Ca2+ Signaling, Intracellular pH and Cell Volume in Cell Proliferation

2005 ◽  
Vol 205 (3) ◽  
pp. 129-137 ◽  
Author(s):  
R. Schreiber
1992 ◽  
Vol 2 (3-4) ◽  
pp. 159-179 ◽  
Author(s):  
R.J. Gillies ◽  
R. Martinez-Zaguilan ◽  
E.P. Peterson ◽  
R. Perona

2012 ◽  
Vol 113 (12) ◽  
pp. 3721-3729 ◽  
Author(s):  
Gisela Di Giusto ◽  
Pilar Flamenco ◽  
Valeria Rivarola ◽  
Juan Fernández ◽  
Luciana Melamud ◽  
...  

1991 ◽  
Vol 112 (4) ◽  
pp. 711-718 ◽  
Author(s):  
N Grandin ◽  
M Charbonneau

In Xenopus embryos, previous results failed to detect changes in the activity of free calcium ions (Ca2+i) during cell division using Ca2(+)-selective microelectrodes, while experiments with aequorin yielded uncertain results complicated by the variation during cell division of the aequorin concentration to cell volume ratio. We now report, using Ca2(+)-selective microelectrodes, that cell division in Xenopus embryos is accompanied by periodic oscillations of the Ca2+i level, which occur with a periodicity of 30 min, equal to that of the cell cycle. These Ca2+i oscillations were detected in 24 out of 35 experiments, and had a mean amplitude of 70 nM, around a basal Ca2+i level of 0.40 microM. Ca2+i oscillations did not take place in the absence of cell division, either in artificially activated eggs or in cleavage-blocked embryos. Therefore, Ca2+i oscillations do not represent, unlike intracellular pH oscillations (Grandin, N., and M. Charbonneau. J. Cell Biol. 111:523-532. 1990), a component of the basic cell cycle ("cytoplasmic clock" or "master oscillator"), but appear to be more likely related to some events of mitosis.


Author(s):  
Florian Lang ◽  
Michael Föller ◽  
Karl Lang ◽  
Philipp Lang ◽  
Markus Ritter ◽  
...  

Author(s):  
Florian Lang ◽  
Ekaterina Shumilina ◽  
Markus Ritter ◽  
Erich Gulbins ◽  
Alexey Vereninov ◽  
...  

1992 ◽  
Vol 262 (1) ◽  
pp. L1-L14 ◽  
Author(s):  
R. L. Lubman ◽  
E. D. Crandall

Alveolar type II epithelial cells in adult mammalian lungs actively transport salt and water, secrete surfactant, and differentiate into type I cells under normal conditions and following lung injury. It has become increasingly apparent that, like all epithelial cells, alveolar pneumocytes have evolved specialized ion transport mechanisms by which they regulate their intracellular pH (pHi). pHi is an important biological parameter in all living cells whose regulation is necessary for normal cellular homeostasis. pHi, and the ion transport mechanisms by which it is regulated, may contribute to many cellular processes, including transcellular transport, cell volume and osmolarity regulation, and intracellular transport, cell volume and osmolarity regulation, and intracellular electrolyte composition. Moreover, changes in pHi may serve as intracellular signals for biological processes such as cell growth, proliferation, and differentiation. We review herein the general principles of pHi regulation in epithelia and describe the mechanisms and effects of pHi regulation in alveolar pneumocytes. Many of the critical issues in current pulmonary research involve processes that pHi is most likely to affect, including maintenance of alveolar epithelial barrier integrity, development and maintenance of epithelial polarity, epithelial proliferation and differentiation, and regulation of transepithelial transport with respect to alveolar fluid balance in normal individuals and in those with excess alveolar fluid (i.e., pulmonary edema). Investigations into the regulation of pHi in alveolar pneumocytes and the regulatory effects of pHi in turn on other cellular processes are likely to yield information important to the understanding of lung biology and pulmonary disease.


1991 ◽  
Vol 261 (4) ◽  
pp. F634-F639 ◽  
Author(s):  
J. S. Beck ◽  
S. Breton ◽  
H. Mairbaurl ◽  
R. Laprade ◽  
G. Giebisch

The effect of alterations in sodium transport on cell ATP content and pH in the isolated perfused proximal convoluted tubule (PCT) of the rabbit was examined. Stimulating sodium transport by the addition of luminal glucose and alanine decreased cell ATP from 4.44 +/- 0.93 to 2.69 +/- 0.62 mM (n = 4), increased intracellular pH by 0.13 +/- 0.02 (n = 7), and increased cell volume by 0.10 +/- 0.02 nl/mm (n = 4). Blocking the sodium pump with 10(-4) M strophanthidin in tubules in which sodium transport had been stimulated increased cell ATP from 2.04 +/- 0.24 to 2.42 +/- 0.32 mM (n = 6). In parallel experiments the same dose of strophanthidin depolarized the basolateral membrane from -52.6 +/- 1.9 to -6.4 +/- 1.6 mV, depolarized the transepithelial potential from -3.2 +/- 0.3 to -0.1 +/- 0.1 mV, and reduced the basolateral membrane potassium transference number from 0.47 to 0.26 indicating a reduction in basolateral potassium conductance. Since strophanthidin caused a cell alkalinization of 0.15 +/- 0.03, this latter effect cannot be due to changes of intracellular pH. Strophanthidin caused no change in cell volume over the period studied, suggesting that stretch-activated potassium channels are not involved either. Instead, potassium conductance inhibition may be the result of the closure of ATP-sensitive potassium channels. These same channels might thus be partly responsible for the increase in potassium conductance commonly observed during stimulation of sodium transport.


Physiology ◽  
1999 ◽  
Vol 14 (2) ◽  
pp. 58-64 ◽  
Author(s):  
Joseph H. Sellin

Short-chain fatty acids are the predominant luminal anions in the colon (>75 mM) and thus create a rather unique environment for transporting epithelium. The colon absorbs short-chain fatty acids, either by diffusion of the protonated species across the apical membrane or by an anion exchange process with bicarbonate. Additionally, short-chain fatty acids modulate Na absorption, Cl secretion, intracellular pH, and cell volume.


1980 ◽  
Vol 85 (3) ◽  
pp. 786-797 ◽  
Author(s):  
A Schonbrunn ◽  
Westendorf J Krasnoff M ◽  
A Tashjian

GH(4)C(1) cells are a clonal strain of rat pituitary cells that synthesize and secrete prolactin and growth hormone. Chronic treatment (longer than 24 h) of GH(4)C(1) cells with epidermal growth factor (EGF) (10(-8) M) decreased by 30-40 percent both the rate of cell proliferation and the plateau density reached by cultures. Inhibition of cell proliferation was accompanied by a change in cellular morphology from a spherical appearance to an elongated flattened shape and by a 40-60 percent increase in cell volume. These actions of EGF were qualitatively similar to those of the hypothalamic tripeptide thyrotropin-releasing hormone (TRH) (10(-7) M) which decreased the rate of cell proliferation by 10-20 percent and caused a 15 percent increase in cell volume. The presence of supramaximal concentrations of both EGF (10(-8)M) and TRH (10(-7)M) resulted in greater effects on cell volume and cell multiplication than either peptide alone. EGF also altered hormone production by GH(4)C(1) cells in the same manner as TRH. Treatment of cultures with 10(-8) M EGF for 2-6 d increased prolactin synthesis five- to ninefold compared to a two- to threefold stimulation by 10(-7) M TRH. Growth hormone production by the same cultures was inhibited 40 percent by EGF and 15 percent by TRH. The half- maximal effect of EGF to increase prolactin synthesis, decrease growth hormone production, and inhibit cell proliferation occurred at a concentration of 5 x 10 (-11) M. Insulin and multiplication stimulating activity, two other growth factors tested, did not alter cell proliferation, cell morphology, or hormone production by GH(4)C(1) cells, indicating the specificity of the EGF effect. Fibroblast growth factor, however, had effects similar to those of EGF and TRH. Of five pituitary cell strains tested, all but one responded to chronic EGF treatment with specifically altered hormone production. Acute chronic EGF treatment with specifically altered hormone production. Acute treatment (30 min) of GH(4)C(1) cells with 10(-8) M EGF caused a 30 percent enhancement of prolactin release compared to a greater than twofold increase caused by 10(-7) M TRH. Therefore, although EGF and TRH have qualitatively similar effects on GH(4)C(1) cells, their powers to affect hormone release acutely or hormone synthesis and cell proliferation chronically are distinct.


1988 ◽  
Vol 256 (2) ◽  
pp. 585-592 ◽  
Author(s):  
A D Whetton ◽  
S J Vallance ◽  
P N Monk ◽  
E J Cragoe ◽  
T M Dexter ◽  
...  

Interleukin 3 (IL-3) is an important regulator of haemopoietic stem cell proliferation both in vivo and in vitro. Little is known about the possible mechanisms whereby this growth factor acts on stem cells to stimulate cell survival and proliferation. Here we have investigated the role of intracellular pH and the Na+/H+ antiport in stem cell proliferation using the multipotential IL-3-dependent stem cell line, FDCP-Mix 1. Evidence is presented that IL-3 can stimulate the activation of an amiloride-sensitive Na+/H+ exchange via protein kinase C activation. IL-3-mediated activation of the Na+/H+ exchange is not observed in FDCP-Mix 1 cells where protein kinase C levels have been down-modulated by treatment with phorbol esters. Also the protein kinase C inhibitor H7 can inhibit IL-3-mediated increases in intracellular pH. This activation of Na+/H+ exchange via protein kinase C has been shown to occur with no measurable effects of IL-3 on inositol lipid hydrolysis or on cytosolic Ca2+ levels. Evidence is also presented that this IL-3-stimulated alkalinization acts as a signal for cellular proliferation in stem cells.


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