Regulatory volume increase (RVI) and apoptotic volume decrease (AVD) in U937 cells in hypertonic medium

2011 ◽  
Vol 5 (5) ◽  
pp. 487-494 ◽  
Author(s):  
V. E. Yurinskaya ◽  
A. A. Rubashkin ◽  
A. V. Shirokova ◽  
A. A. Vereninov
Keyword(s):  
U937 Cells ◽  
Hypertonic Medium ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Apoptotic Volume Decrease ◽  
Volume Decrease

scholarly journals Dual Response of Human Leukemia U937 Cells to Hypertonic Shrinkage: Initial Regulatory Volume Increase (RVI) and Delayed Apoptotic Volume Decrease (AVD)

2012 ◽  
Vol 30 (4) ◽  
pp. 964-973 ◽  
Author(s):  
Valentina E. Yurinskaya ◽  
Alexey V. Moshkov ◽  
Anna V. Wibberley ◽  
Florian Lang ◽  
Michael A. Model ◽  
...  
Keyword(s):  
Human Leukemia ◽  
U937 Cells ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Apoptotic Volume Decrease ◽  
Dual Response ◽  
Volume Decrease

Responses of lymphocytes to anisotonic media: volume-regulating behavior

1984 ◽  
Vol 246 (3) ◽  
pp. C204-C215 ◽  
Author(s):  
S. Grinstein ◽  
A. Rothstein ◽  
B. Sarkadi ◽  
E. W. Gelfand
Keyword(s):  
Regulatory Volume Decrease ◽  
Lymphocyte Subpopulations ◽  
Lymphoid Cells ◽  
Ionophore A23187 ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Cytoplasmic Acidification ◽  
Tissue Of Origin ◽  
Volume Decrease ◽  
Media Volume

The regulatory responses elicited in lymphoid cells suspended in anisotonic media are reviewed. The immediate response approximates osmometric behavior. In addition, in hypotonic media, the initial osmometric swelling is followed by a regulatory volume decrease (RVD), which is associated with KCl loss. The volume-induced effluxes of K+ and Cl- are mediated by two independent conductive pathways. Ca2+-depletion experiments and studies of inhibitor susceptibility suggest that Ca2+ may mediate the activation of the K+ pathway. The responses of the two main lymphocyte subpopulations to hypotonic challenge are different. RVD is much more rapid in T- than in B-cells, regardless of their tissue of origin. Under certain conditions, shrunken lymphocytes will regain their initial volume. This regulatory volume increase (RVI) is due to NaCl uptake, followed by a secondary exchange of Na+ for K+ via the Na+-K+ pump. Na+ is primarily taken up in exchange for H+ through an amiloride-sensitive pathway, whereas Cl- enters in exchange for HCO-3 (or OH-). Anion and cation fluxes responsible for RVI are electroneutral. Some of the volume-sensitive pathways can also be activated in isotonic cells. The conductive K+ pathway is activated by Ca2+ plus ionophore A23187, and the Na+-H+ exchanger can be activated by cytoplasmic acidification. The responses of lymphocytes to anisotonic challenge are compared with those of other cells, and the possible significance of the volume-induced fluxes is discussed.

Does the intracellular ionic concentration or the cell water content (cell volume) determine the activity of TonEBP in NIH3T3 cells?

2008 ◽  
Vol 295 (6) ◽  
pp. C1528-C1534 ◽  
Author(s):  
Tina Rødgaard ◽  
Kenneth Schou ◽  
Martin B. Friis ◽  
Else K. Hoffmann
Keyword(s):  
Regulatory Volume Decrease ◽  
Ionic Concentration ◽  
Luciferase Assay ◽  
Cell Shrinkage ◽  
Nih3t3 Cells ◽  
Hypertonic Medium ◽  
Volume Increase ◽  
Expression Of Genes ◽  
Enhancer Binding Protein ◽  
Volume Decrease

The transcription factor, tonicity-responsive enhancer binding protein (TonEBP), is involved in the adaptive response against hypertonicity. TonEBP regulates the expression of genes that catalyze the accumulation of osmolytes, and its transcriptional activity is increased by hypertonicity. The goal of the present investigation was to investigate whether cell shrinkage or high intracellular ionic concentration induced the activation of TonEBP. We designed a model system for isotonically shrinking cells over a prolonged period of time. Cells swelled in hypotonic medium and performed a regulatory volume decrease. Upon return to the original isotonic medium, cells shrank initially, followed by a regulatory volume increase. To maintain cell shrinkage, the RVI process was inhibited as follows: ethyl-isopropyl-amiloride inhibited the Na+/H+ antiport, bumetanide inhibited the Na+-K+-2Cl− cotransporter, and gadolinium inhibited shrinkage-activated Na+ channels. Cells remained shrunken for at least 4 h (isotonically shrunken cells). The activity of TonEBP was investigated with a Luciferase assay after isotonic shrinkage and after shrinkage in a high-NaCl hypertonic medium. We found that TonEBP was strongly activated after 4 and 16 h in cells in high-NaCl hypertonic medium, but not after 4 or 16 h in isotonically shrunken cells. Cells treated with high-NaCl hypertonic medium for 4 h had significantly higher intracellular concentrations of both K+ and Na+ than isotonically shrunken cells. This strongly suggested that an increase in intracellular ionic concentration and not cell shrinkage is involved in TonEBP activation.

Na+/H+ exchange and osmotic shrinkage in isolated trout hepatocytes

1997 ◽  
Vol 200 (17) ◽  
pp. 2369-2376 ◽  
Author(s):  
B Fossat ◽  
J Porthé-Nibelle ◽  
S Pedersen ◽  
B Lahlou
Keyword(s):  
Rainbow Trout ◽  
Intracellular Ph ◽  
Extracellular Ph ◽  
Hypertonic Medium ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Hypertonic Stress ◽  
Amiloride Derivatives ◽  
Na Uptake ◽  
Rainbow Trout Liver

The ability of rainbow trout liver cells to regulate their intracellular pH (pHi) was studied using two methods on hepatocytes isolated by collagenase digestion: (i) by monitoring pHi with the fluorescent dye BCECF-AM, and (ii) by measuring the amiloride-sensitive uptake of 22Na, which represents Na+/H+ exchange. In low-Na+ medium (¾16mmoll-1), Na+ uptake was reduced by approximately 70% in the presence of amiloride derivatives (DMA or MPA, 10(-4)moll-1). Changing separately either the extracellular pH (pHe) or the intracellular pH (pHi, clamped by treating the cells with nigericin in the presence of 140mmoll-1 K+) between 6 and 8 induced an increase in the rate of Na+ uptake when pHe was raised or when pHi was reduced. When transferred to hypertonic medium, hepatocytes shrank to nearly 72% of their initial volume, and thereafter a slow and partial regulatory volume increase phase was observed, with an increase in the amiloride-sensitive rate of Na+ uptake and an increase in intracellular pH. As DIDS-sensitive Cl- uptake was concomitantly enhanced, it is suggested that hypertonic stress activates Na+/H+ and Cl-/HCO3- exchange.

Ion transport asymmetry and functional coupling in bovine pigmented and nonpigmented ciliary epithelial cells

1994 ◽  
Vol 266 (5) ◽  
pp. C1210-C1221 ◽  
Author(s):  
J. L. Edelman ◽  
G. Sachs ◽  
J. S. Adorante
Keyword(s):  
Transport Properties ◽  
Aqueous Humor ◽  
Lucifer Yellow ◽  
Regulatory Volume Decrease ◽  
Ciliary Epithelium ◽  
Functional Coupling ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Cell Sizing ◽  
Volume Decrease

The solute and water transport properties of the bovine ciliary epithelium were studied using isolated pigmented (PE) and nonpigmented (NPE) cells. It was shown that these cells were functionally coupled by demonstrating dye diffusion between paired PE and NPE cells after microinjection of lucifer yellow. Electronic cell sizing was used to measure cell volume changes of isolated PE and NPE cells in suspension after anisosmotic perturbations and after transport inhibition under isosmotic conditions. The PE cells showed the presence of a regulatory volume increase when subjected to osmotic shrinkage with NaCl, whereas the NPE cells did not demonstrate a regulatory volume increase under these conditions. In contrast, the NPE cells exhibited a regulatory volume decrease when subjected to osmotic swelling, whereas the PE cells did not recover from swelling. The regulatory volume decrease in NPE cells was inhibited by increased bath K or pretreatment with quinine (1 mM). The presence of a bumetanide-sensitive mechanism capable of moving measurable amounts of solute and water, probably Na-K-2Cl cotransport, was demonstrated in the PE cells but absent in the NPE cells. Bumetanide produced a dose-dependent shrinkage of PE cells at concentrations as low as 1 microM. Isosmotically reducing bath Cl, Na, or K concentration caused a rapid shrinkage of PE cells that was bumetanide inhibitable. The asymmetry of transport properties in PE and NPE cells supports a functional syncytium model of aqueous humor formation (39) across the two layers of the ciliary epithelium wherein ion uptake from the blood is carried out by the PE cells and ion extrusion by the NPE cells. Gap-junction coupling between the cells allows the ions taken up by the PE cells to move into the NPE cells. Extrusion of Na by the Na-K pump across the aqueous facing (basolateral) membranes of the NPE cells, most likely accompanied by Cl, determines the formation of the aqueous humor.

scholarly journals Regulatory Volume Increase and Regulatory Volume Decrease Responses in HL-1 Atrial Myocytes

2014 ◽  
Vol 33 (6) ◽  
pp. 1745-1757 ◽  
Author(s):  
Veronica I. Cacace ◽  
Andres G. Finkelsteyn ◽  
Laura M. Tasso ◽  
Carlos F. Kusnier ◽  
Karina A. Gomez ◽  
...  
Keyword(s):  
Regulatory Volume Decrease ◽  
Atrial Myocytes ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Volume Decrease

scholarly journals Vasopressin Neurons Respond to Hyperosmotic Stimulation with Regulatory Volume Increase and Secretory Volume Decrease by Activating Ion Transporters and Ca2+ Channels

2021 ◽  
Vol 55 (S1) ◽  
pp. 119-134
Keyword(s):  
Regulatory Volume Decrease ◽  
The Body ◽  
Cell Swelling ◽  
Ion Transporters ◽  
Cell Shrinkage ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Vasopressin Neurons ◽  
Ca2 Channels ◽  
Volume Decrease

BACKGROUND/AIMS: Arginine vasopressin (AVP) neurons play an important role for sensing a change in the plasma osmolarity and thereby responding with regulated AVP secretion in order to maintain the body fluid homeostasis. The osmo-sensing processes in magnocellular neurosecretory cells (MNCs) including AVP and oxytocin (OXT) neurons of the hypothalamus were reported to be coupled to sustained osmotic shrinkage or swelling without exhibiting discernible cell volume regulation. Since increasing evidence has shown some important differences in properties between AVP and OXT neurons, osmotic volume responses are to be reexamined with distinguishing these cell types from each other. We previously reported that AVP neurons identified by transgenic expression of enhanced green fluorescence protein (eGFP) possess the ability of regulatory volume decrease (RVD) after hypoosmotic cell swelling. Thus, in the present study, we examined the ability of regulatory volume increase (RVI) after hyperosmotic cell shrinkage in AVP neurons. METHODS: Here, we used eGFP-identified AVP neurons acutely dissociated from AVP-eGFP transgenic rats. We performed single-cell size measurements, cytosolic RT-PCR analysis, AVP secretion measurements, and patch-clamp studies. RESULTS: The AVP neurons were found to respond to a hyperosmotic challenge with physiological cell shrinkage caused by massive secretion of AVP, called a secretory volume decrease (SVD), superimposed onto physical osmotic cell shrinkage, and also to exhibit the ability of RVI coping with osmotic and secretory cell shrinkage. Furthermore, our pharmacological and molecular examinations indicated that AVP secretion and its associated SVD event are triggered by activation of T-type Ca2+ channels, and the RVI event is attained by parallel operation of Na+/H+ exchanger and Cl-/HCO3- anion exchanger. CONCLUSION: Thus, it is concluded that AVP neurons respond to hyperosmotic stimulation with the regulatory volume increase and the secretory volume increase by activating ion transporters and Ca2+ channels, respectively.

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