scholarly journals Cell Volume Regulation in the Epidermis

2021 ◽  
Vol 55 (S1) ◽  
pp. 57-70
Keyword(s):  
Cell Volume ◽  
Current Knowledge ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Skin Layer ◽  
Cell Swelling ◽  
Volume Changes ◽  
Barrier Formation ◽  
Molecular Machinery ◽  
Volume Decrease

In order to cope with external stressors such as changes in humidity and temperature or irritating substances, the epidermis as the outermost skin layer forms a continuously renewing and ideally intact protective barrier. Under certain circumstances, this barrier can be impaired and epidermal cells have to counteract cell swelling or shrinkage induced by osmotic stress via regulatory volume decrease (RVD) or increase (RVI). Here, we will review the current knowledge regarding the molecular machinery underlying RVD and RVI in the epidermis. Furthermore, we will discuss the current understanding how cell volume changes and its regulators are associated with epidermal renewal and barrier formation.

scholarly journals Human trabecular meshwork cell volume regulation

2002 ◽  
Vol 283 (1) ◽  
pp. C315-C326 ◽  
Author(s):  
Claire H. Mitchell ◽  
Johannes C. Fleischhauer ◽  
W. Daniel Stamer ◽  
K. Peterson-Yantorno ◽  
Mortimer M. Civan
Keyword(s):  
Cell Volume ◽  
Trabecular Meshwork ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Channel Blockers ◽  
Uptake Mechanism ◽  
Fluid Uptake ◽  
Intracellular Ca ◽  
Predominant Effect ◽  
Volume Decrease

The volume of certain subpopulations of trabecular meshwork (TM) cells may modify outflow resistance of aqueous humor, thereby altering intraocular pressure. This study examines the contribution that Na+/H+, Cl−/HCO[Formula: see text]exchange, and K+-Cl− efflux mechanisms have on the volume of TM cells. Volume, Cl− currents, and intracellular Ca2+ activity of cultured human TM cells were studied with calcein fluorescence, whole cell patch clamping, and fura 2 fluorescence, respectively. At physiological bicarbonate concentration, the selective Na+/H+ antiport inhibitor dimethylamiloride reduced isotonic cell volume. Hypotonicity triggered a regulatory volume decrease (RVD), which could be inhibited by the Cl− channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), the K+channel blockers Ba2+ and tetraethylammonium, and the K+-Cl− symport blocker [(dihydroindenyl)oxy]alkanoic acid. The fluid uptake mechanism in isotonic conditions was dependent on bicarbonate; at physiological levels, the Na+/H+ exchange inhibitor dimethylamiloride reduced cell volume, whereas at low levels the Na+-K+-2Cl− symport inhibitor bumetanide had the predominant effect. Patch-clamp measurements showed that hypotonicity activated an outwardly rectifying, NPPB-sensitive Cl− channel displaying the permeability ranking Cl− > methylsulfonate > aspartate. 2,3-Butanedione 2-monoxime antagonized actomyosin activity and both increased baseline [Ca2+] and abolished swelling-activated increase in [Ca2+], but it did not affect RVD. Results indicate that human TM cells display a Ca2+-independent RVD and that volume is regulated by swelling-activated K+ and Cl− channels, Na+/H+ antiports, and possibly K+-Cl− symports in addition to Na+-K+-2Cl− symports.

scholarly journals Release of taurine and glutamate contributes to cell volume regulation in human retinal Müller cells: differences in modulation by calcium

2018 ◽  
Vol 120 (3) ◽  
pp. 973-984 ◽  
Author(s):  
Vanina Netti ◽  
Alejandro Pizzoni ◽  
Martha Pérez-Domínguez ◽  
Paula Ford ◽  
Herminia Pasantes-Morales ◽  
...  
Keyword(s):  
Cell Volume ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Müller Cells ◽  
Anion Channel ◽  
Müller Cell ◽  
Regulatory Mechanisms ◽  
Muller Cells ◽  
Muller Cell ◽  
Volume Decrease

Neuronal activity in the retina generates osmotic gradients that lead to Müller cell swelling, followed by a regulatory volume decrease (RVD) response, partially due to the isoosmotic efflux of KCl and water. However, our previous studies in a human Müller cell line (MIO-M1) demonstrated that an important fraction of RVD may also involve the efflux of organic solutes. We also showed that RVD depends on the swelling-induced Ca2+ release from intracellular stores. Here we investigate the contribution of taurine (Tau) and glutamate (Glu), the most relevant amino acids in Müller cells, to RVD through the volume-regulated anion channel (VRAC), as well as their Ca2+ dependency in MIO-M1 cells. Swelling-induced [3H]Tau/[3H]Glu release was assessed by radiotracer assays and cell volume by fluorescence videomicroscopy. Results showed that cells exhibited an osmosensitive efflux of [3H]Tau and [3H]Glu (Tau > Glu) blunted by VRAC inhibitors 4-(2-butyl-6,7-dichloro-2-cyclopentylindan-1-on-5-yl)-oxybutyric acid and carbenoxolone reducing RVD. Only [3H]Tau efflux was mainly dependent on Ca2+ release from intracellular stores. RVD was unaffected in a Ca2+-free medium, probably due to Ca2+-independent Tau and Glu release, but was reduced by chelating intracellular Ca2+. The inhibition of phosphatidylinositol-3-kinase reduced [3H]Glu efflux but also the Ca2+-insensitive [3H]Tau fraction and decreased RVD, providing evidence of the relevance of this Ca2+-independent pathway. We propose that VRAC-mediated Tau and Glu release has a relevant role in RVD in Müller cells. The observed disparities in Ca2+ influence on amino acid release suggest the presence of VRAC isoforms that may differ in substrate selectivity and regulatory mechanisms, with important implications for retinal physiology. NEW & NOTEWORTHY The mechanisms for cell volume regulation in retinal Müller cells are still unknown. We show that swelling-induced taurine and glutamate release mediated by the volume-regulated anion channel (VRAC) largely contributes the to the regulatory volume decrease response in a human Müller cell line. Interestingly, the hypotonic-induced efflux of these amino acids exhibits disparities in Ca2+-dependent and -independent regulatory mechanisms, which strongly suggests that Müller cells may express different VRAC heteromers formed by the recently discovered leucine-rich repeat containing 8 (LRRC8) proteins.

Dihydropyridine-sensitive cell volume regulation in proximal tubule: the calcium window

1990 ◽  
Vol 259 (6) ◽  
pp. F950-F960 ◽  
Author(s):  
N. A. McCarty ◽  
R. G. O'Neil
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Channel Blockers ◽  
Ca Channel ◽  
Hypotonic Solution ◽  
Dependent Manner ◽  
Intracellular Ca

The mechanism underlying the activation of hypotonic cell volume regulation was studied in rabbit proximal straight tubule (PST). When isolated non-perfused tubules were exposed to hypotonic solution, cells swelled rapidly and then underwent a regulatory volume decrease (RVD). The extent of regulation after swelling was highly dependent on extracellular Ca concentration ([Ca2+]o), with a half-maximal inhibition (K1/2) for [Ca2+]o of approximately 100 microM. RVD was blocked by the Ca-channel blockers verapamil, lanthanum, and the dihydropyridines (DHP) nifedipine and nitrendipine, implicating voltage-activated Ca channels in the RVD response. Using the fura-2 fluorescence-ratio technique, we observed that cell swelling caused a sustained rise in intracellular Ca ([Ca2+]i) only when [Ca2+]o was normal (1 mM) but not when [Ca2+]o was low (1-10 microM). Furthermore, external Ca was required early on during swelling to induce RVD. If RVD was initially blocked by reducing [Ca2+]o or by addition of verapamil during hypotonic swelling, volume regulation could only be restored by subsequently inducing Ca entry within the first 1 min or less of exposure to hypotonic solution. These data indicate a "calcium window" of less than 1 min, during which RVD is sensitive to Ca, and that part of the Ca-dependent mechanism responsible for achieving RVD undergoes inactivation after swelling. It is concluded that RVD in rabbit PST is modulated by Ca via a DHP-sensitive mechanism in a time-dependent manner.

Regulation of cellular volume in rabbit ventricular myocytes: bumetanide, chlorothiazide, and ouabain

1991 ◽  
Vol 260 (1) ◽  
pp. C122-C131 ◽  
Author(s):  
K. Drewnowska ◽  
C. M. Baumgarten
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Ventricular Myocytes ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Volume Response ◽  
Rabbit Ventricular Myocytes ◽  
Cell Volumes ◽  
Measured Volume ◽  
Volume Decrease

Video microscopy was used to study the regulation of cell volume in isolated rabbit ventricular myocytes. Myocytes rapidly (less than or equal to 2 min) swelled and shrank in hyposmotic and hyperosmotic solutions, respectively, and this initial volume response was maintained without a regulatory volume decrease or increase for 20 min. Relative cell volumes (normalized to isosmotic solution, 1T) were as follows: 1.41 +/- 0.01 in 0.6T, 1.20 +/- 0.04 in 0.8T, 0.71 +/- 0.04 in 1.8T, and 0.57 +/- 0.03 in 2.6T. These volume changes were significantly less than expected if all of the measured volume was osmotically active water. Changes in width and thickness were significantly greater than changes in cell length. The idea that cotransport contributes to cell volume regulation was tested by inhibiting Na(+)-K(+)-2Cl- cotransport with bumetanide (BUM) and Na(+)-Cl- cotransport with chlorothiazide (CTZ). Under isotonic conditions, a 10-min exposure to BUM (1 microM), CTZ (100 microM), or BUM (10 microM) plus CTZ (100 microM) decreased relative cell volume to 0.87 +/- 0.01, 0.86 +/- 0.02, and 0.82 +/- 0.04, respectively. BUM plus CTZ also modified the response to osmotic stress. Swelling in 2.6T medium was 76% greater and shrinkage in 0.6T medium was 29% less than in the absence of diuretics. In contrast to the rapid effects of diuretics, inhibition of the Na(+)-K+ pump with 10 microM ouabain for 20 min did not affect cell volume in 1T solution. Nevertheless, ouabain decreased swelling in 0.6T medium by 52% and increased shrinkage in 1.8T medium by 34%. These data suggest that under isotonic conditions Na(+)-K(+)-2Cl- and Na(+)-Cl- cotransport are critical in establishing cell volume, but osmoregulation can compensate for Na(+)-K+ pump inhibition for at least 20 min. Under anisotonic conditions, the Na(+)-K+ pump and Na(+)-K(+)-2Cl- and/or Na(+)-Cl- cotransport are important in myocyte volume regulation.

Role of concentration and size of intracellular macromolecules in cell volume regulation

1997 ◽  
Vol 273 (2) ◽  
pp. C360-C370 ◽  
Author(s):  
J. C. Summers ◽  
L. Trais ◽  
R. Lajvardi ◽  
D. Hergan ◽  
R. Buechler ◽  
...  
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Molecular Physiology ◽  
Average Molecular Mass ◽  
Membrane Stretch ◽  
Ca2 Channels ◽  
Volume Decrease

To gain insight into the mechanism(s) by which cells sense volume changes, specific predictions of the macromolecular crowding theory (A. P. Minton. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 181-190. A. P. Minton, C. C. Colclasure, and J. C. Parker. Proc. Natl. Acad. Sci. USA 89: 10504-10506, 1992) were tested on the volume of internally perfused barnacle muscle cells. This preparation was chosen because it allows assessment of the effect on cell volume of changes in the intracellular macromolecular concentration and size while maintaining constant the ionic strength, membrane stretch, and osmolality. The predictions tested were that isotonic replacement of large macromolecules by smaller ones should induce volume decreases proportional to the initial macromolecular concentration and size as well as to the magnitude of the concentration reduction. The experimental results were consistent with these predictions: isotonic replacement of proteins or polymers with sucrose induced volume reductions, but this effect was only observed when the replacement was > or = 25% and the particular macromolecule had an average molecular mass of < or = 20 kDa and a concentration of at least 18 mg/ml. Volume reduction was effected by a mechanism identical with that of hypotonicity-induced regulatory volume decrease, namely, activation of verapamil-sensitive Ca2+ channels.

scholarly journals TRPing on Cell Swelling - TRPV4 Senses It

2021 ◽  
Vol 12 ◽  
Author(s):  
Trine L. Toft-Bertelsen ◽  
Nanna MacAulay
Keyword(s):  
Cell Volume ◽  
Transient Receptor Potential ◽  
Current Knowledge ◽  
Receptor Potential ◽  
Cell Swelling ◽  
Transient Receptor Potential Vanilloid ◽  
Volume Changes ◽  
Channel Activation ◽  
Volume Increase ◽  
Transient Receptor

The transient receptor potential vanilloid 4 channel (TRPV4) is a non-selective cation channel that is widely expressed and activated by a range of stimuli. Amongst these stimuli, changes in cell volume feature as a prominent regulator of TRPV4 activity with cell swelling leading to channel activation. In experimental settings based on abrupt introduction of large osmotic gradients, TRPV4 activation requires co-expression of an aquaporin (AQP) to facilitate such cell swelling. However, TRPV4 readily responds to cell volume increase irrespectively of the molecular mechanism underlying the cell swelling and can, as such, be considered a sensor of increased cell volume. In this review, we will discuss the proposed events underlying the molecular coupling from cell swelling to channel activation and present the evidence of direct versus indirect swelling-activation of TRPV4. With this summary of the current knowledge of TRPV4 and its ability to sense cell volume changes, we hope to stimulate further experimental efforts in this area of research to clarify TRPV4’s role in physiology and pathophysiology.

[Ca2+]i rises via G protein during regulatory volume decrease in rabbit proximal tubule cells

1990 ◽  
Vol 258 (3) ◽  
pp. F690-F696
Author(s):  
M. Suzuki ◽  
K. Kawahara ◽  
A. Ogawa ◽  
T. Morita ◽  
Y. Kawaguchi ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Cell Volume ◽  
Pertussis Toxin ◽  
Single Cells ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Hypotonic Solution ◽  
Proximal Tubule Cells ◽  
Tubule Cells ◽  
Volume Decrease

Although animal cells swell in hypotonic medium, their volume is subsequently regulated by a net loss of KCl via Ca2(+)-dependent channels. A rise in intracellular free calcium ([Ca2+]i) thus appears to be an initial event in the adaptation of external tonicity, although details of this mechanism are not known. To investigate cell volume regulation, we measured [Ca2+]i (by use of fura-2) and cell diameters in single cells of cultured renal proximal convoluted tubule. We found that a rapid rise in [Ca2+]i occurred after cells were exposed to hypotonic solution (250 mosM) from 95.8 +/- 3.8 to 468.2 +/- 24 nM (n = 16). The rise in [Ca2+]i was not observed in cells exposed to Ca2(+)-free medium, and exposure to isotonic high-K or low-Na medium did not elicit a rise in [Ca2+]i, suggesting that this rise was a result of Ca2+ influx and not via voltage-dependent Ca2+ influx or decrease of Ca2+ efflux via Na(+)-Ca2+ pump. Pretreatment of cells with pertussis toxin dose dependently blocked the rise in [Ca2+]i. The hypotonic solution enhanced accumulations of inositol tris- and tetra-phosphate after a 1-min exposure. Studies that measured cell diameters suggest that recovery of cell volume may include the rise in [Ca2+]i. These data suggest that the regulatory volume decrease of proximal tubule cells involves a pertussis toxin-sensitive guanine nucleotide binding protein-operated Ca2+ influx.

scholarly journals Indirect Role of AQP4b and AQP4d Isoforms in Dynamics of Astrocyte Volume and Orthogonal Arrays of Particles

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 735 ◽  
Author(s):  
Marjeta Lisjak ◽  
Maja Potokar ◽  
Robert Zorec ◽  
Jernej Jorgačevski
Keyword(s):  
Plasma Membrane ◽  
Cell Volume ◽  
Volume Regulation ◽  
Water Channel ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Orthogonal Arrays ◽  
Cell Swelling ◽  
Early Endosomes ◽  
Orthogonal Arrays Of Particles

Water channel aquaporin 4 (AQP4) plays a key role in the regulation of water homeostasis in the central nervous system (CNS). It is predominantly expressed in astrocytes lining blood–brain and blood–liquor boundaries. AQP4a (M1), AQP4c (M23), and AQP4e, present in the plasma membrane, participate in the cell volume regulation of astrocytes. The function of their splicing variants, AQP4b and AQP4d, predicted to be present in the cytoplasm, is unknown. We examined the cellular distribution of AQP4b and AQP4d in primary rat astrocytes and their role in cell volume regulation. The AQP4b and AQP4d isoforms exhibited extensive cytoplasmic localization in early and late endosomes/lysosomes and in the Golgi apparatus. Neither isoform localized to orthogonal arrays of particles (OAPs) in the plasma membrane. The overexpression of AQP4b and AQP4d isoforms in isoosmotic conditions reduced the density of OAPs; in hypoosmotic conditions, they remained absent from OAPs. In hypoosmotic conditions, the AQP4d isoform was significantly redistributed to early endosomes, which correlated with the increased trafficking of AQP4-laden vesicles. The overexpression of AQP4d facilitated the kinetics of cell swelling, without affecting the regulatory volume decrease. Therefore, although they reside in the cytoplasm, AQP4b and AQP4d isoforms may play an indirect role in astrocyte volume changes.

Effects of arginine vasopressin on cell volume regulation in brain astrocyte in culture

1999 ◽  
Vol 276 (3) ◽  
pp. E596-E601 ◽  
Author(s):  
Darya Sarfaraz ◽  
Cosmo L. Fraser
Keyword(s):  
Cell Volume ◽  
Arginine Vasopressin ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Hypotonic Medium ◽  
Receptor Antagonists ◽  
Volume Increase ◽  
Glucose Water ◽  
Water Space ◽  
Volume Decrease

Astrocytes initially swell when exposed to hypotonic medium but rapidly return to normal volume by the process of regulatory volume decrease (RVD). The role that arginine vasopressin (AVP) plays in hypotonically mediated RVD in astrocytes is unknown. This study was therefore designed to determine whether AVP might play a role in astrocyte RVD. With the use of 3- O-[3H]methyl-d-glucose to determine water space, AVP treatment resulted in significantly increased 3- O-methyl-d-glucose water space within 30 s of hypotonic exposure ( P = 0.0001) and remained significantly elevated above baseline (1.75 μl/mg protein) at 5 min ( P < 0.021). In contrast, in untreated cells, complete RVD was achieved by 5 min. At 30 s, cell volume with AVP treatment was 37% greater than in cells that received no treatment (2.9 vs. 2.26 μl/mg protein, respectively; P < 0.006). The rate of cell volume increase (dV/d t) over 30 s was highly significant (0.038 vs. 0.019 μl ⋅ mg protein−1 ⋅ s−1in the AVP-treated vs. untreated group; P = 0.0004 by regression analysis). Additionally, the rate of cell volume decrease over the next 4.5 min was also significantly greater with vasopressin treatment (−dV/d t = 0.0027 vs. 0.0013 μl ⋅ mg protein−1 ⋅ s−1; P = 0.0306). The effect of AVP was concentration dependent with EC50= 3.5 nM. To determine whether AVP action was receptor mediated, we performed RVD studies in the presence of the V1-receptor antagonists benzamil and ethylisopropryl amiloride and the V2-receptor agonist 1-desamino-8-d-arginine vasopressin (DDAVP). Both V1-receptor antagonists significantly inhibited AVP-mediated volume increase by 40–47% ( P < 0.005), whereas DDAVP had no stimulatory effects above control. Taken together, these data suggest that AVP treatment of brain astrocytes in culture appears to increase 3- O-methyl-d-glucose water space during RVD through V1receptor-mediated mechanisms. The significance of these findings is presently unclear.

Physiology of Cell Volume Regulation in Vertebrates

2009 ◽  
Vol 89 (1) ◽  
pp. 193-277 ◽  
Author(s):  
Else K. Hoffmann ◽  
Ian H. Lambert ◽  
Stine F. Pedersen
Keyword(s):  
Cell Volume ◽  
Cell Function ◽  
Current Knowledge ◽  
Control Cell ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Transepithelial Transport ◽  
Transport Pathways ◽  
Altered Expression ◽  
Shock Proteins

The ability to control cell volume is pivotal for cell function. Cell volume perturbation elicits a wide array of signaling events, leading to protective (e.g., cytoskeletal rearrangement) and adaptive (e.g., altered expression of osmolyte transporters and heat shock proteins) measures and, in most cases, activation of volume regulatory osmolyte transport. After acute swelling, cell volume is regulated by the process of regulatory volume decrease (RVD), which involves the activation of KCl cotransport and of channels mediating K+, Cl−, and taurine efflux. Conversely, after acute shrinkage, cell volume is regulated by the process of regulatory volume increase (RVI), which is mediated primarily by Na+/H+exchange, Na+-K+-2Cl−cotransport, and Na+channels. Here, we review in detail the current knowledge regarding the molecular identity of these transport pathways and their regulation by, e.g., membrane deformation, ionic strength, Ca2+, protein kinases and phosphatases, cytoskeletal elements, GTP binding proteins, lipid mediators, and reactive oxygen species, upon changes in cell volume. We also discuss the nature of the upstream elements in volume sensing in vertebrate organisms. Importantly, cell volume impacts on a wide array of physiological processes, including transepithelial transport; cell migration, proliferation, and death; and changes in cell volume function as specific signals regulating these processes. A discussion of this issue concludes the review.

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