Calcium Capacitance

Cadmium, 85 Calcium electrode, 152 Capacitance, 20, 21, 22, 129 Capacitor, 20 Calixarine, 155... 

Calcium fluoride, solid electrolyte, 92, 420 Capacitance charging current, 2... 

Genetic evidence supports the importance of coordinated expression and distributions of a2 or a3 Na+/K+ pump isoforms with the Na+/Ca2+ exchanger (NCX) and Ca2+ pumps to function in excitable and contractile cells deletion of one copy of the a2 Na+/K+ pump gene in mice leads to increased contractile force in cardiac and skeletal muscle while deletion of one copy of the al gene leads to reduction of contractile force [25]. In rat optic nerve astrocytes, deletion of the a2 gene or ouabain treatment of cells expressing a2 leads to increased capacitative calcium entrance responses, which reflect a decreased ability to rapidly remove cytosolic Ca2+ [26]. 

The functions of the calcium-storage capacity of the ER are at least threefold the association of Ca2+ with Ca2+-binding proteins in the ER is part of a chaperone function that is essential for normal protein synthesis the rapid rate of Ca2+ uptake by endoplasmic pumps provides shortterm cytoplasmic Ca2+ buffering that resists untoward and transient changes in [Ca2+] and, finally, many signaling pathways employ elevated [Ca2+] to activate physiological processes. Extensive Ca2+ release from ER is coupled to activation of Ca2+ entry across the plasma membrane, a process known as capacitative calcium entry, which is discussed below. 

Ca2+ can enter cells via voltage- or ligand-dependent channels and by capacitative entry. These three fundamental mechanisms of regulated calcium ion entry across the plasma membrane involve, respectively, voltage-dependent Ca2+ channels, ligand-gated Ca2+ channels and capacitative Ca2+ entry associated with phospholipase C-coupled receptors. 

Capacitative Ca2+ entry is the predominant mode of regulated Ca2+ entry in nonexcitable cells but it also occurs in a number of excitable cell types. This pathway of Ca2+ entry is usually associated with the activation of phospholipase C, which mediates the formation of IP3 (see Ch. 20). Intracellular application of IP3 mimics the ability of hormones and neurotransmitters to activate calcium ion entry, and activation of calcium ion entry by hormones and neurotransmitters can be blocked by intracellular application of low-molecular-weight heparin, which potently antagonizes IP3 binding to its receptor. There is considerable evidence for the presence of an IP3 receptor in the plasma membrane of some cells types. 1(1,3,4,5)P4, a product of IP3 phosphorylation, has been shown in some cells to augment this action of IP3 in activating PM calcium ion entry, but in others IP3 alone is clearly sufficient. 

However, the current view of the regulation of calcium ion entry into the cytoplasm by PLC-linked stimuli holds that activation occurs not as a direct result of the action of IP3 on the plasma membrane but indirectly, as a result of depletion of calcium ions from an intracellular store by IP3 [14]. In the context of this capacitative model , the actions of intracellularly applied IP3 and heparin reflect the effects of these maneuvers on intracellular release process from ER into cytosol, rather than via the plasma membrane. The reported actions of I(1,3,4,5)P4, if in fact they do represent physiological control mechanisms, may reflect an ability of I(1,3,4,5)P4 to augment the calcium-releasing ability of IP3, rather than a distinct and... 

Channels associated with capacitative calcium ion entry have been characterized electrophysiologically. In leukocytes, the current associated with the depletion of intracellular Ca2+ stores is highly Ca2+-selective and, on the basis of noise analysis, is believed to involve minute single channels [16] (see Ch. 6). This is the calcium release-activated calcium current (ICrac)- In other cell types, currents with significantly different properties have been identified, including in some instances store-operated nonse-lective cation channels. These marked electrophysiological distinctions may be indicative of distinct channel types mediating capacitative calcium ion entry in different cell types. 

While the molecular identity of the capacitative Ca2+ entry channel is not known, a candidate is a homolog of the Drosophila mutant trp. This photoreceptor mutant is incapable of maintaining a sustained photoreceptor potential. This phenotype could be mimicked by the calcium entry blocker lanthanum, and it was suggested that the related defect is a failure of Ca2+ entry. 

Now described as a trp superfamily, more than 20 vertebrate trp homologs have been identified and these can be divided phylogenetically into three subfamilies trpC (termed canonical as they are most closely related to Drosophila trp), trpV and trpM. Some of these proteins are potential contenders for the capacitative calcium ion entry channel. In particular, expression of members of the TRPC and TRPV families in mammalian cells has been shown to augment capacitative calcium ion entry, but their role is still a matter for debate [17]. 

Putney, J. W. Jr Capacitative Calcium Entry. Austin, TX Landes Bioscience,1997. 

Bimbaumer L, Zhu X, J iang M et al 1996 On the molecular basis and regulation of cellular capacitative calcium entry roles for Trp proteins. Proc Natl Acad Sci USA 93 15195—15202... 

Wayman CP, Gibson A, McFadzean I 1998 Depletion of either ryanodine- or IP3-sensitive calcium stores activates capacitative calcium entry in mouse anococcygeus smooth muscle cells. Pfliiger s Arch 435 231—239... 

Berridge MJ 1997 Elementary and global aspects of calcium signalling. J Physiol 499 291—306 Broad LM, Cannon TR, Taylor CW 1999 A non-capacitative pathway activated by arachidonic acid is the major Ca2+ entry mechanism in rat A7r5 smooth muscle cells stimulated with low concentrations of vasopressin. J Physiol 517 121-134 Byron KL, Taylor CW 1995 Vasopressin stimulation of Ca2+ mobilization, two bivalent cation entry pathways and Ca2+ efflux in A7r5 rat smooth muscle cells. J Physiol 485 455—468... 

Kiselyov K, Mignery GA, Zhu MX, Muallem S 1999 The N-terminal domain of the IP3 receptor gates store-operated hTrp3 channels. Mol Cell 4 423-429 Lee HC 2000 NAADP An emerging calcium signaling molecule. J Membr Biol 173 1 -8 Lin S, Fagan KA, Li K-X, Shaul PW, Cooper DMF, Rodman DM 2000 Sustained endothelial nitric-oxide synthase activation requires capacitative Ca2+ entry. J Biol Chem 275 17979-17985... 

Luo D, Broad LM, Bird GSJ, Putney JW Jr 2001 Mutual antagonism of calcium entry by capacitative and arachidonic acid-mediated calcium entry pathways. J Biol Chem 276 20186-20189... 

Putney JW Jr 1997 Capacitative calcium entry. Springer-Verlag, Heidelberg Putney JW Jr 1999 TRP, inositol 1,4,5-trisphosphate receptors, and capacitative calcium entry. Proc Natl Acad Sci USA 96 14669-14671... 

Parekh AB, Penner R 1997 Store depletion and calcium influx. Physiol Rev 77 901-930 Potocnik SJ, Hill MA 2001 Pharmacological evidence for capacitative Ca2+ entry in cannulated and pressurized skeletal muscle arterioles. Br J Pharmacol 134 247-256 Pozzan T, Rizzuto R, Volpe P, Meldolesi J 1994 Molecular and cellular physiology of intracellular calcium stores. Physiol Rev 74 595—636 Putney JW Jr, Broad LM, Braun FJ, Lievremont JP, Bird GS 2001 Mechanisms of capacitative calcium entry. J Cell Sci 114 2223—2229... 

CASH CBM CBO CBPC CC CCB CCM CCP CDB CEC CFBC CFC CFR CMM COP CSH CT Calcium aluminosilicate hydrate Coal bed methane Carbon burn-out Chemically-bonded phosphate ceramics Carbonate carbon Coal combustion byproducts Constant capacitance model Coal combustion product Citrate-dithionate-bicarbonate Cation exchange capacity Circulating fluidized bed combustion Chlorofluorocarbon Cumulative fraction Coal mine methane Coefficient of performance Calcium silicate hydrate Collision theory... 

The increase in capacitance with prothrombin concentration is presented in Figure 5. Even in the absence of Ca++ there is an appreciable increase in capacitance upon addition of prothrombin. However, the initial increase of capacitance with prothrombin concentration is less steep in the absence or at very low concentrations of calcium 10"3mM) than at the higher concentrations. In the low Ca++ concentration region the capacitance increases almost linearly with prothrombin up to concentrations of about 5 /ig/mL. In this concentration region the surface concentrations as seen from Figure 2 are also a linear function of the bulk concentration of prothrombin. Every adsorbed prothrombin molecule up to a given surface concentration contributes by the same value to the surface-layer capacitance Ca... 

Figure 5. Differential capacitance at —0.5 V relative to the N-Ag/AgCl electrode as a function of the concentration of prothrombin at different concentrations of calcium OmM (O) 10 3mM (M) 2mM ( 3) 0.5mM ...

In Figure 6 the dependence of capacitance on calcium concentration for different concentrations of prothrombin is shown. Curves a and b were reconstructed from the curves obtained by changing the concentration of prothrombin at different constant concentrations of Ca+. Curve c was obtained by changing the concentration of Ca++ at a prothrombin concentration of 2.4 jug/mL. We obtain a very good agreement by the two different ways at the prothrombin concentration of 2.4 /ig/mL. It is evident from the increase in the capacitance that substantial penetration of the lipid layer by the prothrombin is observed even in the absence of Ca++. A further pronounced increase in penetration is observed ca. O.lmM Ca++. 

Enfissi, A., Prigent, S., Colosetti, P. and Capiod, T., 2004, The blocking of capacitative calcium entry by 2-aminoethyl diphenylborate (2-APB) and carboxyamidotriazole (CAI) inhibits proliferation in Hep G2 and Huh-7 human hepatoma cells. Cell Calcium 36, 459-467. 

Mignen, O., Brink, C., Enfissi, A., Nadkarni, A., Shuttleworth, T. J., Giovannucci, D. R. and Capiod, T., 2005, Carboxyamidotriazole-induced inhibition of mitochondrial calcium import blocks capacitative calcium entry and cell proliferation in HEK-293 cells. J Cell Sci 118, 5615-23. 

Varadi, A., Cirulli, V. and Rutter, G. A., 2004, Mitochondrial localization as a determinant of capacitative Ca2+ entry in HeLa cells. Cell Calcium 36, 499—508. 

Williams, S. S., French, J. N., Gilbert, M., Rangaswami, A. A., Walleczek, J. and Knox, S. J., 2000, Bcl-2 overexpression results in enhanced capacitative calcium entry and resistance to SKF-96365-induced apoptosis. Cancer lies 60, 4358-61. 

Hopf, F.W., Reddy, P., Hong, J., and Steinhardt, R.A., 1996a, A capacitative calcium current in cultured skeletal muscle cells is mediated by the calcium-specific leak channel and inhibited by dihydropyridine compounds, J Biol Chem, 271, pp 22358-22367. 

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