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Journal articles on the topic 'Calcium exchanger (NCX)'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

Chovancova, Barbora, Veronika Liskova, Petr Babula, and Olga Krizanova. "Role of Sodium/Calcium Exchangers in Tumors." Biomolecules 10, no. 9 (August 31, 2020): 1257. http://dx.doi.org/10.3390/biom10091257.

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The sodium/calcium exchanger (NCX) is a unique calcium transport system, generally transporting calcium ions out of the cell in exchange for sodium ions. Nevertheless, under special conditions this transporter can also work in a reverse mode, in which direction of the ion transport is inverted—calcium ions are transported inside the cell and sodium ions are transported out of the cell. To date, three isoforms of the NCX have been identified and characterized in humans. Majority of information about the NCX function comes from isoform 1 (NCX1). Although knowledge about NCX function has evolved

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2

Roome, Chris J., Emmet M. Power, and Ruth M. Empson. "Transient reversal of the sodium/calcium exchanger boosts presynaptic calcium and synaptic transmission at a cerebellar synapse." Journal of Neurophysiology 109, no. 6 (March 15, 2013): 1669–80. http://dx.doi.org/10.1152/jn.00854.2012.

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The sodium/calcium exchanger (NCX) is a widespread transporter that exchanges sodium and calcium ions across excitable membranes. Normally, NCX mainly operates in its “forward” mode, harnessing the electrochemical gradient of sodium ions to expel calcium. During membrane depolarization or elevated internal sodium levels, NCX can instead switch the direction of net flux to expel sodium and allow calcium entry. Such “reverse”-mode NCX operation is frequently implicated during pathological or artificially extended periods of depolarization, not during normal activity. We have used fast calcium im

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3

Smith, L., and J. B. Smith. "Activation of adenylyl cyclase downregulates sodium/calcium exchanger of arterial myocytes." American Journal of Physiology-Cell Physiology 269, no. 6 (December 1, 1995): C1379—C1384. http://dx.doi.org/10.1152/ajpcell.1995.269.6.c1379.

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Chronic elevation of adenosine 3',5'-cyclic monophosphate (cAMP) is known to inhibit the proliferation of cultured vascular smooth muscle cells. The present findings show that the activation of adenylyl cyclase with forskolin decreased Na+/Ca2+ exchanger (NCX) mRNA and activity. Fetal bovine serum restored NCX transcript and activity. The changes in NCX transcript preceded the changes in NCX activity. Incubation of low-passage immortalized myocytes with forskolin plus 3-isobutyl-1-methylxanthine (IBMX), which inhibits cAMP phosphodiesterase, decreased NCX mRNA by 60% in 6 h and 80% in 24 h. Af

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4

Chernysh, Olga, Madalina Condrescu, and John P. Reeves. "Sodium-dependent inactivation of sodium/calcium exchange in transfected Chinese hamster ovary cells." American Journal of Physiology-Cell Physiology 295, no. 4 (October 2008): C872—C882. http://dx.doi.org/10.1152/ajpcell.00221.2008.

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High concentrations of cytosolic Na+ ions induce the time-dependent formation of an inactive state of the Na+/Ca2+ exchanger (NCX), a process known as Na+-dependent inactivation. NCX activity was measured as Ca2+ uptake in fura 2-loaded Chinese hamster ovary (CHO) cells expressing the wild-type (WT) NCX or mutants that are hypersensitive (F223E) or resistant (K229Q) to Na+-dependent inactivation. As expected, 1) Na+-dependent inactivation was promoted by high cytosolic Na+ concentration, 2) the F223E mutant was more susceptible than the WT exchanger to inactivation, whereas the K229Q mutant wa

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5

Münch, Götz, Kai Rosport, Christine Baumgartner, Zhongmin Li, Silvia Wagner, Andreas Bültmann, and Martin Ungerer. "Functional alterations after cardiac sodium-calcium exchanger overexpression in heart failure." American Journal of Physiology-Heart and Circulatory Physiology 291, no. 2 (August 2006): H488—H495. http://dx.doi.org/10.1152/ajpheart.01324.2005.

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The sodium-calcium exchanger (NCX) is discussed as one of the key proteins involved in heart failure. However, the causal role and the extent to which NCX contributes to contractile dysfunction during heart failure are poorly understood. NCX overexpression was induced by infection with an adenovirus coding for NCX, which coexpressed green fluorescence protein (GFP) (AdNCX) by ex vivo gene transfer to nonfailing and failing rabbit cardiomyocytes. Myocardial gene transfer in rabbits in vivo was achieved by adenoviral delivery via aortic cross-clamping. Peak cell shortening of cardiomyocytes was

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6

Torrente, Angelo G., Rui Zhang, Audrey Zaini, Jorge F. Giani, Jeanney Kang, Scott T. Lamp, Kenneth D. Philipson, and Joshua I. Goldhaber. "Burst pacemaker activity of the sinoatrial node in sodium–calcium exchanger knockout mice." Proceedings of the National Academy of Sciences 112, no. 31 (July 20, 2015): 9769–74. http://dx.doi.org/10.1073/pnas.1505670112.

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In sinoatrial node (SAN) cells, electrogenic sodium–calcium exchange (NCX) is the dominant calcium (Ca) efflux mechanism. However, the role of NCX in the generation of SAN automaticity is controversial. To investigate the contribution of NCX to pacemaking in the SAN, we performed optical voltage mapping and high-speed 2D laser scanning confocal microscopy (LSCM) of Ca dynamics in an ex vivo intact SAN/atrial tissue preparation from atrial-specific NCX knockout (KO) mice. These mice lack P waves on electrocardiograms, and isolated NCX KO SAN cells are quiescent. Voltage mapping revealed disorga

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7

de Ruijter, Wouter, Ger J. M. Stienen, Jan van Klarenbosch, and Jacob J. de Lange. "Negative and Positive Inotropic Effects of Propofol via L-type Calcium Channels and the Sodium-Calcium Exchanger in Rat Cardiac Trabeculae." Anesthesiology 97, no. 5 (November 1, 2002): 1146–55. http://dx.doi.org/10.1097/00000542-200211000-00019.

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Background Conflicting opinions are present in the literature regarding the origin of the negative inotropic effect of propofol on the myocardium. This study aims to resolve these discrepancies by investigating the inotropic effects of propofol the L-type calcium channels and the sodium-calcium exchanger (NCX). Methods The effect of 20 microg/ml propofol on force development was determined in rat cardiac trabeculae at different pacing frequencies and different extracellular calcium concentrations. Postrest potentiation, sodium withdrawal during quiescence, and the NCX inhibitor KB-R7943 were u

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8

Padín, Juan-Fernando, José-Carlos Fernández-Morales, Román Olivares, Stefan Vestring, Juan-Alberto Arranz-Tagarro, Enrique Calvo-Gallardo, Ricardo de Pascual, Luís Gandía, and Antonio G. García. "Plasmalemmal sodium-calcium exchanger shapes the calcium and exocytotic signals of chromaffin cells at physiological temperature." American Journal of Physiology-Cell Physiology 305, no. 2 (July 15, 2013): C160—C172. http://dx.doi.org/10.1152/ajpcell.00016.2013.

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The activity of the plasmalemmal Na+/Ca2+ exchanger (NCX) is highly sensitive to temperature. We took advantage of this fact to explore here the effects of the NCX blocker KB-R7943 (KBR) at 22 and 37°C on the kinetics of Ca2+ currents ( ICa), cytosolic Ca2+ ([Ca2+]c) transients, and catecholamine release from bovine chromaffin cells (BCCs) stimulated with high K+, caffeine, or histamine. At 22°C, the effects of KBR on those parameters were meager or nil. However, at 37°C whereby the NCX is moving Ca2+ at a rate fivefold higher than at 22°C, various of the effects of KBR were pronounced, namely

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9

Haug-Collet, K., B. Pearson, R. Webel, R. T. Szerencsei, R. J. Winkfein, P. P. M. Schnetkamp, and N. J. Colley. "Cloning and Characterization of a Potassium-Dependent Sodium/Calcium Exchanger in Drosophila." Journal of Cell Biology 147, no. 3 (November 1, 1999): 659–70. http://dx.doi.org/10.1083/jcb.147.3.659.

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Sodium/calcium(-potassium) exchangers (NCX and NCKX) are critical for the rapid extrusion of calcium, which follows the stimulation of a variety of excitable cells. To further understand the mechanisms of calcium regulation in signaling, we have cloned a Drosophila sodium/calcium-potassium exchanger, Nckx30C. The overall deduced protein topology for NCKX30C is similar to that of mammalian NCKX, having five membrane-spanning domains in the NH2 terminus separated from six at the COOH-terminal end by a large intracellular loop. We show that NCKX30C functions as a potassium-dependent sodium/calciu

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10

Li, Sen, Anant Chopra, Wendy Keung, Camie W. Y. Chan, Kevin D. Costa, Chi-Wing Kong, Roger J. Hajjar, Christopher S. Chen, and Ronald A. Li. "Sarco/endoplasmic reticulum Ca2+-ATPase is a more effective calcium remover than sodium-calcium exchanger in human embryonic stem cell-derived cardiomyocytes." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 5 (November 1, 2019): H1105—H1115. http://dx.doi.org/10.1152/ajpheart.00540.2018.

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Human pluripotent stem cell (hPSCs)-derived ventricular (V) cardiomyocytes (CMs) display immature Ca2+–handing properties with smaller transient amplitudes and slower kinetics due to such differences in crucial Ca2+-handling proteins as the poor sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump but robust Na+-Ca2+ exchanger (NCX) activities in human embryonic stem cell (ESC)-derived VCMs compared with adult. Despite their fundamental importance in excitation-contraction coupling, the relative contribution of SERCA and NCX to Ca2+-handling of hPSC-VCMs remains unexplored. We systematically a

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11

Linask, Kersti K., Ming-Da Han, Michael Artman, and Cheryl A. Ludwig. "Sodium-calcium exchanger (NCX-1) and calcium modulation: NCX protein expression patterns and regulation of early heart development." Developmental Dynamics 221, no. 3 (2001): 249–64. http://dx.doi.org/10.1002/dvdy.1131.

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12

Loffing, Johannes, Dominique Loffing-Cueni, Victor Valderrabano, Lea Kläusli, Steven C. Hebert, Bernard C. Rossier, Joost G. J. Hoenderop, René J. M. Bindels, and Brigitte Kaissling. "Distribution of transcellular calcium and sodium transport pathways along mouse distal nephron." American Journal of Physiology-Renal Physiology 281, no. 6 (December 1, 2001): F1021—F1027. http://dx.doi.org/10.1152/ajprenal.0085.2001.

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First published August 15, 2001; 10.1152/ajprenal. 00085.2001.—The organization of Na+ and Ca2+ transport pathways along the mouse distal nephron is incompletely known. We revealed by immunohistochemistry a set of Ca2+ and Na+transport proteins along the mouse distal convolution. The thiazide-sensitive Na+-Cl− cotransporter (NCC) characterized the distal convoluted tubule (DCT). The amiloride-sensitive epithelial Na+ channel (ENaC) colocalized with NCC in late DCT (DCT2) and extended to the downstream connecting tubule (CNT) and collecting duct (CD). In early DCT (DCT1), the basolateral Ca2+-e

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13

Jha, Brajesh Kumar, and Amrita Jha. "Two dimensional finite element estimation of calcium ions in presence fo NCX and Buffers in Astrocytes." Boletim da Sociedade Paranaense de Matemática 36, no. 1 (January 1, 2018): 151. http://dx.doi.org/10.5269/bspm.v36i1.29137.

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Sodium calcium exchanger (NCX) plays effective role in signal transduction in most of the nerve cells like neuron, astrocytes. Sodium ion affects the cytosolic calcium concentration label in Astrocytes via various channels. This affects the movement of the nerve impulse from one cell to other cell. In this paper two dimensional model is developedin the form of diffusion equation to study the effect of NCX in presence and negligence of buffer in Astrocytes. Finite element method is employed to solve the problem and simulated in Matlab to estimate the affect of various parameter like flux, diffu

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14

Shiraga, Masamichi, Yoshiaki Tomiyama, Shigenori Honda, Hidenori Suzuki, Satoru Kosugi, Seiji Tadokoro, Yuzuru Kanakura, Kenjiro Tanoue, Yoshiyuki Kurata та Yuji Matsuzawa. "Involvement of Na+/Ca2+ Exchanger in Inside-Out Signaling Through the Platelet Integrin IIbβ3". Blood 92, № 10 (15 листопада 1998): 3710–20. http://dx.doi.org/10.1182/blood.v92.10.3710.

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Abstract The platelet integrin IIbβ3 has become a new target for the treatment of pathological thrombosis. It becomes apparent that the affinity of IIbβ3 for its ligands is dynamically regulated by inside-out signaling. However, the components that couple diverse intracellular signals to the cytoplasmic domains of IIbβ3 remain obscure. Employing a chymotrypsin-induced IIbβ3 activation model, we previously proposed the hypothesis that Na+/Ca2 +exchanger (NCX) may be involved in inside-out signaling (Shiraga et al:Blood 88:2594, 1996). In the present study, employing two unrelated Na+/Ca2+ e

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15

Shiraga, Masamichi, Yoshiaki Tomiyama, Shigenori Honda, Hidenori Suzuki, Satoru Kosugi, Seiji Tadokoro, Yuzuru Kanakura, Kenjiro Tanoue, Yoshiyuki Kurata та Yuji Matsuzawa. "Involvement of Na+/Ca2+ Exchanger in Inside-Out Signaling Through the Platelet Integrin IIbβ3". Blood 92, № 10 (15 листопада 1998): 3710–20. http://dx.doi.org/10.1182/blood.v92.10.3710.422k13_3710_3720.

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The platelet integrin IIbβ3 has become a new target for the treatment of pathological thrombosis. It becomes apparent that the affinity of IIbβ3 for its ligands is dynamically regulated by inside-out signaling. However, the components that couple diverse intracellular signals to the cytoplasmic domains of IIbβ3 remain obscure. Employing a chymotrypsin-induced IIbβ3 activation model, we previously proposed the hypothesis that Na+/Ca2 +exchanger (NCX) may be involved in inside-out signaling (Shiraga et al:Blood 88:2594, 1996). In the present study, employing two unrelated Na+/Ca2+ exchange i

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16

Galli, Gina L. J., Edwin W. Taylor, and Holly A. Shiels. "Calcium flux in turtle ventricular myocytes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 6 (December 2006): R1781—R1789. http://dx.doi.org/10.1152/ajpregu.00421.2006.

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The relative contribution of the sarcoplasmic reticulum (SR), the L-type Ca2+ channel and the Na+/Ca2+ exchanger (NCX) were assessed in turtle ventricular myocytes using epifluorescent microscopy and electrophysiology. Confocal microscopy images of turtle myocytes revealed spindle-shaped cells, which lacked T-tubules and had a large surface area-to-volume ratio. Myocytes loaded with the fluorescent Ca2+-sensitive dye Fura-2 elicited Ca2+ transients, which were insensitive to ryanodine and thapsigargin, indicating the SR plays a small role in the regulation of contraction and relaxation in the

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17

Polo-Parada, Luis, and Amol A. Modgi. "Differences in Expression and Function in the Atrium versus Ventricle of the Sodium-Calcium Exchanger in the Embryonic Chicken Heart." ISRN Physiology 2013 (September 1, 2013): 1–12. http://dx.doi.org/10.1155/2013/921527.

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Heart function is well known to be dependent on intrinsic electrical activity. This electrical activity is primarily mediated by a combination of interactions among various ionic channels and transporters. In this study, we demonstrate that the Na+-Ca2+ exchanger (NCX) is equally present in both atrial and ventricular cells at early stages of development (st. 13). However, ventricular cells exhibit an increase in NCX messenger ribonucleic acid (mRNA) levels during later stages of development, while levels in atrial cells remain constant. We demonstrate that the current density of the NCX incre

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18

Pittner, János, Kristie Rhinehart, and Thomas L. Pallone. "Ouabain modulation of endothelial calcium signaling in descending vasa recta." American Journal of Physiology-Renal Physiology 291, no. 4 (October 2006): F761—F769. http://dx.doi.org/10.1152/ajprenal.00326.2005.

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Using fura 2-loaded vessels, we tested whether ouabain modulates endothelial cytoplasmic calcium concentration ([Ca2+]CYT) in rat descending vasa recta (DVR). Over a broad range between 10−10 and 10−4 M, ouabain elicited biphasic peak and plateau [Ca2+]CYT elevations. Blockade of voltage-gated Ca2+ entry with nifedipine did not affect the response to ouabain mitigating against a role for myo-endothelial gap junctions. Reduction of extracellular Na+ concentration ([Na+]o) or Na+/Ca2+ exchanger (NCX) inhibition with SEA-0400 (10−6 M) elevated [Ca2+]CYT, supporting a role for NCX in the setting o

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Kurnellas, M. P., K. C. Donahue, and S. Elkabes. "Mechanisms of neuronal damage in multiple sclerosis and its animal models: role of calcium pumps and exchangers." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 923–26. http://dx.doi.org/10.1042/bst0350923.

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Multiple sclerosis is an inflammatory, demyelinating and neurodegenerative disorder of the central nervous system. Increasing evidence indicates that neuronal pathology and axonal injury are early hallmarks of multiple sclerosis and are major contributors to progressive and permanent disability. Yet, the mechanisms underlying neuronal dysfunction and damage are not well defined. Elucidation of such mechanisms is of critical importance for the development of therapeutic strategies that will prevent neurodegeneration and confer neuroprotection. PMCA2 (plasma-membrane Ca2+-ATPase 2) and the NCX (

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Giladi, Moshe, Reut Shor, Michal Lisnyansky, and Daniel Khananshvili. "Structure-Functional Basis of Ion Transport in Sodium–Calcium Exchanger (NCX) Proteins." International Journal of Molecular Sciences 17, no. 11 (November 22, 2016): 1949. http://dx.doi.org/10.3390/ijms17111949.

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21

Kang, Beom Seok, Bo Young Choi, A. Ra Kho, Song Hee Lee, Dae Ki Hong, Jeong Hyun Jeong, Dong Hyeon Kang, Min Kyu Park, and Sang Won Suh. "An Inhibitor of the Sodium–Hydrogen Exchanger-1 (NHE-1), Amiloride, Reduced Zinc Accumulation and Hippocampal Neuronal Death after Ischemia." International Journal of Molecular Sciences 21, no. 12 (June 14, 2020): 4232. http://dx.doi.org/10.3390/ijms21124232.

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Acidosis in the brain plays an important role in neuronal injury and is a common feature of several neurological diseases. It has been reported that the sodium–hydrogen exchanger-1 (NHE-1) is a key mediator of acidosis-induced neuronal injury. It modulates the concentration of intra- and extra-cellular sodium and hydrogen ions. During the ischemic state, excessive sodium ions enter neurons and inappropriately activate the sodium–calcium exchanger (NCX). Zinc can also enter neurons through voltage-gated calcium channels and NCX. Here, we tested the hypothesis that zinc enters the intracellular

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Boscia, Francesca, Rosaria Gala, Giuseppe Pignataro, Andrea de Bartolomeis, Maria Cicale, Alberto Ambesi-Impiombato, Gianfranco Di Renzo, and Lucio Annunziato. "Permanent Focal Brain Ischemia Induces Isoform-Dependent Changes in the Pattern of Na+/Ca2+ Exchanger Gene Expression in the Ischemic Core, Periinfarct Area, and Intact Brain Regions." Journal of Cerebral Blood Flow & Metabolism 26, no. 4 (August 17, 2005): 502–17. http://dx.doi.org/10.1038/sj.jcbfm.9600207.

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Dysregulation of sodium [Na+]i and calcium [Ca2+]i homeostasis plays a pivotal role in the pathophysiology of cerebral ischemia. Three gene products of the sodium–calcium exchanger family NCX1, NCX2, and NCX3 couple, in a bidirectional way, the movement of these ions across the cell membrane during cerebral ischemia. Each isoform displays a selective distribution in the rat brain. To determine whether NCX gene expression can be regulated after cerebral ischemia, we used NCX isoform-specific antisense radiolabeled probes to analyze, by radioactive in situ hybridization histochemistry, the patte

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Roberts, Diane E., Archibald McNicol, and Ratna Bose. "Mechanism of Collagen Activation in Human Platelets." Journal of Biological Chemistry 279, no. 19 (February 23, 2004): 19421–30. http://dx.doi.org/10.1074/jbc.m308864200.

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The mechanism of collagen-induced human platelet activation was examined using Ca2+, Na+, and the pH-sensitive fluorescent dyes calcium green/fura red, sodium-binding benzofuran isophthalate, and 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Administration of a moderate dose of collagen (10 μg/ml) to human platelets resulted in an increase in [Ca2+]iand platelet aggregation. The majority of this increase in [Ca2+]iresulted from the influx of calcium from the extracellular milieu via the Na+/Ca2+exchanger (NCX) functioning in the reverse mode and was reduced in a dose-dependent manner by t

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Geramipour, Amir, Zsófia Kohajda, Claudia Corici, János Prorok, Zsolt Szakonyi, Kinga Oravecz, Zoltán Márton, et al. "The investigation of the cellular electrophysiological and antiarrhythmic effects of a novel selective sodium–calcium exchanger inhibitor, GYKB-6635, in canine and guinea-pig hearts." Canadian Journal of Physiology and Pharmacology 94, no. 10 (October 2016): 1090–101. http://dx.doi.org/10.1139/cjpp-2015-0566.

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The sodium–calcium exchanger (NCX) is considered as the major transmembrane transport mechanism that controls Ca2+ homeostasis. Its contribution to the cardiac repolarization has not yet been directly studied due to lack of specific inhibitors, so that an urgent need for more selective compounds. In this study, the electrophysiological effects of GYKB-6635, a novel NCX inhibitor, on the NCX, L-type calcium, and main repolarizing potassium currents as well as action potential (AP) parameters were investigated. Ion currents and AP recordings were investigated by applying the whole-cell patch cla

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Biner, Helena Lagger, Marie-Pierre Arpin-Bott, Johannes Loffing, Xiaoyan Wang, Mark Knepper, Steve C. Hebert, and Brigitte Kaissling. "Human Cortical Distal Nephron: Distribution of Electrolyte and Water Transport Pathways." Journal of the American Society of Nephrology 13, no. 4 (April 2002): 836–47. http://dx.doi.org/10.1681/asn.v134836.

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ABSTRACT. The exact distributions of the different salt transport systems along the human cortical distal nephron are unknown. Immunohistochemistry was performed on serial cryostat sections of healthy parts of tumor nephrectomized human kidneys to study the distributions in the distal convolution of the thiazide-sensitive Na-Cl cotransporter (NCC), the β subunit of the amiloride-sensitive epithelial Na channel (ENaC), the vasopressin-sensitive water channel aquaporin 2 (AQP2), and aquaporin 3 (AQP3), the H+ ATPase, the Na-Ca exchanger (NCX), plasma membrane calcium-ATPase, and calbindin-D28k (

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Lowie, Bobbi-Jo, Xuan-Yu Wang, Elizabeth J. White, and Jan D. Huizinga. "On the origin of rhythmic calcium transients in the ICC-MP of the mouse small intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 5 (November 2011): G835—G845. http://dx.doi.org/10.1152/ajpgi.00077.2011.

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Interstitial cells of Cajal associated with the myenteric plexus (ICC-MP) are pacemaker cells of the small intestine, producing the characteristic omnipresent electrical slow waves, which orchestrate peristaltic motor activity and are associated with rhythmic intracellular calcium oscillations. Our objective was to elucidate the origins of the calcium transients. We hypothesized that calcium oscillations in the ICC-MP are primarily regulated by the sarcoplasmic reticulum (SR) calcium release system. With the use of calcium imaging, study of the effect of T-type calcium channel blocker mibefrad

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Saini, Harjot K., and Naranjan S. Dhalla. "Sarcolemmal cation channels and exchangers modify the increase in intracellular calcium in cardiomyocytes on inhibiting Na+-K+-ATPase." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 1 (July 2007): H169—H181. http://dx.doi.org/10.1152/ajpheart.00007.2007.

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Although inhibition of the sarcolemmal (SL) Na+-K+-ATPase is known to cause an increase in the intracellular concentration of Ca2+ ([Ca2+]i) by stimulating the SL Na+/Ca2+ exchanger (NCX), the involvement of other SL sites in inducing this increase in [Ca2+]i is not fully understood. Isolated rat cardiomyocytes were treated with or without different agents that modify Ca2+ movements by affecting various SL sites and were then exposed to ouabain. Ouabain was observed to increase the basal levels of both [Ca2+]i and intracellular Na+ concentration ([Na+]i) as well as to augment the KCl-induced i

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Limbu, Bijay, Kushal Shah, Seth H. Weinberg, and Makarand Deo. "Role of Cytosolic Calcium Diffusion in Murine Cardiac Purkinje Cells." Clinical Medicine Insights: Cardiology 10s1 (January 2016): CMC.S39705. http://dx.doi.org/10.4137/cmc.s39705.

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Cardiac Purkinje cells (PCs) are morphologically and electrophysiologically different from ventricular myocytes and, importantly, exhibit distinct calcium (Ca2+) homeostasis. Recent studies suggest that PCs are more susceptible to action potential (AP) abnormalities than ventricular myocytes; however, the exact mechanisms are poorly understood. In this study, we utilized a detailed biophysical mathematical model of a murine PC to systematically examine the role of cytosolic Ca2+ diffusion in shaping the AP in PCs. A biphasic spatiotemporal Ca2+ diffusion process, as recorded experimentally, wa

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Giladi, Moshe, Reuben Hiller, Joel A. Hirsch, and Daniel Khananshvili. "Population Shift Underlies Ca2+-induced Regulatory Transitions in the Sodium-Calcium Exchanger (NCX)." Journal of Biological Chemistry 288, no. 32 (June 24, 2013): 23141–49. http://dx.doi.org/10.1074/jbc.m113.471698.

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Duman, Joseph G., Liangyi Chen, and Bertil Hille. "Calcium Transport Mechanisms of PC12 Cells." Journal of General Physiology 131, no. 4 (March 17, 2008): 307–23. http://dx.doi.org/10.1085/jgp.200709915.

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Many studies of Ca2+ signaling use PC12 cells, yet the balance of Ca2+ clearance mechanisms in these cells is unknown. We used pharmacological inhibition of Ca2+ transporters to characterize Ca2+ clearance after depolarizations in both undifferentiated and nerve growth factor-differentiated PC12 cells. Sarco-endoplasmic reticulum Ca2+ ATPase (SERCA), plasma membrane Ca2+ ATPase (PMCA), and Na+/Ca2+ exchanger (NCX) account for almost all Ca2+ clearance in both cell states, with NCX and PMCA making the greatest contributions. Any contribution of mitochondrial uniporters is small. The ATP pool in

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Oceandy, D., P. J. Stanley, E. J. Cartwright, and L. Neyses. "The regulatory function of plasma-membrane Ca2+-ATPase (PMCA) in the heart." Biochemical Society Transactions 35, no. 5 (October 25, 2007): 927–30. http://dx.doi.org/10.1042/bst0350927.

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The PMCA (plasma-membrane Ca2+-ATPase) is a ubiquitously expressed calcium-extruding enzymatic pump important in the control of intracellular calcium concentration. Unlike in non-excitable cells, where PMCA is the only system for calcium extrusion, in excitable cells, such as cardiomyocytes, PMCA has been shown to play only a minor role in calcium homoeostasis compared with the NCX (sodium/calcium exchanger), another system of calcium extrusion. However, increasing evidence points to an important role for PMCA in signal transduction; of particular interest in cardiac physiology is the modulati

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Ibáñez, Ignacio, David Bartolomé-Martín, Dolores Piniella, Cecilio Giménez, and Francisco Zafra. "Activity dependent internalization of the glutamate transporter GLT-1 requires calcium entry through the NCX sodium/calcium exchanger." Neurochemistry International 123 (February 2019): 125–32. http://dx.doi.org/10.1016/j.neuint.2018.03.012.

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Shlosman, Irina, Fabrizio Marinelli, José D. Faraldo-Gómez, and Joseph A. Mindell. "The prokaryotic Na+/Ca2+ exchanger NCX_Mj transports Na+ and Ca2+ in a 3:1 stoichiometry." Journal of General Physiology 150, no. 1 (December 13, 2017): 51–65. http://dx.doi.org/10.1085/jgp.201711897.

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Intracellular Ca2+ signals control a wide array of cellular processes. These signals require spatial and temporal regulation of the intracellular Ca2+ concentration, which is achieved in part by a class of ubiquitous membrane proteins known as sodium–calcium exchangers (NCXs). NCXs are secondary-active antiporters that power the translocation of Ca2+ across the cell membrane by coupling it to the flux of Na+ in the opposite direction, down an electrochemical gradient. Na+ and Ca2+ are translocated in separate steps of the antiport cycle, each of which is thought to entail a mechanism whereby i

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Wan, Qun-Fang, Everett Nixon, and Ruth Heidelberger. "Regulation of presynaptic calcium in a mammalian synaptic terminal." Journal of Neurophysiology 108, no. 11 (December 1, 2012): 3059–67. http://dx.doi.org/10.1152/jn.00213.2012.

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Ca2+ signaling in synaptic terminals plays a critical role in neurotransmitter release and short-term synaptic plasticity. In the present study, we examined the role of synaptic Ca2+ handling mechanisms in the synaptic terminals of mammalian rod bipolar cells, neurons that play a pivotal role in the high-sensitivity vision pathway. We found that mitochondria sequester Ca2+ under conditions of high Ca2+ load, maintaining intraterminal Ca2+ near resting levels. Indeed, the effect of the mitochondria was so powerful that the ability to clamp intraterminal Ca2+ with a somatically positioned whole

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Shenoy, Rajesh, Irwin Klein, and Kaie Ojamaa. "Differential regulation of SR calcium transporters by thyroid hormone in rat atria and ventricles." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 4 (October 1, 2001): H1690—H1696. http://dx.doi.org/10.1152/ajpheart.2001.281.4.h1690.

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Thyroid hormone exerts positive inotropic effects on the heart mediated in part by its regulation of calcium transporter proteins, including sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2), phospholamban (PLB), and Na+/Ca2+ exchanger (NCX). To further understand the potential cardiac chamber-specific effects of thyroid hormone action, we compared the triiodo-l-thyronine (T3) responsiveness of calcium transporter proteins in atrial versus ventricular tissues. Rats were rendered hypothyroid by ingestion of propylthiouracil, and a subgroup of animals was treated with T3 for 7 days (7 μg/day by

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Zhang, Zijuan, Shuguang Sun, Caixia Du, Wei Li, Juan Zhang, Yanqin Zhu, Peilin Liu, and Ying Xing. "Effects of Leptin on Na+/Ca2+ Exchanger in PC12 Cells." Cellular Physiology and Biochemistry 40, no. 6 (2016): 1529–37. http://dx.doi.org/10.1159/000453203.

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Background/Aims: Alzheimer's disease (AD) is known to be related to alterations in neuronal intracellular calcium activity ([Ca2+]i). The present study revealed the distinct role of leptin in Na+/Ca2+-exchanger activity. Methods: [Ca2+]i was determined utilizing Fura-2 fluorescence. The activity of NCX was measured by removal of extracellular Na+ in the presence of external Ca2+. Na+/Ca2+-exchanger activity was further quantified from whole cell currents following removal of extracellular Na+. Na+/Ca2+-exchanger isoform NCX1 transcript levels and protein abundance were quantified by RT-PCR and

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Newton, Jamila, Luli Rebecca Akinfiresoye, and Prosper N’Gouemo. "Inhibition of the Sodium Calcium Exchanger Suppresses Alcohol Withdrawal-Induced Seizure Susceptibility." Brain Sciences 11, no. 2 (February 23, 2021): 279. http://dx.doi.org/10.3390/brainsci11020279.

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Calcium influx plays important roles in the pathophysiology of seizures, including acoustically evoked alcohol withdrawal-induced seizures (AWSs). One Ca2+ influx route of interest is the Na+/Ca2+ exchanger (NCX) that, when operating in its reverse mode (NCXrev) activity, can facilitate Ca2+ entry into neurons, possibly increasing neuronal excitability that leads to enhanced seizure susceptibility. Here, we probed the involvement of NCXrev activity on AWS susceptibility by quantifying the effects of SN-6 and KB-R7943, potent blockers of isoform type 1 (NCX1rev) and 3 (NCX3rev), respectively. M

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Romero, Jose R., Dennis A. Ricupero, Alicia Rivera, Ronald H. Goldstein, and Paul R. Conlin. "Activation of Na + /Ca 2+ Exchanger in Kinin B 1 Receptor-Stimulated Human Fibroblast Is Associated with Collagen Production." Hypertension 36, suppl_1 (October 2000): 710–20. http://dx.doi.org/10.1161/hyp.36.suppl_1.710.

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P148 The arterial wall in hypertension is characterized by thickening of the media, in part due to increased deposition of connective tissue. Autocrine and paracrine factors may participate in this process; including products of the kallikrein-kinin system. We evaluated early signal transduction events and effects on collagen formation in B 1 -stimulated human myofibroblast cells (IMR-90). We measured cytosolic calcium (Ca cyt ) levels in cells loaded with FURA-2AM. Gene expression of connective tissue growth factor (CTGF) and α1(I) collagen was determined by estimating mRNA levels using North

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Wheatly, M., Z. Zhang, J. Weil, J. Rogers, and L. Stiner. "Novel subcellular and molecular tools to study Ca(2+) transport mechanisms during the elusive moulting stages of crustaceans: flow cytometry and polyclonal antibodies." Journal of Experimental Biology 204, no. 5 (March 1, 2001): 959–66. http://dx.doi.org/10.1242/jeb.204.5.959.

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Our understanding of calcium homeostasis during the crustacean moulting cycle derives from research on intermoult animals that has been extrapolated to other stages. In terms of transepithelial Ca(2+) flux, the more interesting stages are those surrounding ecdysis since crustaceans experience a sizeable negative calcium balance in immediate premoult and a significant positive calcium balance in immediate postmoult. These stages are elusive in the sense that larger species such as lobsters are rarely captured at this time, and smaller species such as blue crabs and crayfish are seldom synchroni

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Liu, Ai-Hua, Yi-Min Bao, Xing-Yu Wang, and Zhi-Xiong Zhang. "Cardio-Protection by Ginkgo biloba Extract 50 in Rats with Acute Myocardial Infarction is Related to Na+–Ca2+ Exchanger." American Journal of Chinese Medicine 41, no. 04 (January 2013): 789–800. http://dx.doi.org/10.1142/s0192415x13500535.

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Ginkgo biloba has been used for medical purposes for centuries in traditional Chinese medicine. Ginkgo biloba extract 50 (GBE50) is a new standardized GBE product that matches the standardized German product as EGb761. This paper is aimed at studying the cardio-protection effects of GBE50 Salvia miltiorrhiza on myocardial function, area at risk, myocardial ultra-structure, and expression of calcium handling proteins in rat ischemic myocardium. Myocardium ischemia was induced by the left anterior descending (LAD) coronary artery occlusion and myocardial function was recorded by a transducer adv

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Plank, David M., Atsuko Yatani, Honda Ritsu, Sandra Witt, Betty Glascock, M. Jane Lalli, Muthu Periasamy та ін. "Calcium dynamics in the failing heart: restoration by β-adrenergic receptor blockade". American Journal of Physiology-Heart and Circulatory Physiology 285, № 1 (липень 2003): H305—H315. http://dx.doi.org/10.1152/ajpheart.00425.2002.

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Changes in calcium (Ca2+) regulation contribute to loss of contractile function in dilated cardiomyopathy. Clinical treatment using β-adrenergic receptor antagonists (β-blockers) slows deterioration of cardiac function in end-stage heart failure patients; however, the effects of β-blocker treatment on Ca2+ dynamics in the failing heart are unknown. To address this issue, tropomodulin-overexpressing transgenic (TOT) mice, which suffer from dilated cardiomyopathy, were treated with a nonselective β-receptor blocker (5 mg · kg-1 · day-1 propranolol) for 2 wk. Ca2+ dynamics in isolated cardiomyocy

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Estacion, M., B. P. S. Vohra, S. Liu, J. Hoeijmakers, C. G. Faber, I. S. J. Merkies, G. Lauria, J. A. Black, and S. G. Waxman. "Ca2+ toxicity due to reverse Na+/Ca2+ exchange contributes to degeneration of neurites of DRG neurons induced by a neuropathy-associated Nav1.7 mutation." Journal of Neurophysiology 114, no. 3 (September 2015): 1554–64. http://dx.doi.org/10.1152/jn.00195.2015.

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Gain-of-function missense mutations in voltage-gated sodium channel Nav1.7 have been linked to small-fiber neuropathy, which is characterized by burning pain, dysautonomia and a loss of intraepidermal nerve fibers. However, the mechanistic cascades linking Nav1.7 mutations to axonal degeneration are incompletely understood. The G856D mutation in Nav1.7 produces robust changes in channel biophysical properties, including hyperpolarized activation, depolarized inactivation, and enhanced ramp and persistent currents, which contribute to the hyperexcitability exhibited by neurons containing Nav1.8

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Moonga, Baljit S., Robert Davidson, Li Sun, Olugbenga A. Adebanjo, James Moser, Mohammad Abedin, Neeha Zaidi, Christopher L. H. Huang, and Mone Zaidi. "Identification and Characterization of a Sodium/Calcium Exchanger, NCX-1, in Osteoclasts and Its Role in Bone Resorption." Biochemical and Biophysical Research Communications 283, no. 4 (May 2001): 770–75. http://dx.doi.org/10.1006/bbrc.2001.4870.

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Li, Jing-Ping, Hiroshi Kajiya, Fujio Okamoto, Akihiro Nakao, Takahiro Iwamoto, and Koji Okabe. "Three Na+/Ca2+Exchanger (NCX) Variants Are Expressed in Mouse Osteoclasts and Mediate Calcium Transport during Bone Resorption." Endocrinology 148, no. 5 (May 2007): 2116–25. http://dx.doi.org/10.1210/en.2006-1321.

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Huang, Jingbo, Leif Hove-Madsen, and Glen F. Tibbits. "SR Ca2+ refilling upon depletion and SR Ca2+ uptake rates during development in rabbit ventricular myocytes." American Journal of Physiology-Cell Physiology 293, no. 6 (December 2007): C1906—C1915. http://dx.doi.org/10.1152/ajpcell.00241.2007.

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While it has been reported that a sparse sarcoplasmic reticulum (SR) and a low SR Ca2+ pump density exist at birth, we and others have recently shown that significant amounts of Ca2+ are stored in the neonatal rabbit heart SR. Here we try to determine developmental changes in SR Ca2+ loading mechanisms and Ca2+ pump efficacy in rabbit ventricular myocytes. SR Ca2+ loading (loadSR) and k0.5 (Ca2+ concentration at half-maximal SR Ca2+ uptake) were higher and lower, respectively, in younger age groups. Inhibition of the L-type calcium current ( ICa) with 15 μM nifedipine dramatically reduced load

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TEWARI, SHIVENDRA G., and K. R. PARDASANI. "MODELING EFFECT OF SODIUM PUMP ON CALCIUM OSCILLATIONS IN NEURON CELLS." Journal of Multiscale Modelling 04, no. 03 (September 2012): 1250010. http://dx.doi.org/10.1142/s1756973712500102.

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Calcium plays a significant role in a number of processes like muscle contraction, gene expression, synaptic plasticity, signal transduction etc. but the significance of calcium oscillation is not yet completely understood in most of the cell types. A number of investigators have reported the oscillatory behavior of calcium due to intracellular concentration of inositol 1,4,5-trisphosphate (IP3). In this paper, an attempt has been made to study the oscillations induced in calcium due to dynamically changing membrane potential with special relevance to sodium pump. A mathematical model is devel

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Armoundas, Antonis A., Jochen Rose, Rajesh Aggarwal, Bruno D. Stuyvers, Brian O'Rourke, David A. Kass, Eduardo Marbán, Stephen R. Shorofsky, Gordon F. Tomaselli, and C. William Balke. "Cellular and molecular determinants of altered Ca2+ handling in the failing rabbit heart: primary defects in SR Ca2+ uptake and release mechanisms." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 3 (March 2007): H1607—H1618. http://dx.doi.org/10.1152/ajpheart.00525.2006.

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Myocytes from the failing myocardium exhibit depressed and prolonged intracellular Ca2+ concentration ([Ca2+]i) transients that are, in part, responsible for contractile dysfunction and unstable repolarization. To better understand the molecular basis of the aberrant Ca2+ handling in heart failure (HF), we studied the rabbit pacing tachycardia HF model. Induction of HF was associated with action potential (AP) duration prolongation that was especially pronounced at low stimulation frequencies. L-type calcium channel current ( ICa,L) density (−0.964 ± 0.172 vs. −0.745 ± 0.128 pA/pF at +10 mV) a

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Moon, H. S., E. Choi, and C. Hyun. "The Cardiac Sodium-Calcium Exchanger Gene (NCX-1) is a Potential Canine Cardiac Biomarker of Chronic Mitral Valvular Insufficiency." Journal of Veterinary Internal Medicine 22, no. 6 (November 2008): 1360–65. http://dx.doi.org/10.1111/j.1939-1676.2008.0209.x.

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JHA, AMRITA, NEERU ADLAKHA, and BRAJESH KUMAR JHA. "FINITE ELEMENT MODEL TO STUDY EFFECT OF Na+−Ca2+ EXCHANGERS AND SOURCE GEOMETRY ON CALCIUM DYNAMICS IN A NEURON CELL." Journal of Mechanics in Medicine and Biology 16, no. 02 (March 2016): 1650018. http://dx.doi.org/10.1142/s0219519416500184.

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The study of calcium diffusion in neuron cells has gained interest among research workers during the last two decades, due to its wide variety of roles in human body like muscle contraction, secretion, metabolism, signal transduction etc. Na[Formula: see text] is the first ion that comes in the hierarchy of ions affecting cytosolic Ca[Formula: see text] concentration. This Na[Formula: see text] ion helps in intracellular Ca[Formula: see text] regulation in cytosol via Na[Formula: see text]/Ca[Formula: see text] exchanger protein (NCX protein). Most of the theoretical investigations on calcium

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Pallafacchina, Giorgia, Sofia Zanin, and Rosario Rizzuto. "Recent advances in the molecular mechanism of mitochondrial calcium uptake." F1000Research 7 (November 28, 2018): 1858. http://dx.doi.org/10.12688/f1000research.15723.1.

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In the last few decades, a large body of experimental evidence has highlighted the complex role for mitochondria in eukaryotic cells: they are not only the site of aerobic metabolism (thus providing most of the ATP supply for endergonic processes) but also a crucial checkpoint of cell death processes (both necrosis and apoptosis) and autophagy. For this purpose, mitochondria must receive and decode the wide variety of physiological and pathological stimuli impacting on the cell. The “old” notion that mitochondria possess a sophisticated machinery for accumulating and releasing Ca2+, the most c

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