How Do Animal Cells Control Their Volume
maintenance of a constant volume in the face of extracellular and intracellular osmotic perturbations is a critical problem faced past all cells. Most cells respond to swelling or shrinkage by activating specific membrane transport and/or metabolic processes that serve to render cell volume to its normal resting state. These processes are essential for normal jail cell role and survival. This paper provides an overview of the cellular and molecular events underlying cell volume homeostasis.
Osmosis
The bulk movement of water beyond a semipermeable membrane is termed osmosis. An ideal semipermeable membrane is i that is permeable only to water. If such as membrane separates solutions with different solute concentrations, say, 0.ane M NaCl on 1 side and 1 M NaCl on the other, h2o will move from the dilute into the concentrated NaCl solution (Fig. 1). Water flow will continue until the NaCl concentrations in both solutions are equalized. The driving force for h2o period is the concentration gradient for water. The concentration of water is higher in the 0.i M NaCl solution compared with the ane One thousand NaCl solution.
Fig. ane.Osmotic water flow across a semipermeable membrane. Pointer indicates direction of water period. Water flows from an expanse of loftier water concentration (i.east., 0.1 K NaCl) into an area of lower h2o concentration (i.east., 1 Chiliad NaCl). If pressure level is applied to the bedroom on the left with the piston, water flow beyond the membrane will exist reduced. The pressure level required to stop water period is defined as the osmotic force per unit area (Eq. 1).
Osmotic water period beyond the membrane can exist prevented past applying an opposing hydrostatic force (Fig. ane). The pressure required to end water menstruation is termed the osmotic pressure. The mathematical expression that defines osmotic pressure was derived by van't Hoff and is
(ane)
where Δπ is osmotic pressure difference, R is the gas constant, T is the absolute temperature, and ΔC i is the deviation in solute concentration across the membrane.
Osmotic force per unit area is dependent on the total concentration of dissolved solute particles. The terms osmolality and osmolarity indicate the total number of particles present in a kilogram of solvent and a liter of solution, respectively. One osmole is 1 mol of particle, which are 6.02 × ten23 individual particles. Osmolality and osmolarity are used interchangeably when referring to the relatively dilute solutions of the body.
The above discussion of osmosis is based on the simplifying concept that water flow is occurring across a membrane permeable but to water. Real membranes are non quite so tidy. All membranes take finite solute permeabilities. While many biologically relevant solutes have permeabilities substantially lower than water and behave as though they were effectively impermeable, some solutes accept permeabilities approaching that of h2o. These high-permeability solutes diffuse beyond the membrane downwards their concentration gradient. Equally they do so, the osmotic pressure driving water catamenia is reduced. If the motion of solute is fast enough, the concentrations of the solute on the two sides of the membrane can become equalized earlier significant osmotic water menses occurs.
To account for the nonideal beliefs of membranes, Staverman derived the term reflection coefficient for solute i, σ i , as
(ii)
where Δπobs is the observed osmotic pressure and Δπth is the theoretical osmotic force per unit area obtained from Eq. i. The reflection coefficient is a dimensionless term that ranges from 1 for a solute that behaves as though it were finer impermeant (i.due east., the solute is "reflected" by the membrane), to 0 for a solute whose permeability is similar to that of water. The effective osmotic pressure, Δπeff, across a membrane generated past solute i is therefore
(3)
The flow of water Jv beyond a membrane is defined as
(iv)
where Lp is the hydraulic electrical conductivity coefficient of the membrane and ΔP the hydrostatic pressure difference across the membrane. The hydraulic conductivity coefficient is a measure of the water permeability of the membrane. Prison cell membranes do not generate and maintain significant hydrostatic force per unit area gradients. Thus, when because water catamenia into and out of animal cells, the ΔP term in Eq. 4 can be ignored. Even so, in organisms with relatively rigid prison cell walls, such as bacteria, plants, and yeast, significant hydrostatic pressure gradients can be generated and play important roles in driving water menses.
Water flow across most biological membranes occurs by uncomplicated improvidence of water molecules through the lipid bilayer. However, some cells possess specialized proteins that form transmembrane water-selective pores termed aquaporins (1, 28). Aquaporins dramatically increase the water permeability of cell membranes.
Fundamentals of Cell Volume Regulation
Water is effectively in thermodynamic equilibrium across the plasma membrane. In other words, the osmotic concentration of cytoplasmic (πι) and extracellular (π°) fluids are equal under steady-state atmospheric condition. Changes in intracellular or extracellular solute content generate a transmembrane osmotic gradient (Δπ). Because jail cell membranes are freely permeable to h2o, whatsoever such gradient results in the firsthand flow of h2o into or out of the cell until equilibrium is again achieved. Since fauna cell membranes are unable to generate or sustain significant hydrostatic force per unit area gradients, water flow causes cell swelling or shrinkage.
Cell volume changes are usually grouped into ii wide categories, anisosmotic and isosmotic. Anisosmotic volume changes are induced by alterations in extracellular osmolality. Under normal physiological conditions, nearly mammalian cells, with a few noteworthy exceptions (due east.g., cells in the renal medulla and gastrointestinal tract), are protected from anisosmotic volume changes by the kidney's precise regulation of plasma osmolality. Notwithstanding, plasma osmolality can be disrupted past a multifariousness of affliction states and their treatments (17, 18).
Isosmotic volume changes are brought about by alterations in intracellular solute content. All cells are threatened by possible isosmotic swelling or shrinkage. Under steady-land weather, intracellular solute levels are held constant by a precise balance between solute influx and efflux beyond the plasma membrane, and past the metabolic production and removal of osmotically active substances. A diversity of physiological and pathophysiological conditions, nonetheless, can disrupt this balance (17, 18). For example, the cell swelling that occurs in the brain subsequently a stroke or head trauma is an example of isosmotic volume increase and is due to intracellular accumulation of NaCl and other solutes.
Experimental Measurement of Jail cell Volume
A variety of methods are available for measuring absolute and relative prison cell volume changes under experimental weather condition including electronic sizing by Coulter-type impedance techniques, calorie-free scattering, ion-sensitive microelectrode methods that measure the concentration of intra- or extracellular impermeant molecules, and radioactive tracer methods. Microscopy methods are widely used for measuring jail cell volume changes. Unmarried cells tin can be imaged by bright field microscopy and volume changes quantified by three-dimensional reconstruction. If cell shape is spherical, relative volume changes can exist quantified simply by measuring jail cell bore. Fluorescence microscopy methods can be used to measure changes in the intensity of fluorescent probes trapped inside the cell. As long every bit the probes are non sensitive to other cellular parameters such as pH, Ca2+ levels, etc., changes in fluorescence intensity reliably track swelling- and shrinkage-induced volume perturbations.
Regulation of Prison cell Volume
Cells respond to volume perturbations by activating book regulatory mechanisms. The processes past which bloated and shrunken cells return to normal book are collectively termed regulatory book decrease and regulatory book increment, respectively (Fig. two). Cell volume tin only exist regulated by the gain or loss of osmotically active solutes, primarily inorganic ions such equally Na+, Thousand+, Cl−, or small-scale organic molecules termed organic osmolytes.
Fig. 2.Cells activate volume regulatory mechanisms in response to volume perturbations. Book regulatory solute loss and gain are termed regulatory volume decrease (RVD) and regulatory volume increase (RVI), respectively. The time course of RVD and RVI varies with jail cell type and experimental conditions. Typically, however, RVI mediated past electrolyte uptake and RVD mediated by electrolyte and organic osmolyte loss occur over a period of minutes.
Volume regulatory electrolyte loss and gain are mediated exclusively by membrane transport processes (12, xiii, twenty). In most animal cells, regulatory book decrease occurs through loss of KCl via activation of separate K+ and Cl− channels or by activation of the G-Cl cotransporter. Regulatory volume increase occurs past uptake of both KCl and NaCl. Aggregating of these salts is brought well-nigh by activation of Na+/H+ and Cl−/HCO3− exchangers or the Na-Thousand-2Cl cotransporter. Figure 3 illustrates the ion send systems commonly involved in prison cell volume regulation. Activation of these ship pathways is rapid and occurs inside seconds to minutes after book perturbation. Rapid stimulation of electrolyte transport is possible because the channels and transporters past which information technology is mediated reside continuously in the plasma membrane or are stored in submembrane cytoplasmic vesicles. Sure volume-sensitive ion transport systems play multiple roles, participating in volume regulation besides as transepithelial salt and water movement, and intracellular pH control.
Fig. 3.Volume regulatory electrolyte loss and accumulation is mediated by changes in the activity of membrane carriers and channels. Activation of these ship pathways occurs rapidly later on the volume perturbation. This indicates that the aqueduct and carrier proteins are either resident in the cell membrane or are rapidly inserted from a preexisting cytoplasmic puddle.
Organic osmolytes are establish in high (tens to hundreds of millimolar) concentrations in the cytosol of all organisms from leaner to humans (3, 4, 12, 31). These solutes play cardinal roles in prison cell book homeostasis and may besides function every bit general cytoprotectants. In brute cells, organic osmolytes are grouped into three distinct classes: 1) polyols (e.g., sorbitol and myo-inositol), 2) amino acids and their derivatives (e.k., taurine, alanine, and proline), and iii) methylamines (e.g., betaine, glycerophosphorylcholine) (Fig. 4).
Fig. four.Major classes of organic osmolytes institute in animal cells. Organic osmolytes used past animal cells are grouped into three classes: 1) amino acids and their derivatives, 2) polyols, and 3) methylamines.
Organic osmolytes are "compatible" or "nonperturbing" solutes (three, 4, 31). They have unique biophysical and biochemical backdrop that allow cells to accrue them to loftier levels or to withstand big shifts in their concentration without deleterious effects on cellular structure and function. In dissimilarity, and so-called "perturbing" solutes, such as electrolytes or urea tin harm cells or disrupt metabolic processes when they are nowadays at high concentrations or when big shifts in their concentrations occur. For example, elevated electrolyte levels and intracellular ionic force tin denature or precipitate cell macromolecules. Fifty-fifty smaller changes in cellular inorganic ion levels can alter resting membrane potential, the rates of enzymatically catalyzed reactions and membrane solute transport that is coupled to ion gradients.
Aggregating of organic osmolytes is mediated either by free energy-dependent transport from the external medium or by changes in the rates of osmolyte synthesis and degradation (Fig. 5) (iii, 4, 12, 31). Volume regulatory organic osmolyte accumulation is typically a boring process relative to electrolyte uptake and requires many hours later on initial activation to reach completion. This slow time course is observed because activation of organic osmolyte accumulation pathways unremarkably requires transcription and translation of genes coding for organic osmolyte transporters and synthesis enzymes.
Fig. 5.Mechanisms of organic osmolyte accumulation and loss. Volume regulatory organic osmolyte accumulation in animal cells is mediated largely by changes in the activity of Na+-coupled membrane transporters and by changes in the rates of synthesis and degradation. Organic osmolyte accumulation is typically a boring process relative to volume regulatory electrolyte uptake and requires many hours after initial activation to reach completion. This dull fourth dimension course is observed considering activation of organic osmolyte accumulation pathways usually requires transcription and translation of genes coding for organic osmolyte transporters and synthesis enzymes. Organic osmolyte loss appears to be mediated largely by passive efflux mechanisms. Activation of organic osmolyte efflux mechanisms is rapid and typically occurs within seconds afterwards cell swelling is initiated.
Loss of organic osmolytes from cells is elicited by swelling and occurs in two distinct steps. First, swelling induces a very rapid (i.eastward., seconds) increase in passive organic osmolyte efflux (Fig. five) (9–11). Downregulation of organic osmolyte synthesis and uptake mechanisms also contributes to the loss of these solutes from the jail cell. Overall, this process is boring. Cell swelling inhibits transcription of the genes coding for organic osmolyte transporters and synthesis enzymes (three, 31). Every bit transcription decreases, mRNA levels driblet and the number of functional proteins declines over a period of many hours to days.
How Do Cells Sense Their Size?
Volume sensing mechanisms appear to be extremely sensitive. For example, studies by Lohr and Grantham (14) on the renal proximal tubule have demonstrated that cells can sense and reply to volume changes of <iii%. However, our understanding of the mechanisms by which cells sense volume perturbations and transduce those changes into regulatory responses is rudimentary.
Several possible volume signals have been postulated including swelling- and shrinkage-induced changes in membrane tension, cytoskeletal architecture, cellular ion concentrations and the concentration of cytoplasmic macromolecules (12, twenty, 21). All of these hypotheses have their strengths and weaknesses. At present, information technology appears that no i signaling mechanism can business relationship for the book sensitivity of the diverse genes and membrane transport pathways that are activated or inactivated in response to cell volume perturbations. To further complicate the film, recent evidence suggests that cells can observe more than simple swelling or shrinkage. Cells most likely possess a wide assortment of volume detector and effector mechanisms that reply selectively to both the magnitude and nature of the volume pertubation (7, 16, 24). Such functionally singled-out sensor and effector pathways may beget the cell simultaneous control over a diverseness of parameters (e.g., intracellular pH and ionic limerick) in addition to volume.
Molecular insight into the signals that initiate volume regulatory responses has been gained from studies on bacteria and kidney cells. The large conductance mechanosensitive channel, thousandechanosouthwardensitive channel large conductance (MscL), in Escherichia coli mediates osmolyte efflux in response to hypotonic shock. MscL has been purified, reconstituted and characterized structurally using 10-ray crystallography (2, 25, 26). The purified channel protein reconstituted into planar lipid bilayers is activated by membrane stretch demonstrating that the channel protein itself senses directly membrane tension transmitted through the bilayer (2, 25, 26).
The mechanisms by which hypertonic stress induces increased expression of genes encoding organic osmolyte transporters and enzymes involved in their synthesis have been studied extensively in the kidney. The major organic osmolytes nowadays in the hypertonic medulla of the mammalian kidney include sorbitol, betaine and myo-inositol. Sorbitol is accumulated by increased synthesis mediated by the enzyme aldose reductase (AR). Betaine and myo-inositol accumulation is mediated past transport from the extracellular space via the Na-Cl-betaine (BGT1) and the Na-myo-inositol (SMIT) cotransporters (3).
Early on studies by Burg and co-workers (3) suggested that increases in intracellular ionic forcefulness brought about by hypertonic shrinkage and subsequent regulatory volume increment triggered increased gene transcription. For example, Uchida et al. (27) observed a linear relationship between AR action and total intracellular Na+ and K+ levels.
The promoter regions of AR, SMIT, and BGT1 comprise regulatory domains termed tonicity-responsive enhancers (TonE) that modulates gene expression in response to hypertonic stress (three). Kwon and co-workers (19) cloned the transcription factor TonEBP (TonE bounden protein) that binds to this regulatory domain and initiates gene transcription. TonEBP is a member of the Rel family of transcription factors. In response to hypertonic stupor, TonEBP translocates from the cytoplasm into the nucleus where it binds to genes containing TonE sites (29, 30). Nuclear translocation and TonEBP binding may exist mediated by increases in cytoplasmic ionic force.
As with the initial volume signal sensed by the cell, there is little clear-cut understanding of the signaling mechanisms by which cell volume changes are transduced into regulatory responses. Numerous signal transduction pathways have been implicated in the command of volume regulatory transport pathways including changes in intracellular Ca2+ concentration, GTPase activity, serine/threonine and tyrosine phosphorylation/dephosphosphorylation, and eicosanoid levels (12).
Perchance the almost extensively studied and best understood volume regulatory signaling mechanisms are the phosphorylation/dephosphorylation reactions that regulate swelling- and shrinkage-induced activation of the K-Cl and Na-K-2Cl cotransporters. Swelling-induced activation and shrinkage-induced inactivation of the K-Cl cotransporter are mediated by serine/threonine dephosphorylation and phosphorylation, respectively. The converse is truthful for the Na-K-2Cl cotransporter; shrinkage-induced activation is mediated past phosphorylation and swelling-induced inactivation is brought by dephosphorylation. Pharmacological studies advise that blazon ane protein phosphatase mediates protein dephosphorylation (8, 12, xv, 21).
Detailed transport studies advise that both transporters are regulated by a mutual kinase whose activity is modulated by cell volume changes (8, 12, fifteen, 21). The identity of this putative common volume-sensitive kinase is non firmly established. Still, Delpire and co-workers (22) demonstrated recently that the STE20-related kinase PASK (Proline-Alanine-rich SouthwardTE20-related Yardinase) interacts with the NH2 termini of both the G-Cl and Na-K-2Cl cotransporters. PASK is a member of a big kinase superfamily that is divided into p21-activated kinase (PAK) and germinal heart kinase (GCK) subfamilies (v). Members of this superfamily regulate numerous fundamental physiological processes including apoptosis, cellular stress responses, morphogenesis, cytoskeletal architecture, jail cell cycle, and oocyte meiotic maturation (five).
STE20 was identified originally in yeast, where it functions equally a mitogen-activated protein kinase kinase kinase kinase (MAP4K) that is activated in response to hypertonic stress and regulates aggregating of the organic osmolyte glycerol (23). Dowd and Forbush (half-dozen) have shown that PASK plays a function in activation of Na-K-2Cl cotransporter NKCC1 in response to hypertonic shrinkage. The regulatory office of PASK is most likely mediated through direct phosphorylation of the cotransporter (6). The studies in yeast and mammalian cells suggest that STE20-related kinases may be important components of the indicate transduction pathways that control jail cell book regulatory mechanisms.
In determination, the ability to tightly control solute and water balance during osmotic challenge is an essential prerequisite for cellular life. Cellular osmotic homeostasis is maintained by the regulated accumulation and loss of inorganic ions and small organic solutes termed organic osmolytes. Organic osmolytes are "uniform" or "nonperturbing" solutes and are typically found in concentrations of tens to hundreds of millimolars in the cytosol of all organisms from bacteria to humans. The effector mechanisms responsible for osmoregulatory solute accumulation and loss in beast cells are more often than not well understood. Even so, major gaps be in our understanding of the signals and signaling pathways past which animal cells detect volume perturbations and activate book regulatory mechanisms. Elucidation of book sensing mechanisms and signaling pathways represents the most pressing and meaning challenge in the field and is essential for understanding fully cell volume control and related cellular processes.
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