusing solution. The cell capillary was connected in series with a blank reference capillary, and differential pressure changes across each tube were monitored. The advantages of this method include 1) ability to continuously monitor changes in volume during rapid solution changes, 2) independence from cell morphology, 3) presence of physiological conditions with cell surface contacts and cell-cell interactions, 4) no phototoxic effects such as those associated with fluorescent methods, and 5) ability to report from large populations of cells. With this method, we could detect the previously demonstrated enhanced volume regulation of cells overexpressing the membrane phosphoprotein phospholemman, which has been implicated in osmolyte transport.

Colloid osmotic pressure changes of dog's blood exposed to different mixtures of CO2 and air

1978 ◽  
Vol 44 (2) ◽  
pp. 254-257 ◽  
Author(s):  
Y. Kakiuchi ◽  
A. B. DuBois ◽  
D. Gorenberg
Keyword(s):  
Red Blood Cells ◽  
Osmotic Pressure ◽  
Cell Volume ◽  
Blood Cells ◽  
Freezing Point ◽  
Colloid Osmotic Pressure ◽  
Red Cell ◽  
Freezing Point Depression ◽  
Pressure Changes ◽  
Different Levels

Hansen's membrane manometer method for measuring plasma colloid osmotic pressure was used to obtain the osmolality changes of dogs breathing different levels of CO2. Osmotic pressure was converted to osmolality by calibration of the manometer with saline and plasma, using freezing point depression osmometry. The addition of 10 vol% of CO2 to tonometered blood caused about a 2.0 mosmol/kg H2O increase of osmolality, or 1.2% increase of red blood cell volume. The swelling of the red blood cells was probably due to osmosis caused by Cl- exchanged for the HCO3- which was produced rapidly by carbonic anhydrase present in the red blood cells. The change in colloid osmotic pressure accompanying a change in co2 tension was measured on blood obtained from dogs breathing different CO2 mixtures. It was approximately 0.14 mosmol/kg H2O per Torr Pco2. The corresponding change in red cell volume could not be calculated from this because water can exchange between the plasma and tissues.

scholarly journals Role of glutathione on cell adhesion and volume.

2021 ◽  
Author(s):  
Alain Geloen ◽  
Emmanuelle Danty
Keyword(s):  
Cell Adhesion ◽  
Cell Volume ◽  
Reduced Glutathione ◽  
Self Regulation ◽  
Cell Types ◽  
Self Control ◽  
Animal Cells ◽  
Cellular Processes ◽  
Proliferation And Apoptosis ◽  
Glutamylcysteine Synthetase

Glutathione is the most abundant thiol in animal cells. Reduced glutathione (GSH) is a major intracellular antioxidant neutralizing free radicals and detoxifying electrophiles. It plays important roles in many cellular processes, including cell differentiation, proliferation, and apoptosis. In the present study we demonstrate that extracellular concentration of reduced glutathione markedly increases cell volume within few hours, in a dose-response manner. Pre-incubation of cells with BSO, the inhibitor of 7-glutamylcysteine synthetase, responsible for the first step in intracellular glutathione synthesis did not change the effect of reduced glutathione on cell volume suggesting a mechanism limited to the interaction of extracellular reduced glutathione on cell membrane. Results show that reduced GSH decreases cell adhesion resulting in an increased cell volume. Since many cell types are able to transport of GSH out, the present results suggest that this could be a fundamental self-regulation of cell volume, giving the cells a self-control on their adhesion proteins.

scholarly journals Multivalent proteins rapidly and reversibly phase-separate upon osmotic cell volume change

2019 ◽  
Author(s):  
Ameya P. Jalihal ◽  
Sethuramasundaram Pitchiaya ◽  
Lanbo Xiao ◽  
Pushpinder Bawa ◽  
Xia Jiang ◽  
...  
Keyword(s):  
Phase Separation ◽  
Cell Volume ◽  
Volume Change ◽  
Mammalian Cells ◽  
Internal State ◽  
Transcription Termination ◽  
Cell Types ◽  
List Type ◽  
Molecular Crowding ◽  
Minimal Impact

SUMMARYProcessing bodies (PBs) and stress granules (SGs) are prominent examples of sub-cellular, membrane-less compartments that are observed under physiological and stress conditions, respectively. We observe that the trimeric PB protein DCP1A rapidly (within ∼10 s) phase-separates in mammalian cells during hyperosmotic stress and dissolves upon isosmotic rescue (over ∼100 s) with minimal impact on cell viability even after multiple cycles of osmotic perturbation. Strikingly, this rapid intracellular hyperosmotic phase separation (HOPS) correlates with the degree of cell volume compression, distinct from SG assembly, and is exhibited broadly by homo-multimeric (valency ≥ 2) proteins across several cell types. Notably, HOPS sequesters pre-mRNA cleavage factor components from actively transcribing genomic loci, providing a mechanism for hyperosmolarity-induced global impairment of transcription termination. Together, our data suggest that the multimeric proteome rapidly responds to changes in hydration and molecular crowding, revealing an unexpected mode of globally programmed phase separation and sequestration that adapts the cell to volume change.GRAPHICAL ABSTRACTIN BRIEFCells constantly experience osmotic variation. These external changes lead to changes in cell volume, and consequently the internal state of molecular crowding. Here, Jalihal and Pitchiaya et al. show that multimeric proteins respond rapidly to such cellular changes by undergoing rapid and reversible phase separation.HIGHLIGHTSDCP1A undergoes rapid and reversible hyperosmotic phase separation (HOPS)HOPS of DCP1A depends on its trimerization domainSelf-interacting multivalent proteins (valency ≥ 2) undergo HOPSHOPS of CPSF6 explains transcription termination defects during osmotic stress

A mathematical model of rat distal convoluted tubule. II. Potassium secretion along the connecting segment

2005 ◽  
Vol 289 (4) ◽  
pp. F721-F741 ◽  
Author(s):  
Alan M. Weinstein
Keyword(s):  
Water Permeability ◽  
Collecting Duct ◽  
Cell Types ◽  
Distal Convoluted Tubule ◽  
Cortical Collecting Duct ◽  
Transport Activity ◽  
Luminal Membrane ◽  
In Series ◽  
Potassium Secretion ◽  
Osmotic Equilibration

A simulation of the rat distal convoluted tubule (DCT) is completed with a model of the late portion, or connecting tubule (CNT). This CNT model is developed by relying on a prior cortical collecting duct (CCD) model (Weinstein AM. Am J Physiol Renal Physiol 280: F1072–F1092, 2001), and scaling up transport activity of the three cell types to a level appropriate for DCT. The major difference between the two tubule segments is the lower CNT water permeability. In early CNT the luminal solution is hypotonic, with a K+ concentration less than that of plasma, and it is predicted that osmotic equilibration requires the whole length of CNT, to end with a nearly isotonic fluid, whose K+ concentration is severalfold greater than plasma. With respect to potassium secretion, early CNT conditions are conducive to maximal fluxes, whereas late conditions require the capacity to transport against a steep electrochemical gradient. The parameter dependence for K+ secretion under each condition is different: maximal secretion depends on luminal membrane K+ permeability, but the limiting luminal K+ concentration does not. However, maximal secretion and the limiting gradient are both enhanced by greater Na+ reabsorption. While higher CNT water permeability depresses K+ secretion, it favors Na+ reabsorption. Thus in antidiuresis there is a trade-off between enhanced Na+-dependent K+ secretion and the attenuation of K+ secretion by slow flow. When the CNT model is configured in series with the early DCT, thiazide diuretics promote renal K+ wasting by shifting Na+ reabsorption from early DCT to CNT; they promote alkalosis by shifting the remaining early DCT Na+ reabsorption to Na+/H+ exchange. This full DCT is suitable for simulating the defects of hyperkalemic hypertension, but the model offers no suggestion of a tight junction abnormality that might contribute to the phenotype.

Ion Channels and Cell Volume Regulation: Chaos in an Organized System

Physiology ◽  
1990 ◽  
Vol 5 (3) ◽  
pp. 112-119 ◽  
Author(s):  
SA Lewis ◽  
P Donaldson
Keyword(s):  
Ion Channels ◽  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Cell Types ◽  
Initial Increase ◽  
Normal Value ◽  
Basic Strategy

Exposure of many vertebrate cells to solutions more dilute or concentrated than the physiological "norm" results in an initial increase or decrease in cell volume followed by a recovery of volume toward a normal value. Although the basic strategy for volume regulation is the same for cell types studied, the mechanism by which the cell regulates ion channels appears to be tissue dependent.

Focal adhesion kinase PTK2 autophosphorylation is not required for the activation of sodium–hydrogen exchange by decreased cell volume in the preimplantation mouse embryo

Zygote ◽  
2019 ◽  
Vol 27 (3) ◽  
pp. 173-179
Author(s):  
Jane C. Fenelon ◽  
Baozeng Xu ◽  
Jay M. Baltz
Keyword(s):  
Focal Adhesion Kinase ◽  
Cell Volume ◽  
Focal Adhesion ◽  
Mouse Embryo ◽  
Hydrogen Exchange ◽  
Cell Types ◽  
Mouse Embryos ◽  
Cell Stage ◽  
Early Embryos ◽  
Early Mouse

SummaryRecovery from decreased cell volume is accomplished by a regulated increase of intracellular osmolarity. The acute response is activation of inorganic ion transport into the cell, the main effector of which is the Na+/H+ exchanger NHE1. NHE1 is rapidly activated by a cell volume decrease in early embryos, but how this occurs is incompletely understood. Elucidating cell volume-regulatory mechanisms in early embryos is important, as it has been shown that their dysregulation results in preimplantation developmental arrest. The kinase JAK2 has a role in volume-mediated NHE1 activation in at least some cells, including 2-cell stage mouse embryos. However, while 2-cell embryos show partial inhibition of NHE1 when JAK2 activity is blocked, NHE1 activation in 1-cell embryos is JAK2-independent, implying a requirement for additional signalling mechanisms. As focal adhesion kinase (FAK aka PTK2) becomes phosphorylated and activated in some cell types in response to decreased cell volume, we sought to determine whether it was involved in NHE1 activation in the early mouse embryo. FAK activity requires initial autophosphorylation of a tyrosine residue, Y397. However, FAK Y397 phosphorylation levels were not increased in either 1- or 2-cell embryos after cell volume was decreased. Furthermore, the selective FAK inhibitor PF-562271 did not affect NHE1 activation at concentrations that essentially eliminated Y397 phosphorylation. Thus, autophosphorylation of FAK Y397 does not appear to be required for NHE1 activation induced by a decrease in cell volume in early mouse embryos.

A novel method for reducing harmonics in series-connected rectifiers

2008 ◽  
Vol 78 (7) ◽  
pp. 1256-1264
Author(s):  
Kaili Xu ◽  
Kala Meah ◽  
A.H.M. Sadrul Ula
Keyword(s):  
In Series ◽  
Novel Method
Sign in / Sign up

Export Citation Format

Share Document