Cell content of phosphatidylinositol (4,5)bisphosphate in Ehrlich mouse ascites tumour cells in response to cell volume perturbations in anisotonic and in isosmotic media

Nielsen, Doris K.; Jensen, Annelie Kolbjørn; Harbak, Henrik; Christensen, Søren; Simonsen, Leif

doi:10.1113/jphysiol.2007.132308

Cited by 17 publications

(15 citation statements)

References 28 publications

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“…In EAT cells, the steady-state volume obtained after RVD is greater than the initial cell volume (Figs. 1 and 2), which could reflect that the volume set point is elevated in cells which have undergone an RVD or RVI response (358,706). As seen in Figure 2B, the recovery after swelling in 225 mosM medium is almost complete, whereas the "missing" recovery is Ͼ20% after swelling in 150 mosM medium (358,706).…”

Section: Volume Set Pointmentioning

confidence: 86%

“…537), and the one for which the volume-dependent changes are most widely documented. Thus the cellular PtdIns(4,5)P 2 level has been shown to increase rapidly after osmotic cell shrinkage in a variety of cell types (695, 706, 1122), and conversely, several studies have demonstrated a decrease in the cellular PtdIns(4,5)P 2 level after osmotic swelling (135,694,706). However, there are also reports describing osmotically induced changes in the cellular levels of other phosphoinositides (639,695,889,890,1023).…”

Section: Phosphoinositide Kinases and Phospholipases C And Dmentioning

confidence: 94%

“…Recent studies in EAT cells established that it was not the volume change per se, but the change in ionic strength, which was required for the changes in PtdIns(4,5)P 2 levels after osmotic shrinkage and swelling (706). In HeLa cells, the shrinkage-induced increase in PtdIns(4,5)P 2 was proposed to be mediated through increased recruitment and activity of PIP5KI␤ in a manner dependent on Ser/Thr dephosphorylation (1122).…”

Section: Phosphoinositide Kinases and Phospholipases C And Dmentioning

confidence: 99%

“…Phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P 2 ], the concentration of which is decreased after cell swelling and increased after shrinkage, respectively (see sect. IVC), was also recently suggested to orchestrate the volume set point in EAT cells (706).…”

Section: Volume Set Pointmentioning

confidence: 99%

“…1 and 2), which could reflect that the volume set point is elevated in cells which have undergone an RVD or RVI response (358,706). As seen in Figure 2B, the recovery after swelling in 225 mosM medium is almost complete, whereas the "missing" recovery is Ͼ20% after swelling in 150 mosM medium (358,706). One possible interpretation is that the volume set point increases with decreasing intracellular ionic strength in these cells, although obviously many other conditions in the swollen cells could affect the open FIG. 2.…”

Section: Volume Set Pointmentioning

confidence: 99%

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Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,306

1,677

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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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Section: Volume Set Pointmentioning

confidence: 86%

Section: Phosphoinositide Kinases and Phospholipases C And Dmentioning

confidence: 94%

Section: Phosphoinositide Kinases and Phospholipases C And Dmentioning

confidence: 99%

Section: Volume Set Pointmentioning

confidence: 99%

Section: Volume Set Pointmentioning

confidence: 99%

See 3 more Smart Citations

Physiology of Cell Volume Regulation in Vertebrates

Hoffmann

Lambert²,

Pedersen³

2009

Physiological Reviews

1,306

1,677

View full text Add to dashboard Cite

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Roles of Ion Transport in Control of Cell Motility

Stock

Ludwig

Hanley

et al. 2013

Comprehensive Physiology

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Cell motility is an essential feature of life. It is essential for reproduction, propagation, embryonic development, and healing processes such as wound closure and a successful immune defense. If out of control, cell motility can become life-threatening as, for example, in metastasis or autoimmune diseases. Regardless of whether ciliary/flagellar or amoeboid movement, controlled motility always requires a concerted action of ion channels and transporters, cytoskeletal elements, and signaling cascades. Ion transport across the plasma membrane contributes to cell motility by affecting the membrane potential and voltage-sensitive ion channels, by inducing local volume changes with the help of aquaporins and by modulating cytosolic Ca(2+) and H(+) concentrations. Voltage-sensitive ion channels serve as voltage detectors in electric fields thus enabling galvanotaxis; local swelling facilitates the outgrowth of protrusions at the leading edge while local shrinkage accompanies the retraction of the cell rear; the cytosolic Ca(2+) concentration exerts its main effect on cytoskeletal dynamics via motor proteins such as myosin or dynein; and both, the intracellular and the extracellular H(+) concentration modulate cell migration and adhesion by tuning the activity of enzymes and signaling molecules in the cytosol as well as the activation state of adhesion molecules at the cell surface. In addition to the actual process of ion transport, both, channels and transporters contribute to cell migration by being part of focal adhesion complexes and/or physically interacting with components of the cytoskeleton. The present article provides an overview of how the numerous ion-transport mechanisms contribute to the various modes of cell motility.

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Thermal inactivation of volume-sensitive K+,Cl− cotransport and plasma membrane relief changes in human erythrocytes

Parshina

Yusipovich

Platonova

et al. 2013

Pflugers Arch - Eur J Physiol

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Previously, we reported that in mammalian erythrocytes irreversible annealing of spectrin heterodimers at 49-50 °C abolished cell volume-dependent regulation of ion carriers, thus suggesting an implication of a two-dimensional (2D) membrane carcass in volume sensing and/or signal transduction. To further examine this hypothesis, we employed atomic force microscopy. This method revealed folded membrane relief of fixed human erythrocytes with an average wave height of 3-5 nm covered by globular structures with a diameter of 40-50 nm and an average height of 1-2 nm. Erythrocyte swelling caused by reduction of medium osmolality decreased the height of membrane surface waves by 40 % and increased K(+),Cl(-) cotransport by approximately sixfold. Both volume-sensitive changes of membrane relief and activity of K(+),Cl(-) cotransporter were abolished by a 10-min preincubation at 50 °C. Our results strongly suggest that volume-dependent alterations of the human erythrocyte membrane relief are caused by reorganization of the 2D spectrin-actin network contributing to regulation of the activity of volume-sensitive ion transporters.

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Cell content of phosphatidylinositol (4,5)bisphosphate in Ehrlich mouse ascites tumour cells in response to cell volume perturbations in anisotonic and in isosmotic media

Cited by 17 publications

References 28 publications

Physiology of Cell Volume Regulation in Vertebrates

Physiology of Cell Volume Regulation in Vertebrates

Roles of Ion Transport in Control of Cell Motility

Thermal inactivation of volume-sensitive K+,Cl− cotransport and plasma membrane relief changes in human erythrocytes

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