Journal articles: 'Osmotic cell swelling'

1

Lepple-Wienhues, Albrecht, Ildikò Szabò, Tilmann Laun, Nubia Kristen Kaba, Erich Gulbins, and Florian Lang. "The Tyrosine Kinase p56lck Mediates Activation of Swelling-induced Chloride Channels in Lymphocytes." Journal of Cell Biology 141, no. 1 (April 6, 1998): 281–86. http://dx.doi.org/10.1083/jcb.141.1.281.

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Osmotic cell swelling activates Cl− channels to achieve anion efflux. In this study, we find that both the tyrosine kinase inhibitor herbimycin A and genetic knockout of p56lck, a src-like tyrosine kinase, block regulatory volume decrease (RVD) in a human T cell line. Activation of a swelling-activated chloride current (ICl−swell) by osmotic swelling in whole-cell patch-clamp experiments is blocked by herbimycin A and lavendustin. Osmotic activation of ICl−swell is defective in p56lck-deficient cells. Retransfection of p56lck restores osmotic current activation. Furthermore, tyrosine kinase activity is sufficient for activation of ICl−swell. Addition of purified p56lck to excised patches activates an outwardly rectifying chloride channel with 31 pS unitary conductance. Purified p56lck washed into the cytoplasm activates ICl−swell in native and p56lck-deficient cells even when hypotonic intracellular solutions lead to cell shrinkage. When whole-cell currents are activated either by swelling or by p56lck, slow single-channel gating events can be observed revealing a unitary conductance of 25–28 pS. In accordance with our patch-clamp data, osmotic swelling increases activity of immunoprecipitated p56lck. We conclude that osmotic swelling activates ICl−swell in lymphocytes via the tyrosine kinase p56lck.

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Tomassen, Sebastian F. B., Thea van der Wijk, Hugo R. de Jonge, and Ben C. Tilly. "Activation of phospholipase D by osmotic cell swelling." FEBS Letters 566, no. 1-3 (May 4, 2004): 287–90. http://dx.doi.org/10.1016/j.febslet.2004.04.063.

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Häussinger, D., C. Hallbrucker, N. Saha, F. Lang, and W. Gerok. "Cell volume and bile acid excretion." Biochemical Journal 288, no. 2 (December 1, 1992): 681–89. http://dx.doi.org/10.1042/bj2880681.

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The interaction between cell volume and taurocholate excretion into bile was studied in isolated perfused rat liver. Cell swelling due to hypo-osmotic exposure, addition of amino acids or insulin stimulated taurocholate excretion into bile and bile flow, whereas hyperosmotic cell shrinkage inhibited these. These effects were explained by changes in Vmax of taurocholate excretion into bile: Vmax. increased from about 300 to 700 nmol/min per g after cell swelling by 12-15% caused by either hypo-osmotic exposure or addition of amino acids under normo-osmotic conditions. Steady-state taurocholate excretion into bile was not affected when the influent K+ concentration was increased from 6 to 46 mM or decreased to 1 mM with iso-osmoticity being maintained by corresponding changes in the influent Na+ concentration. Replacement of 40 mM-NaCl by 80 mM-sucrose decreased taurocholate excretion into bile by about 70%; subsequent hypo-osmotic exposure by omission of sucrose increased taurocholate excretion to 160%. Only minor, statistically insignificant, effects of aniso-osmotic cell volume changes on the appearance of bolus-injected horseradish peroxidase in bile were observed. Taurocholate (400 microM) exhibited a cholestatic effect during hyperosmotic cell shrinkage, but not during hypo-osmotic cell swelling. Both taurocholate and tauroursodeoxycholate increased liver cell volume. Tauroursodeoxycholate stimulated taurocholate (100 microM) excretion into bile. This stimulatory effect was strongly dependent on the extent of tauroursodeoxycholate-induced cell swelling. During continuous infusion of taurocholate (100 microM) further addition of tauroursodeoxycholate at concentrations of 20, 50 and 100 microM increased cell volume by 10, 8 and 2% respectively, in parallel with a stimulation of taurocholate excretion into bile by 29, 27 and 9% respectively. There was a close relationship between the extent of cell volume changes and taurocholate excretion into bile, regardless of whether cell volume was modified by tauroursodeoxycholate, amino acids or aniso-osmotic exposure. The data suggest that: (i) liver cell volume is one important factor determining bile flow and biliary taurocholate excretion; (ii) swelling-induced stimulation of taurocholate excretion into bile is probably not explained by alterations of the membrane potential; (iii) bile acids modulate liver cell volume; (iv) taurocholate-induced cholestasis may depend on cell volume; (v) stimulation of taurocholate excretion into bile by tauroursodeoxycholate can largely be explained by tauroursodeoxycholate-induced cell swelling.

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Häussinger, D., C. Hallbrucker, S. vom Dahl, F. Lang, and W. Gerok. "Cell swelling inhibits proteolysis in perfused rat liver." Biochemical Journal 272, no. 1 (November 15, 1990): 239–42. http://dx.doi.org/10.1042/bj2720239.

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Exposure of isolated single-pass-perfused rat liver to hypo-osmotic media resulted in liver cell swelling and an inhibition of release of branched-chain amino acids. Similarly, cell swelling inhibited [3H]leucine release from perfused livers from rats in which liver proteins were prelabelled in vivo by intraperitoneal injection of L-[4,5-3H]leucine 16-20 h before the experiment. The effects of cell swelling on [3H]leucine release were fully reversible. [3H]Leucine release was also inhibited when cell swelling was induced by addition of glutamine (0.5-2 mM). There was a close relationship between the inhibition of [3H]leucine release and the degree of liver cell swelling, regardless of whether cell swelling was induced by hypo-osmotic perfusion or addition of glutamine. The data suggest that the known anti-proteolytic effect of glutamine is in large part due to glutamine-induced hepatocyte swelling.

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Ahkong, Q. F., and J. A. Lucy. "Localized osmotic swelling and cell fusion in erythrocytes: possible implications for exocytosis." Journal of Cell Science 91, no. 4 (December 1, 1988): 597–601. http://dx.doi.org/10.1242/jcs.91.4.597.

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Factors that govern the experimentally induced fusion of erythrocytes with one another may generally be relevant to whether or not osmotic forces drive membrane fusion in exocytosis because, under appropriate conditions, osmotic swelling can drive the fusion of erythrocytes. It is now reported that these cells fuse when they are subjected to osmotic swelling caused by exposure to small permeant molecules. The behaviour of erythrocytes in fusion induced by treatment with a concentrated solution of high molecular weight poly(ethylene glycol) (PEG) is also of specific interest in relation to exocytosis because the haemoglobin of erythrocytes that are dehydrated by concentrated solutions of the polymer may be regarded as a model for the tightly packed, dehydrated contents of the granules in secretory cells. We have observed that, under certain conditions of rehydration, the swelling of aqueous microdroplets between the dehydrated haemoglobin and the plasma membrane is closely associated with the fusion of partially rehydrated but still shrunken, PEG-treated erythrocytes. It is therefore apparent that osmotic forces, acting locally at the sites of aqueous microdroplets, can drive the fusion of membranes that encapsulate a dehydrated, concentrated protein, even though gross osmotic swelling at the level of the light microscope is absent. This finding is consistent with the possibility that osmotic swelling may play a role in exocytotic membrane fusion if it is restricted to a small zone immediately under the granule membrane.

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van der Wijk, Thea, Sebastian F. B. Tomassen, Adriaan B. Houtsmuller, Hugo R. de Jonge, and Ben C. Tilly. "Increased Vesicle Recycling in Response to Osmotic Cell Swelling." Journal of Biological Chemistry 278, no. 41 (July 18, 2003): 40020–25. http://dx.doi.org/10.1074/jbc.m307603200.

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Barfod, Elisabeth T., Ann L. Moore, Benjamin G. Van de Graaf, and Steven D. Lidofsky. "Myosin light chain kinase and Src control membrane dynamics in volume recovery from cell swelling." Molecular Biology of the Cell 22, no. 5 (March 2011): 634–50. http://dx.doi.org/10.1091/mbc.e10-06-0514.

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The expansion of the plasma membrane, which occurs during osmotic swelling of epithelia, must be retrieved for volume recovery, but the mechanisms are unknown. Here we have identified myosin light chain kinase (MLCK) as a regulator of membrane internalization in response to osmotic swelling in a model liver cell line. On hypotonic exposure, we found that there was time-dependent phosphorylation of the MLCK substrate myosin II regulatory light chain. At the sides of the cell, MLCK and myosin II localized to swelling-induced membrane blebs with actin just before retraction, and MLCK inhibition led to persistent blebbing and attenuated cell volume recovery. At the base of the cell, MLCK also localized to dynamic actin-coated rings and patches upon swelling, which were associated with uptake of the membrane marker FM4-64X, consistent with sites of membrane internalization. Hypotonic exposure evoked increased biochemical association of the cell volume regulator Src with MLCK and with the endocytosis regulators cortactin and dynamin, which colocalized within these structures. Inhibition of either Src or MLCK led to altered patch and ring lifetimes, consistent with the concept that Src and MLCK form a swelling-induced protein complex that regulates volume recovery through membrane turnover and compensatory endocytosis under osmotic stress.

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Okada, Yasunobu, Akihiro Hazama, Akira Hashimoto, Yoshio Maruyama, and Machiko Kubo. "Exocytosis upon osmotic swelling in human epithelial cells." Biochimica et Biophysica Acta (BBA) - Biomembranes 1107, no. 1 (June 1992): 201–5. http://dx.doi.org/10.1016/0005-2736(92)90348-p.

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Granitzer, Marita, Peter Bakos, Wolfram Nagel, and Jean Crabbé. "Osmotic swelling and membrane conductances in A6 cells." Biochimica et Biophysica Acta (BBA) - Biomembranes 1110, no. 2 (October 1992): 239–42. http://dx.doi.org/10.1016/0005-2736(92)90365-s.

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Maloney, John M., and Krystyn J. Van Vliet. "Chemoenvironmental modulators of fluidity in the suspended biological cell." Soft Matter 10, no. 40 (2014): 8031–42. http://dx.doi.org/10.1039/c4sm00743c.

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Schliess, F., R. Schreiber, and D. Häussinger. "Activation of extracellular signal-regulated kinases Erk-1 and Erk-2 by cell swelling in H4IIE hepatoma cells." Biochemical Journal 309, no. 1 (July 1, 1995): 13–17. http://dx.doi.org/10.1042/bj3090013.

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Hepatic metabolism and gene expression are among the factors controlled by the cellular hydration state, which changes within minutes in response to aniso-osmotic environments, cumulative substrate uptake, oxidative stress and under the influence of hormones such as insulin. The signalling events coupling cell-volume changes to altered cell function were studied in H4IIE rat hepatoma cells. Hypo-osmotic cell swelling resulted within 1 min in a tyrosine kinase-mediated activation of the extracellular signal-regulated protein kinases Erk-1 and Erk-2, which was independent of protein kinase C and cytosolic calcium. Activation of mitogen-activated protein kinases was followed by an increased phosphorylation of c-Jun, which may explain our recently reported finding of an about 5-fold increase in c-jun mRNA level in response to cell swelling. Pretreatment of cells with pertussis or cholera toxin abolished the swelling-induced activation of Erk-1 and Erk-2, suggesting the involvement of G-proteins. Thus, a signal-transduction pathway resembling growth factor signalling is activated already by osmotic water shifts across the plasma membrane, thereby providing a new perspective for adaption of cell function to alterations of the environment.

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Ishida-Ishihara, Sumire, Masakazu Akiyama, Kazuya Furusawa, Isao Naguro, Hiroki Ryuno, Takamichi Sushida, Seiichiro Ishihara, and Hisashi Haga. "Osmotic gradients induce stable dome morphogenesis on extracellular matrix." Journal of Cell Science 133, no. 14 (June 23, 2020): jcs243865. http://dx.doi.org/10.1242/jcs.243865.

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ABSTRACTOne of the fundamental processes in morphogenesis is dome formation, but many of the mechanisms involved are unexplored. Previous in vitro studies showed that an osmotic gradient is the driving factor of dome formation. However, these investigations were performed without extracellular matrix (ECM), which provides structural support to morphogenesis. With the use of ECM, we observed that basal hypertonic stress induced stable domes in vitro that have not been seen in previous studies. These domes developed as a result of ECM swelling via aquaporin water transport activity. Based on computer simulation, uneven swelling, with a positive feedback between cell stretching and enhanced water transport, was a cause of dome formation. These results indicate that osmotic gradients induce dome morphogenesis via both enhanced water transport activity and subsequent ECM swelling.

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Rothstein, A., and E. Mack. "Volume-activated calcium uptake: its role in cell volume regulation of Madin-Darby canine kidney cells." American Journal of Physiology-Cell Physiology 262, no. 2 (February 1, 1992): C339—C347. http://dx.doi.org/10.1152/ajpcell.1992.262.2.c339.

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Immediately after osmotic swelling of Madin-Darby canine kidney (MDCK) cells, a transient (1-2 min) increase in Ca2+ influx and internal Ca2+ (Ca2+i) is observed. The normal Ca2+ influx appears to be mediated by the 3Na(+)-Ca2+ exchange system [Borle et al. Am. J. Physiol. 259 (Cell Physiol. 28): C19-C25, 1990], but the swelling-induced component is different in 1) Na+ dependence, 2) affinity for Ca2+, 3) inhibition by La3+, and 4) direction of net flux at low external Ca2+. Swelling appears to activate an uncoupled Ca2+ flow, perhaps through cation-nonspecific stretch-activated channels. The regulatory volume decrease (RVD) is dependent on the swelling-induced pulse of Ca2+ influx and associated rise in Ca2+i. Swelling also induces a biphasic change in membrane potential, a hyperpolarization followed by depolarization, reflecting sequential increases in K+ and Cl- permeabilities. The time dependence of the former corresponds closely with the transient peak in Ca2+i, but the latter does not. Ca2+i appears to have a direct activating effect on K+ channels but an indirect effect on Cl- channels, mediated via other Ca(2+)-triggered systems. The sequence of events following cell swelling appears to be transient increases in Ca2+ permeability, Ca2+ influx, Ca2+i, K+ permeability, followed by triggering of a mediating system that increases Cl- permeability. The net result is KCl, osmotic water loss, and volume adjustment.

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Noulin, J. F., E. Fayolle-Julien, J. F. Desaphy, J. P. Poindessault, and M. Joffre. "Swelling and cAMP on hyperpolarization-activated Cl- conductance in rat Leydig cells." American Journal of Physiology-Cell Physiology 271, no. 1 (July 1, 1996): C74—C84. http://dx.doi.org/10.1152/ajpcell.1996.271.1.c74.

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We have used the whole cell patch-clamp technique to characterize changes in membrane conductance induced by osmotic swelling in mature rat Leydig cells dialyzed with ATP (control cells) or adenosine 3',5'-cyclic monophosphate (cAMP) plus ATP (cAMP cells). A spontaneous current activation occurs in both groups in isosmotic conditions (300/295 mosM in/out). This development is entirely counteracted in control cells and partly inhibited in cAMP cells by exposing them to a hyperosmotic (350 mosM) bath solution, and these currents increase again in a hyposmotic (205 mosM) bath solution. These currents are sensitive to 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, a Cl- channel blocker. Taken together, the results indicate that, in the control cells (ATP alone) as well as in the presence of intracellular cAMP, osmotic swelling activates the background hyperpolarization-activated Cl- conductance, osmotic swelling and cAMP appearing to act synergistically.

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Hazama, Akihiro, Takahiro Shimizu, Yuhko Ando-Akatsuka, Seiji Hayashi, Shoko Tanaka, Emi Maeno, and Yasunobu Okada. "Swelling-Induced, Cftr-Independent Atp Release from a Human Epithelial Cell Line." Journal of General Physiology 114, no. 4 (September 13, 1999): 525–33. http://dx.doi.org/10.1085/jgp.114.4.525.

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To examine a possible relation between the swelling-induced ATP release pathway and the volume-sensitive Cl− channel, we measured the extracellular concentration of ATP released upon osmotic swelling and whole-cell volume-sensitive Cl− currents in a human epithelial cell line, Intestine 407, which lacks expression of cystic fibrosis transmembrane conductance regulator (CFTR). Significant release of ATP was observed within several minutes after a hypotonic challenge (56–80% osmolality) by the luciferin/luciferase assay. A carboxylate analogue Cl− channel blocker, 5-nitro-2-(3-phenylpropylamino)-benzoate, suppressed ATP release in a concentration-dependent manner with a half-maximal inhibition concentration of 6.3 μM. However, swelling-induced ATP release was not affected by a stilbene-derivative Cl− channel blocker, 4-acetamido-4′-isothiocyanostilbene at 100 μM. Glibenclamide (500 μM) and arachidonic acid (100 μM), which are known to block volume-sensitive outwardly rectifying (VSOR) Cl− channels, were also ineffective in inhibiting the swelling-induced ATP release. Gd3+, a putative blocker of stretch-activated channels, inhibited swelling-induced ATP release in a concentration-dependent manner, whereas the trivalent lanthanide failed to inhibit VSOR Cl− currents. Upon osmotic swelling, the local ATP concentration in the immediate vicinity of the cell surface was found to reach ∼13 μM by a biosensor technique using P2X2 receptors expressed in PC12 cells. We have raised antibodies that inhibit swelling-induced ATP release from Intestine 407 cells. Earlier treatment with the antibodies almost completely suppressed swelling-induced ATP release, whereas the activity of VSOR Cl− channel was not affected by pretreatment with the antibodies. Taking the above results together, the following conclusions were reached: first, in a CFTR-lacking human epithelial cell line, osmotic swelling induces ATP release and increases the cell surface ATP concentration over 10 μM, which is high enough to stimulate purinergic receptors; second, the pathway of ATP release is distinct from the pore of the volume-sensitive outwardly rectifying Cl− channel; and third, the ATP release is not a prerequisite to activation of the Cl− channel.

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vom Dahl, S., B. Stoll, W. Gerok, and D. Häussinger. "Inhibition of proteolysis by cell swelling in the liver requires intact microtubular structures." Biochemical Journal 308, no. 2 (June 1, 1995): 529–36. http://dx.doi.org/10.1042/bj3080529.

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In the perfused rat liver, proteolysis is inhibited by cell swelling in response to hypo-osmotic media, glutamine and insulin. Colchicine, an inhibitor of microtubules, did not affect cell swelling in response to these agonists. However, the antiproteolytic action of these effectors was largely blunted in the presence of colchicine or the microtubule inhibitors colcemid and taxol. On the other hand, inhibition of proteolysis by phenylalanine, asparagine or NH4Cl, i.e. compounds which exert their antiproteolytic effects by mechanisms distinct from cell swelling, was not sensitive to colchicine. Swelling-induced inhibition of proteolysis was not affected by cytochalasin B. The anti-proteolytic effect of hypo-osmotic cell swelling and insulin was largely abolished in freshly isolated rat hepatocytes; however, it reappeared upon cultivation of the hepatocytes for 6-10 h. The restoration of the sensitivity of proteolysis to cell volume changes was accompanied by a progressive reorganization of microtubule structures, as shown by immunohistochemical staining for tubulin. It is concluded that intact microtubules are required for the control of proteolysis by cell volume, but not for the control of proteolysis by phenylalanine, asparagine or NH4Cl. These findings may explain why others [Meijer, Gustafson, Luiken, Blommaart, Caro, Van Woerkom, Spronk and Boon (1993) Eur. J. Biochem. 215, 449-454] failed to detect an antiproteolytic effect of hypo-osmotic exposure of freshly isolated hepatocytes. This effect, however, which is consistently found in the intact perfused rat liver, also reappeared in isolated hepatocytes when they were allowed to reorganize their microtubular structures in culture.

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Pritzen, Cornelia, and Andreas Herrmann. "Are osmotic forces involved in influenza virus-cell fusion?" Bioscience Reports 8, no. 1 (February 1, 1988): 55–64. http://dx.doi.org/10.1007/bf01128972.

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The kinetics of the fusion process of unsealed and resealed erthyrocyte ghosts with influenza virus (A/PR8/34, A/Chile 1/83), were measured under hypotonic, isotonic and hypertonic conditions using a recently developed fluorescence assay (Hoekstra et al. (1984) Biochemistry23:5675–5681]. No correlation between the external osmotic pressure and kinetics and extent of fusion was observed. Influenza viruses fuse as effectively with unsealed ghosts as with resealed ghosts. It is concluded that osmotic forces as well as osmotic swelling of cells are not necessary for virus-cell membrane fusion.

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Lee, Wing-Kee, and Frank Thévenod. "A role for mitochondrial aquaporins in cellular life-and-death decisions?" American Journal of Physiology-Cell Physiology 291, no. 2 (August 2006): C195—C202. http://dx.doi.org/10.1152/ajpcell.00641.2005.

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Mitochondria dominate the process of life-and-death decisions of the cell. Continuous generation of ATP is essential for cell sustenance, but, on the other hand, mitochondria play a central role in the orchestra of events that lead to apoptotic cell death. Changes of mitochondrial volume contribute to the modulation of physiological mitochondrial function, and several ion permeability pathways located in the inner mitochondrial membrane have been implicated in the mediation of physiological swelling-contraction reactions, such as the K+ cycle. However, the channels and transporters involved in these processes have not yet been identified. Osmotic swelling is also one of the fundamental characteristics exhibited by mitochondria in pathological situations, which activates downstream cascades, culminating in apoptosis. The permeability transition pore has long been postulated to be the primary mediator for water movement in mitochondrial swelling during cell death, but its molecular identity remains obscure. Inevitably, accumulating evidence shows that mitochondrial swelling induced by apoptotic stimuli can also occur independently of permeability transition pore activation. Recently, a novel mechanism for osmotic swelling of mitochondria has been described. Aquaporin-8 and -9 channels have been identified in the inner mitochondrial membrane of various tissues, including the kidney, liver, and brain, where they may mediate water transport associated with physiological volume changes, contribute to the transport of metabolic substrates, and/or participate in osmotic swelling induced by apoptotic stimuli. Hence, the recent discovery that aquaporins are expressed in mitochondria opens up new areas of investigation in health and disease.

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Hallbrucker, C., F. Lang, W. Gerok, and D. Häussinger. "Cell swelling increases bile flow and taurocholate excretion into bile in isolated perfused rat liver." Biochemical Journal 281, no. 3 (February 1, 1992): 593–95. http://dx.doi.org/10.1042/bj2810593.

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The effects of aniso-osmotically and amino-acid-induced cell-volume changes on bile flow and biliary taurocholate excretion were studied in isolated perfused rat liver. With taurocholate (100 microM) in the influent perfusate, hypo-osmotic exposure (225 mosmol/l) increased taurocholate excretion into bile and bile flow by 42 and 27% respectively, whereas inhibition by 32 and 47% respectively was observed after hyperosmotic (385 mosmol/l) exposure. The effects of aniso-moticity on taurocholate excretion into bile was observed throughout aniso-osmotic exposure, even after completion of volume-regulatory ion fluxes and were fully reversible upon re-exposure to normo-osmotic media. Hypo-osmotic cell swelling (225 mosmol/l) increased the Vmax. of taurocholate translocation from the sinusoidal compartment into bile about 2-fold. Also, cell swelling induced by glutamine and glycine stimulated both bile flow and biliary taurocholate excretion. There was a close relationship between the aniso-osmotically and amino-acid-induced change of cell volume and taurocholate excretion into bile. The data suggest that liver cell volume plays an important role in regulating bile-acid-dependent bile flow and biliary taurocholate excretion.

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BUSCH, GILLIAN L., NUBIA KRISTEN KABA, MIRJANA BUKARA, and FLORIAN LANG. "Osmotic Cell Swelling Alkalinizes Acidic Cellular Compartments of Pancreatic Islet and RINm5F Cells." Pancreas 15, no. 4 (November 1997): 420–23. http://dx.doi.org/10.1097/00006676-199711000-00014.

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Offeddu, Giovanni S., Constantin E. Tanase, Sotiria Toumpaniari, Michelle L. Oyen, and Ruth E. Cameron. "Stiffening by Osmotic Swelling Constraint in Cartilage‐Like Cell Culture Scaffolds." Macromolecular Bioscience 18, no. 11 (September 6, 2018): 1800247. http://dx.doi.org/10.1002/mabi.201800247.

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Tilly, Ben C., Matthias Gaestel, Katrin Engel, Marcel J. Edixhoven, and Hugo R. de Jonge. "Hypo-osmotic cell swelling activates the p38 MAP kinase signalling cascade." FEBS Letters 395, no. 2-3 (October 21, 1996): 133–36. http://dx.doi.org/10.1016/0014-5793(96)01028-9.

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Numata, Tomohiro, Takahiro Shimizu, and Yasunobu Okada. "TRPM7 is a stretch- and swelling-activated cation channel involved in volume regulation in human epithelial cells." American Journal of Physiology-Cell Physiology 292, no. 1 (January 2007): C460—C467. http://dx.doi.org/10.1152/ajpcell.00367.2006.

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Stretch- and swelling-activated cation (SSAC) channels play essential roles not only in sensing and transducing external mechanical stresses but also in regulating cell volume in living cells. However, the molecular nature of the SSAC channel has not been clarified. In human epithelial HeLa cells, single-channel recordings in cell-attached and inside-out patches revealed expression of a Mg2+- and Gd3+-sensitive nonselective cation channel that is exquisitely sensitive to membrane stretch. Whole cell recordings revealed that the macroscopic cationic currents exhibit transient receptor potential (TRP) melastatin (TRPM)7-like properties such as outward rectification and sensitivity to Mg2+ and Gd3+. The whole cell cation current was augmented by osmotic cell swelling. RT-PCR and Western blotting demonstrated molecular expression of TRPM7 in HeLa cells. Treatment with small interfering RNA (siRNA) targeted against TRPM7 led to abolition of single stretch-activated cation channel currents and of swelling-activated, whole cell cation currents in HeLa cells. The silencing of TRPM7 by siRNA reduced the rate of cell volume recovery after osmotic swelling. A similar inhibition of regulatory volume decrease was also observed when extracellular Ca2+ was removed or Gd3+ was applied. It is thus concluded that TRPM7 represents the SSAC channel endogenously expressed in HeLa cells and that, by serving as a swelling-induced Ca2+ influx pathway, it plays an important role in cell volume regulation.

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HAYAKAWA, MASAHARU, SATOMI TANIMOTO, AKIO KONDOAND, and TOHRU NAKAZAWA. "Changes in Osmotic Pressure and Swelling in Horseshoe Crab Embryos During Development. (horseshoe crab embryo/swelling/water influx/perivitelline fluid/osmotic pressure)." Development, Growth and Differentiation 27, no. 1 (February 1985): 51–56. http://dx.doi.org/10.1111/j.1440-169x.1985.00051.x.

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Vom Dahl, S., C. Hallbrucker, F. Lang, W. Gerok, and D. Häussinger. "Regulation of liver cell volume and proteolysis by glucagon and insulin." Biochemical Journal 278, no. 3 (September 15, 1991): 771–77. http://dx.doi.org/10.1042/bj2780771.

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The effects of insulin and glucagon on liver cell volume and proteolysis were studied in isolated perfused rat liver. The rate of proteolysis was assessed as [3H]leucine release from single-pass-perfused livers from rats which had been prelabelled in vivo by intraperitoneal injection of [3H]leucine. The intracellular water space was determined from the wash-out profiles of simultaneously added [3H]inulin and [14C]urea. In normo-osmotic (305 mosM) control perfusions the intracellular water space was 548 +/- 10 microliters/g wet mass (n = 44) and was increased by 16.5 +/- 2.6% (n = 6), i.e. by 85 +/- 14 microliters/g, after hypoosmotic exposure (225 mosM). Glucagon (0.1 microM) decreased the intracellular water space by 17 +/- 4% (n = 4), whereas insulin (35 nM) increased the intracellular water space by 9.3 +/- 1.4% (n = 15). Also, in isolated rat hepatocyte suspensions insulin (100 nM) caused cell swelling by 10.7 +/- 1.8% (n = 16), which was fully reversed by glucagon. In perfused liver, insulin-induced cell swelling was accompanied by a hepatic net K+ uptake (4.5 +/- 0.2 mumol/g) and an inhibition of proteolysis by 21 +/- 2% (n = 12); further addition of glucagon led to a net K+ release of 3.8 +/- 0.2 mumol/g (n = 7) and fully reversed the insulin effects on both cell volume and proteolysis. Similarly, insulin-induced cell swelling and inhibition of proteolysis were completely antagonized by hyperosmotic (385 mosM) cell shrinkage. Furthermore, cell swelling and inhibition of proteolysis after hypo-osmotic exposure or amino acid addition were reversed by glucagon-induced cell shrinkage. There was a close relationship between the extent of cell swelling and the inhibition of proteolysis, regardless of whether cell volume was modified by insulin, glucagon or aniso-osmotic exposure. The data show that glucagon and insulin are potent modulators of liver cell volume, at least in part by alterations of cellular K+ balance, and that their opposing effects on hepatic proteolysis can largely be explained by opposing effects on cell volume. It is hypothesized that hormone-induced alterations of cell volume may represent an important, not yet recognized, mechanism mediating hormonal effects on metabolism.

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Cameron, Ivan L., Phillip Merta, and Gary D. Fullerton. "Osmotic and motional properties of intracellular water as influenced by osmotic swelling and shrinkage ofXenopus Oocytes." Journal of Cellular Physiology 142, no. 3 (March 1990): 592–602. http://dx.doi.org/10.1002/jcp.1041420320.

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Niemeyer, M. I., C. Hougaard, E. K. Hoffmann, F. Jørgensen, A. Stutzin, and F. V. Sepúlveda. "K+ conductance activated by osmotic cell swelling or by leukotriene D4 in ehrlich cells." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 126 (July 2000): 135. http://dx.doi.org/10.1016/s1095-6433(00)80268-8.

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Finkenzeller, Günter, William Newsome, Florian Lang, and Dieter Häussinger. "Increase of c-jun mRNA upon hypo-osmotic cell swelling of rat hepatoma cells." FEBS Letters 340, no. 3 (March 7, 1994): 163–66. http://dx.doi.org/10.1016/0014-5793(94)80129-0.

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29

Wang, Xiangbing, Noriyuki Sato, Monte A. Greer, Staci McAdams, and Susan E. Greer. "Dual effect of osmotic cell swelling on prolactin secretion by acutely dispersed adenohypophyseal cells." Life Sciences 48, no. 7 (January 1991): 617–22. http://dx.doi.org/10.1016/0024-3205(91)90536-k.

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30

Greer, M., Fay Hagemenas, and D. Illingworth. "Osmotic Cell Swelling Stimulates Receptor-Mediated Low Density Lipoprotein Endocytosis and Degradation." Hormone and Metabolic Research 24, no. 09 (September 1992): 454. http://dx.doi.org/10.1055/s-2007-1003360.

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31

Guggino, W. B., H. Oberleithner, and G. Giebisch. "Relationship between cell volume and ion transport in the early distal tubule of the Amphiuma kidney." Journal of General Physiology 86, no. 1 (July 1, 1985): 31–58. http://dx.doi.org/10.1085/jgp.86.1.31.

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The roles of apical and basolateral transport mechanisms in the regulation of cell volume and the hydraulic water permeabilities (Lp) of the individual cell membranes of the Amphiuma early distal tubule (diluting segment) were evaluated using video and optical techniques as well as conventional and Cl-sensitive microelectrodes. The Lp of the apical cell membrane calculated per square centimeter of tubule is less than 3% that of the basolateral cell membrane. Calculated per square centimeter of membrane, the Lp of the apical cell membrane is less than 40% that of the basolateral cell membrane. Thus, two factors are responsible for the asymmetry in the Lp of the early distal tubule: an intrinsic difference in the Lp per square centimeter of membrane area, and a difference in the surface areas of the apical and basolateral cell membranes. Early distal tubule cells do not regulate volume after a reduction in bath osmolality. This cell swelling occurs without a change in the intracellular Cl content or the basolateral cell membrane potential. In contrast, reducing the osmolality of the basolateral solution in the presence of luminal furosemide diminishes the magnitude of the increase in cell volume to a value below that predicted from the change in osmolality. This osmotic swelling is associated with a reduction in the intracellular Cl content. Hence, early distal tubule cells can lose solute in response to osmotic swelling, but only after the apical Na/K/Cl transporter is blocked. Inhibition of basolateral Na/K ATPase with ouabain results in severe cell swelling. This swelling in response to ouabain can be inhibited by the prior application of furosemide, which suggests that the swelling is due to the continued entry of solutes, primarily through the apical cotransport pathway.

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32

Tseng, G. N. "Cell swelling increases membrane conductance of canine cardiac cells: evidence for a volume-sensitive Cl channel." American Journal of Physiology-Cell Physiology 262, no. 4 (April 1, 1992): C1056—C1068. http://dx.doi.org/10.1152/ajpcell.1992.262.4.c1056.

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Cardiac cell swelling occurs under abnormal conditions. Currents through volume-sensitive channels, if present in heart, will affect the cardiac electrical activity. Single canine ventricular myocytes were voltage clamped under conditions that largely suppressed Na, K, and Ca channel currents and currents generated by electrogenic transport systems. Cell width and membrane conductance were monitored continuously. Swelling was induced by increasing the osmolarity of the pipette solution or by decreasing the osmolarity of the external solution. During cell swelling, the cell widened and membrane conductance increased. This increase in membrane conductance was sensitive to Cl channel blockers and to external Cl removal, suggesting that a major component was provided by a Cl channel. The current-voltage relationship of the swelling-induced current displayed an outward rectification, with an average zero-current voltage of -60 mV. The activation of the swelling-induced current did not seem to depend on external or internal Ca and was not sensitive to a protein kinase inhibitor (H-8). Shape-altering agents chlorpromazine decreased while dipyridamole and trinitrophenol increased the membrane conductance without osmotic perturbations, suggesting that changes in tension in the cell membrane may play a role in opening and closing of the swelling-induced channels.

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Awayda, Mouhamed S., and Muthangi Subramanyam. "Regulation of the Epithelial Na+ Channel by Membrane Tension." Journal of General Physiology 112, no. 2 (August 1, 1998): 97–111. http://dx.doi.org/10.1085/jgp.112.2.97.

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The sensitivity of αβγ rat epithelial Na+ channel (rENaC) to osmotically or mechanically induced changes of membrane tension was investigated in the Xenopus oocyte expression system, using both dual electrode voltage clamp and cell-attached patch clamp methodologies. ENaC whole-cell currents were insensitive to mechanical cell swelling caused by direct injection of 90 or 180 nl of 100-mM KCl. Similarly, ENaC whole-cell currents were insensitive to osmotic cell swelling caused by a 33% decrease of bathing solution osmolarity. The lack of an effect of cell swelling on ENaC was independent of the status of the actin cytoskeleton, as ENaC remained insensitive to osmotic and mechanical cell swelling in oocytes pretreated with cytochalasin B for 2–5 h. This apparent insensitivity of ENaC to increased cell volume and changes of membrane tension was also observed at the single channel level in membrane patches subjected to negative or positive pressures of 5 or 10 in. of water. However, and contrary to the lack of an effect of cell swelling, ENaC currents were inhibited by cell shrinking. A 45-min incubation in a 260-mosmol solution (a 25% increase of solution osmolarity) caused a decrease of ENaC currents (at −100 mV) from −3.42 ± 0.34 to −2.02 ± 0.23 μA (n = 6). This decrease of current with cell shrinking was completely blocked by pretreatment of oocytes with cytochalasin B, indicating that these changes of current are not likely related to a direct effect of cell shrinking. We conclude that αβγ rENaC is not directly mechanosensitive when expressed in a system that can produce a channel with identical properties to those found in native epithelia.

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al-Habori, M., M. Peak, T. H. Thomas, and L. Agius. "The role of cell swelling in the stimulation of glycogen synthesis by insulin." Biochemical Journal 282, no. 3 (March 15, 1992): 789–96. http://dx.doi.org/10.1042/bj2820789.

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In hepatocyte cultures, insulin stimulates cellular accumulation of K+, partly (approximately 20%) by net replacement of cell Na+, but largely (approximately 80%) by increasing the cell K++Na+ content, with a consequent increase in cell volume. An increase in cation content occurred within 5 min of exposure to insulin and was not secondary to metabolic changes. Insulin also increased the cation content, by increasing the Na+ content, in a K(+)-free medium or when K+ uptake was inhibited with 1 mM-ouabain. However, insulin did not increase the cation content in a Na(+)-free medium. The stimulation of glycogen synthesis by insulin, like the increase in cation content, was blocked in a Na(+)-free medium, but not when K+ uptake was inhibited. Hypo-osmotic swelling restored the stimulation of glycogen synthesis in a Na(+)-free medium, indicating that the lack of effect of insulin in the iso-osmotic Na(+)-free medium was not due to a direct requirement for Na+ for glycogen synthesis, but to a secondary mechanism, dependent on Na+ entry, that can be mimicked by hypo-osmotic swelling. Quinine increased cell volume further and caused a further increase in glycogen synthesis. The hypothesis that cellular uptake of K+ may be part of the mechanism by which insulin controls metabolism was discounted, because inhibition of K+ uptake does not block the metabolic effects of insulin [Czech (1977) Annu. Rev. Biochem. 46, 359-384]. The present results support the hypothesis that an increase in cell cation content, and thereby cell volume, rather than K+ uptake, is part of the mechanism by which insulin stimulates glycogen synthesis in hepatocytes.

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35

Rothstein, A., and E. Mack. "Volume-activated K+ and Cl- pathways of dissociated epithelial cells (MDCK): role of Ca2+." American Journal of Physiology-Cell Physiology 258, no. 5 (May 1, 1990): C827—C834. http://dx.doi.org/10.1152/ajpcell.1990.258.5.c827.

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Osmotic swelling of dissociated Madin-Darby canine kidney (MDCK) cells in NaCl medium is followed by shrinking (regulatory volume decrease, or RVD) or in KCl medium by secondary swelling. The cation ionophore gramicidin has little effect on volumes of isotonic cells but accelerates volume-activated changes in either medium. Immediately after hypotonic exposure, the membrane becomes transiently hyperpolarized followed by depolarization. The depolarization phase is diminished by the anion transport inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Swelling is also associated with an almost immediate increase in Ca2+ influx and elevation of cytoplasmic Ca2+ ([Ca2+]i) preceding RVD. In Ca2(+)-free medium, [Ca2+]i rapidly declines to a low level. Osmotic swelling, under these circumstances, is associated with a small transient increase in [Ca2+]i, but RVD or secondary swelling (in KCl) are minimal. Under these conditions, addition of gramicidin or the Ca2(+)-ionophore A23187 induces significant volume changes, although not as large as those found in the presence of Ca2+. Quinine inhibits RVD in the absence of gramicidin, but not in its presence; oligomycin C, DIDS, and trifluoperazine, on the other hand, inhibit in the presence of the ionophore. These findings suggest that in MDCK cells RVD involves activation of distinct conductive K+ and Cl- pathways which allow escape of KCl and osmotically obligated water and that activation of both pathways is associated with elevated [Ca2+]i derived largely from volume activation of a Ca2(+)-influx pathway.

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Tomita, M., and F. Gotoh. "Cascade of cell swelling: thermodynamic potential discharge of brain cells after membrane injury." American Journal of Physiology-Heart and Circulatory Physiology 262, no. 2 (February 1, 1992): H603—H610. http://dx.doi.org/10.1152/ajpheart.1992.262.2.h603.

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This paper illustrates the principles of volume regulation in brain cells. Animal experiments were first performed ex vivo. Brains of gerbils were removed and incubated in 3 ml of physiological saline for 1 h. Control (0.86 g, n = 8) and swollen hemispheres (1.11 g, n = 8) were analyzed for tissue hydration, electrolytes and osmolality. The incubation media were also analyzed for gains or losses of electrolytes and water. Na+ and Cl- moved into and K+ moved out of the tissue. The ratio of Na+ influx to K+ efflux was calculated to be approximately 2:1. Water shifted into the tissue accompanying the net movements of small ions. In a simulated "cell" model constructed on the basis of the above observations with an outside saline and an inside colloid solution separated by a dialysis membrane, fluid shifts were demonstrated in the absence of (or even against) an osmotic gradient across the membrane under isobaric and isothermal conditions. Such paradoxical fluid shifts, presumably occurring in a similar manner to those in living cells, were shown to be due to the discharge of a huge thermodynamic potential accumulated by the cell as a condensation of ions outside and of proteins inside the cell membrane. We conclude that a loss in barrier function of the cell membrane ignites such a thermodynamic potential discharge causing an environmental fluid shift into the cells even under conditions of no (or even a contrary) osmotic gradient. Under such circumstances, countercotransporters and ion exchangers such as Na(+)-K(+)-2Cl- may work as modulators of the fluid shift, limiting its rate. The thermodynamic potential can explain the cascade of cell swelling (cytotoxic edema) as well as the spontaneous increase in osmolality in the ischemic cell when the cell volume increase is somehow restricted.

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37

Li, Gui-Rong, Min Zhang, Leslie S. Satin, and Clive M. Baumgarten. "Biphasic effects of cell volume on excitation-contraction coupling in rabbit ventricular myocytes." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 4 (April 1, 2002): H1270—H1277. http://dx.doi.org/10.1152/ajpheart.00946.2001.

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We studied the effects of osmotic swelling on the components of excitation-contraction coupling in ventricular myocytes. Myocyte volume rapidly increased 30% in hyposmotic (0.6T) solution and was constant thereafter. Cell shortening transiently increased 31% after 4 min in 0.6T but then decreased to 68% of control after 20 min. In parallel, the L-type Ca2+ current ( I Ca-L) transiently increased 10% and then declined to 70% of control. Similar biphasic effects on shortening were observed under current clamp. In contrast, action potential duration was unchanged at 4 min but decreased to 72% of control after 20 min. Ca2+ transients were measured with fura 2-AM. The emission ratio with excitation at 340 and 380 nm (f340/f380) decreased by 12% after 3 min in 0.6T, whereas shortening and I Ca-L increased at the same time. After 8 min, shortening, I Ca-L, and the f340/f380 ratio decreased 28, 25, and 59%, respectively. The results suggest that osmotic swelling causes biphasic changes in I Ca-L that contribute to its biphasic effects on contraction. In addition, swelling initially appears to reduce the Ca2+ transient initiated by a given I Ca-L, and later, both I Ca-L and the Ca2+ transient are inhibited.

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38

Peterson, Suzanne, and Emil Bogenmann. "Osmotic Swelling Induces p75 Neurotrophin Receptor (p75NTR) Expression via Nitric Oxide." Journal of Biological Chemistry 278, no. 36 (June 23, 2003): 33943–50. http://dx.doi.org/10.1074/jbc.m302376200.

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39

Smikle, Collin B., and Paul J. Turek. "Hypo-osmotic swelling can accurately assess the viability of nonmotile sperm." Molecular Reproduction and Development 47, no. 2 (June 1997): 200–203. http://dx.doi.org/10.1002/(sici)1098-2795(199706)47:2<200::aid-mrd11>3.0.co;2-3.

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40

Sivaramakrishnan, Venketesh, and Samuel J. Fountain. "Evidence for Extracellular ATP as a Stress Signal in a Single-Celled Organism." Eukaryotic Cell 14, no. 8 (June 5, 2015): 775–82. http://dx.doi.org/10.1128/ec.00066-15.

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ABSTRACT ATP is omnipresent in biology and acts as an extracellular signaling molecule in mammals. Information regarding the signaling function of extracellular ATP in single-celled eukaryotes is lacking. Here, we explore the role of extracellular ATP in cell volume recovery during osmotic swelling in the amoeba Dictyostelium . Release of micromolar ATP could be detected during cell swelling and regulatory cell volume decrease (RVD) phases during hypotonic challenge. Scavenging ATP with apyrase caused profound cell swelling and loss of RVD. Apyrase-induced swelling could be rescued by 100 μM βγ-imidoATP. N -Ethylmalemide (NEM), an inhibitor of vesicular exocytosis, caused heightened cell swelling, loss of RVD, and inhibition of ATP release. Amoebas with impaired contractile vacuole (CV) fusion (drainin knockout [KO] cells) displayed increased swelling but intact ATP release. One hundred micromolar Gd 3+ caused cell swelling while blocking any recovery by βγ-imidoATP. ATP release was 4-fold higher in the presence of Gd 3+ . Cell swelling was associated with an increase in intracellular nitric oxide (NO), with NO-scavenging agents causing cell swelling. Swelling-induced NO production was inhibited by both apyrase and Gd 3+ , while NO donors rescued apyrase- and Gd 3+ -induced swelling. These data suggest extracellular ATP released during cell swelling is an important signal that elicits RVD. Though the cell surface receptor for ATP in Dictyostelium remains elusive, we suggest ATP operates through a Gd 3+ -sensitive receptor that is coupled with intracellular NO production.

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Basavappa, Srisaila, Stine F. Pedersen, Nanna K. Jørgensen, J. Clive Ellory, and Else K. Hoffmann. "Swelling-Induced Arachidonic Acid Release via the 85-kDa cPLA2 in Human Neuroblastoma Cells." Journal of Neurophysiology 79, no. 3 (March 1, 1998): 1441–49. http://dx.doi.org/10.1152/jn.1998.79.3.1441.

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Basavappa, Srisaila, Stine F. Pedersen, Nanna K. Jørgensen, J. Clive Ellory, and Else K. Hoffmann. Swelling-induced arachidonic acid release via the 85-kDa cPLA2 in human neuroblastoma cells. J. Neurophysiol. 79: 1441–1449, 1998. Arachidonic acid or its metabolites have been implicated in the regulatory volume decrease (RVD) response after hypotonic cell swelling in some mammalian cells. The present study investigated the role of arachidonic acid (AA) during RVD in the human neuroblastoma cell line CHP-100. During the first nine minutes of hypo-osmotic exposure the rate of 3H-arachidonic acid (3H-AA) release increased to 250 ± 19% (mean ± SE, n = 22) as compared with cells under iso-osmotic conditions. This release was significantly inhibited after preincubation with AACOCF3, an inhibitor of the 85-kDa cytosolic phospholipase A2 (cPLA2). This indicates that a PLA2, most likely the 85-kDa cPLA2 is activated during cell swelling. In contrast, preincubation with U73122, an inhibitor of phospholipase C, did not affect the swelling-induced release of 3H-AA. Swelling-activated efflux of 36Cl and 3H-taurine were inhibited after preincubation with AACOCF3. Thus the swelling-induced activation of cPLA2 may be essential for stimulation of both 36Cl and 3H-taurine efflux during RVD. As the above observation could result from a direct effect of AA or its metabolite leukotriene D4 (LTD4), the effects of these agents were investigated on swelling-induced 36Cl and 3H-taurine effluxes. In the presence of high concentrations of extracellular AA, the swelling-induced efflux of 36Cl and 3H-taurine were inhibited significantly. In contrast, addition of exogenous LTD4 had no significant effect on the swelling-activated 36Cl efflux. Furthermore, exogenous AA increased cytosolic calcium levels as measured in single cells loaded with the calcium sensitive dye Fura-2. On the basis of these results we propose that cell swelling activates phospholipase A2 and that this activation via an increased production of AA or some AA metabolite(s) other than LTD4 is essential for RVD.

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42

Tomassen, Sebastian F. B., Durk Fekkes, Hugo R. de Jonge, and Ben C. Tilly. "Osmotic swelling-provoked release of organic osmolytes in human intestinal epithelial cells." American Journal of Physiology-Cell Physiology 286, no. 6 (June 2004): C1417—C1422. http://dx.doi.org/10.1152/ajpcell.00468.2003.

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Human Intestine 407 cells respond to osmotic cell swelling by the activation of Cl−- and K+-selective ionic channels, as well as by stimulating an organic osmolyte release pathway readily permeable to taurine and phosphocholine. Unlike the activation of volume-regulated anion channels (VRAC), activation of the organic osmolyte release pathway shows a lag time of ∼30–60 s, and its activity persists for at least 8–12 min. In contrast to VRAC activation, stimulation of organic osmolyte release did not require protein tyrosine phosphorylation, active p21rho, or phosphatidylinositol 3-kinase activity and was insensitive to Cl− channel blockers. Treatment of the cells with putative organic anion transporter inhibitors reduced the release of taurine only partially or was found to be ineffective. The efflux was blocked by a subclass of organic cation transporter (OCT) inhibitors (cyanine-863 and decynium-22) but not by other OCT inhibitors (cimetidine, quinine, and verapamil). Brief treatment of the cells with phorbol esters potentiated the cell swelling-induced taurine efflux, whereas addition of the protein kinase C (PKC) inhibitor GF109203X largely inhibited the response, suggesting that PKC is involved. Increasing the level of intracellular Ca2+ by using A-23187- or Ca2+-mobilizing hormones, however, did not affect the magnitude of the response. Taken together, the results indicate that the hypotonicity-induced efflux of organic osmolytes is independent of VRAC and involves a PKC-dependent step.

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SCHLIESS, Freimut, Ralf SINNING, Richard FISCHER, Corinne SCHMALENBACH, and Dieter HÄUSSINGER. "Calcium-dependent activation of Erk-1 and Erk-2 after hypo-osmotic astrocyte swelling." Biochemical Journal 320, no. 1 (November 15, 1996): 167–71. http://dx.doi.org/10.1042/bj3200167.

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The influence of hypo-osmotic cell swelling on the activity of the mitogen-activated protein (MAP) kinases Erk-1 and Erk-2 (where Erk stands for extracellular signal-regulated protein kinase) was studied in cultured rat astrocytes. Hypo-osmotic treatment led within 10 min to an increased activity of Erk-1 and Erk-2, which became maximal at 20 min and returned to the basal level within 60 min. Moreover, exposure to hypo-osmotic conditions induced a biphasic increase in cytosolic Ca2+ concentration ([Ca2+]i): a rapid peak-like increase was followed by a sustained plateau. The absence of extracellular Ca2+ completely abolished Erk activation as well as the plateau of the [Ca2+]i response after hypo-osmotic stimulation. Application of wortmannin and agents to elevate intracellular cAMP levels also completely blocked Erk activation but were without effect on the biphasic [Ca2+]i response to hypo-osmotic treatment of the cells, suggesting a role of PtdIns 3-kinase and the Ras/Raf pathway downstream of the calcium signal. Protein kinase C (PKC) and Ca2+/calmodulin (CaM)-dependent kinases are unlikely to play a role in the hypo-osmolarity-induced signalling towards MAP kinases, as revealed by the blockage of PKC and CaM kinases. Inhibition of tyrosine kinases, pertussis-toxin- or cholera-toxin-sensitive G-proteins and phospholipase C had no effect on the [Ca2+]i response; the Erk response to hypo-osmolarity was also largely unaltered. This is different from the swelling-induced MAP kinase activation in hepatocytes, which was shown to occur via a calcium-independent but G-protein- and tyrosine kinase-dependent mechanism. Thus osmo-signalling towards MAP kinases might exhibit cell-type-specific features.

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Wurm, Antje, Ianors Iandiev, Margrit Hollborn, Peter Wiedemann, Andreas Reichenbach, Herbert Zimmermann, Andreas Bringmann, and Thomas Pannicke. "Purinergic receptor activation inhibits osmotic glial cell swelling in the diabetic rat retina." Experimental Eye Research 87, no. 4 (October 2008): 385–93. http://dx.doi.org/10.1016/j.exer.2008.07.004.

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Lehrenfeld, Christoph, and Stephan Rave. "Mass conservative reduced order modeling of a free boundary osmotic cell swelling problem." Advances in Computational Mathematics 45, no. 5-6 (May 23, 2019): 2215–39. http://dx.doi.org/10.1007/s10444-019-09691-z.

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46

Tilly, B. C., M. J. Edixhoven, L. G. Tertoolen, N. Morii, Y. Saitoh, S. Narumiya, and H. R. de Jonge. "Activation of the osmo-sensitive chloride conductance involves P21rho and is accompanied by a transient reorganization of the F-actin cytoskeleton." Molecular Biology of the Cell 7, no. 9 (September 1996): 1419–27. http://dx.doi.org/10.1091/mbc.7.9.1419.

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Hypo-osmotic stimulation of human Intestine 407 cells rapidly activated compensatory CL- and K+ conductances that limited excessive cell swelling and, finally, restored the original cell volume. Osmotic cell swelling was accompanied by a rapid and transient reorganization of the F-actin cytoskeleton, affecting both stress fibers as well as apical ruffles. In addition, an increase in total cellular F-actin was observed. Pretreatment of the cells with recombinant Clostridium botulinum C3 exoenzyme, but not with mutant enzyme (C3-E173Q) devoid of ADP-ribosyltransferase activity, greatly reduced the activation of the osmo-sensitive anion efflux, suggesting a role for the ras-related GTPase p21rho. In contrast, introducing dominant negative N17-p21rac into the cells did not affect the volume-sensitive efflux. Cell swelling-induced reorganization of F-actin coincided with a transient, C3 exoenzyme-sensitive tyrosine phosphorylation of p125 focal adhesion kinase (p125FAK) as well as with an increase in phosphatidylinositol-3-kinase (PtdIns-3-kinase) activity. Pretreatment of the cells with wortmannin, a specific inhibitor of PtdIns-3-kinase, largely inhibited the volume-sensitive ion efflux. Taken together, our results indicate the involvement of a p21rho signaling cascade and actin filaments in the activation of volume-sensitive chloride channels.

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Avella, Martine, Olivier Ducoudret, Didier F. Pisani, and Philippe Poujeol. "Swelling-activated transport of taurine in cultured gill cells of sea bass: physiological adaptation and pavement cell plasticity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R1149—R1160. http://dx.doi.org/10.1152/ajpregu.90615.2008.

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We have investigated volume-activated taurine transport and ultrastructural swelling response of sea bass gill cells in culture, assuming that euryhaline fish may have developed particularly efficient mechanisms of salinity adaptation. In vivo, when sea basses were progressively transferred from seawater to freshwater, we noticed a decrease in blood osmotic pressure. When gill cells in culture were subjected to 30% hypotonic shock, we observed a five-fold stimulation of [3H]taurine efflux. This transport was reduced by various anion channel inhibitors with the following efficiency: 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) > niflumic acid > DIDS = diphenylamine-2-carboxylic acid. With polarized gill cells in culture, the hypotonic shock produced a five-fold stimulation of apical taurine transport, whereas basolateral exit was 25 times higher. Experiments using ionomycin, thapsigargin, BAPTA-AM, or removal of extracellular calcium suggested that taurine transport was regulated by external calcium. The inhibitory effects of lanthanum and streptomycin support Ca2+ entry through mechanosensitive Ca2+ channels. Branchial cells also showed hypotonically activated anionic currents sensitive to DIDS and NPPB. Similar pharmacology and time course suggested the potential existence of a common pathway for osmosensitive taurine and Cl− efflux through volume-sensitive organic osmolyte and anion channels. A three-dimensional structure study revealed that respiratory gill cells began to swell only 15 s after hypoosmotic shock. Apical microridges showed membrane outfoldings: the cell surface became smoother with a progressive disappearance of ridges. Therefore, osmotic swelling may not actually induce membrane stretch per se, inasmuch as the microridges may provide a reserve of surface area. This work demonstrates mechanisms of functional and morphological plasticity of branchial cells during osmotic stress.

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Severinghaus, J. W. "Hypothetical roles of angiogenesis, osmotic swelling, and ischemia in high-altitude cerebral edema." Journal of Applied Physiology 79, no. 2 (August 1, 1995): 375–79. http://dx.doi.org/10.1152/jappl.1995.79.2.375.

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High-altitude cerebral edema (HACE) has been tentatively attributed to either cellular ion pump failure from ATP depletion or high cerebral blood flow inducing high capillary pressure. These hypotheses are inadequate because 1) ATP decrease occurs only after anoxia has silenced neuronal activity and 2) prolonged hypercapnic hyperemia generates only minor transcapillary protein leakage localized to the less hyperemic brain regions. In connection with this review of HACE and its causes, three other hypothetical mechanisms that might contribute are presented. 1) Osmotic cell swelling: cellular and mitochondrial osmotic pressure may rise 30 mosmol in ischemia or anoxia (potentially a 7–10% expansion). Smaller rises caused by hypoxia may be significant in the closed calvarium. 2) Focal ischemia: this may result from intracranial hypertension from hyperemia and osmotic swelling. 3) Angiogenesis: cellular hypoxia initially attracts and activates macrophages that express vascular endothelial growth factor and other cytokines, dissolving capillary basement membranes and degrading extracellular matrix, resulting in capillary leakage. In HACE, petechial hemorrhages are seen in the nerve cell layers of the retina, and similar changes have been described throughout the brain. Evidence linking HACE to angiogenesis is that dexamethasone, an effective inhibitor of angiogenesis, has demonstrated unique success in preventing and treating HACE.

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Peak, M., M. al-Habori, and L. Agius. "Regulation of glycogen synthesis and glycolysis by insulin, pH and cell volume. Interactions between swelling and alkalinization in mediating the effects of insulin." Biochemical Journal 282, no. 3 (March 15, 1992): 797–805. http://dx.doi.org/10.1042/bj2820797.

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The effects of changes in cell volume and pH on glycogen synthesis and glycolysis and their control by insulin were investigated in hepatocyte cultures. 1. Cell acidification, by increasing [CO2] from 2.5% to 5%, inhibited glycolysis and stimulated glycogen synthesis. The inhibition of glycolysis was also observed in Na(+)-free media and when K+ uptake was inhibited, but the stimulation of glycogen synthesis was abolished under these conditions, suggesting that it is secondary to ionic or volume changes. Alkalinization had converse effects on glycolysis and glycogen synthesis. 2. In HCO3(-)-containing media, replacement of NaCl with sodium acetate or potassium acetate, like acidification with CO2, inhibited glycolysis and stimulated glycogen synthesis. The latter correlated with an increase in cation content. Amiloride, an inhibitor of Na+/H+ exchange, inhibited both the increase in cation content and the stimulation of glycogen synthesis, suggesting that the latter is secondary to cell swelling. 3. Hypo-osmotic swelling increased glycogen synthesis in HCO3(-)-containing media, in both the absence and the presence of Na+ and at both 2.5% and 5% CO2, but it increased glycolysis in the presence of Na+ and at 2.5%, but not at 5%, CO2. In HCO3(-)-free media, during acidification and swelling, glycogen synthesis correlated with pH and not with cell volume, indicating that inhibition by acidification over-rides stimulation by swelling. 4. Stimulation of glycolysis by insulin was not additive with stimulation by alkalinization. The stimulation of glycogen synthesis by insulin was partially suppressed under alkaline conditions; it was markedly suppressed in isosmolar Na(+)-free media and restored by hypo-osmotic swelling. In hypo-osmolar Na(+)-free media insulin prevented the decrease in glycogen synthesis with decreasing [HCO3-], suggesting that it counteracts inhibition by acidification. 5. It is concluded that glycogen synthesis and glycolysis are both stimulated by cell swelling and inhibited by acidification, under certain conditions, but glycolysis is more sensitive to inhibition by acidification and glycogen synthesis to stimulation by swelling. Consequently, simultaneous swelling and acidification is associated with inhibition of glycolysis and stimulation of glycogen synthesis. Stimuli that cause swelling and alkalinization activate both glycogen synthesis and glycolysis, alkalinization being more important in control of glycolysis and swelling in control of glycogen synthesis. Both cell swelling and alkalinization are components of the mechanism by which insulin controls glycogen synthesis and glycolysis.

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Germann, W. J., S. A. Ernst, and D. C. Dawson. "Resting and osmotically induced basolateral K conductances in turtle colon." Journal of General Physiology 88, no. 2 (August 1, 1986): 253–74. http://dx.doi.org/10.1085/jgp.88.2.253.

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Two types of K conductance can be distinguished in the basolateral membranes of polyene-treated colonic epithelial cells (see Germann, W. J., M. E. Lowy, S. A. Ernst, and D. C. Dawson, 1986, Journal of General Physiology, 88:237-251). The significance of these two types of K conductance was investigated by measuring the properties of the basolateral membrane under conditions that we presumed would lead to marked swelling of the epithelial cells. We compared the basolateral conductance under these conditions of osmotic stress with those observed under other conditions where changes in cell volume would be expected to be less dramatic. In the presence of a permeant salt (KCl) or nonelectrolyte (urea), amphotericin-treated colonic cell layers exhibited a quinidine-sensitive conductance. Light microscopy revealed that these conditions were also associated with pronounced swelling of the epithelial cells. Incubation of tissues in solutions containing the organic anion benzene sulfonate led to the activation of the quinidine-sensitive gK and was also associated with dramatic cell swelling. In contrast, tissues incubated with an impermeant salt (K-gluconate) or nonelectrolyte (sucrose) did not exhibit a quinidine-sensitive basolateral conductance in the presence of the polyene. Although such conditions were also associated with changes in cell volume, they did not lead to the extreme cell swelling detected under conditions that activated the quinidine-sensitive gK. The quinidine-sensitive basolateral conductance that was activated under conditions of osmotic stress was also highly selective for K over Rb, in contrast to the behavior of normal Na transport by the tissue, which was supported equally well by K or Rb and was relatively insensitive to quinidine. The results are consistent with the notion that the basolateral K conductance measured in the amphotericin-treated epithelium bathed by mucosal K-gluconate solutions or in the presence of sucrose was due to the same channels that are responsible for the basolateral K conductance under conditions of normal transport. Conditions of extreme osmotic stress, however, which led to pronounced swelling of the epithelial cells, were associated with the activation of a new conductance, which was highly selective for K over Rb and was blocked by quinidine or lidocaine.

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Journal articles on the topic 'Osmotic cell swelling'

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