Relevant bibliographies by topics / Sodium/calcium exchanger (NCX)

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Academic literature on the topic 'Sodium/calcium exchanger (NCX)'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "Sodium/calcium exchanger (NCX)"

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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 rapidly in recent years, little is known about these transport systems in cancer cells. This review aims to summarize current knowledge about NCX functions in individual types of cancer cells.
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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 was resistant, and 3) inactivation was enhanced by cytosolic acidification. However, in contrast to expectations from excised patch studies, 1) the WT exchanger was resistant to Na+-dependent inactivation unless cytosolic pH was reduced, 2) reducing cellular phosphatidylinositol-4,5-bisphosphate levels did not induce Na+-dependent inactivation in the WT exchanger, 3) Na+-dependent inactivation did not increase the half-maximal cytosolic Ca2+ concentration for allosteric Ca2+ activation, 4) Na+-dependent inactivation was not reversed by high cytosolic Ca2+ concentrations, and 5) Na+-dependent inactivation was partially, but transiently, reversed by an increase in extracellular Ca2+ concentration. Thus Na+-dependent inactivation of NCX expressed in CHO cells differs in several respects from the inactivation process measured in excised patches. The refractoriness of the WT exchanger to Na+-dependent inactivation suggests that this type of inactivation is unlikely to be a strong regulator of exchange activity under physiological conditions but would probably act to inhibit NCX-mediated Ca2+ influx during ischemia.
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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 imaging, mathematical simulation, and whole cell electrophysiology to study the role of NCX at the parallel fiber-to-Purkinje neuron synapse in the mouse cerebellum. We show that nontraditional, reverse-mode NCX activity boosts the amplitude and duration of parallel fiber calcium transients during short bursts of high-frequency action potentials typical of their behavior in vivo. Simulations, supported by experimental manipulations, showed that accumulation of intracellular sodium drove NCX into reverse mode. This mechanism fueled additional calcium influx into the parallel fibers that promoted synaptic transmission to Purkinje neurons for up to 400 ms after the burst. Thus we provide the first functional demonstration of transient and fast NCX-mediated calcium entry at a major central synapse. This unexpected contribution from reverse-mode NCX appears critical for shaping presynaptic calcium dynamics and transiently boosting synaptic transmission, and is likely to optimize the accuracy of cerebellar information transfer.
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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. After a 6-h lag, forskolin plus IBMX decreased NCX activity almost linearly to 20% of control at 40 h. 1,9-Dideoxyforskolin, which does not activate adenylyl cyclase, had no effect on NCX mRNA or activity. Forskolin plus IBMX decreased the c-Myc transcript, an immediate-early gene whose expression correlates with cell proliferation, but had no effect on plasma membrane Ca(2+)-ATPase transcripts. Removal of forskolin plus IBMX and addition of fetal bovine serum increased NCX and c-Myc transcripts seven- to eightfold in 6 h and restored NCX activity in 24 h. Inhibition of protein or RNA synthesis by cycloheximide or actinomycin D, respectively, prevented the increase in NCX mRNA. In contrast to blocking NCX induction, cycloheximide potentiated c-Myc induction by serum. Transcription factors that regulate myocyte growth may mediate the opposing influences of serum and forskolin on NCX mRNA and activity.
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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 determined photo-optically. Hemodynamic parameters in vivo were determined by echocardiography (fractional shortening) and tip catheter [maximal first derivative of left ventricular (LV) pressure (dP/d tmax); maximal negative derivative of LV pressure (−dP/d tmax)]. Peak cell shortening was depressed after NCX gene delivery in isolated nonfailing and in failing cardiomyocytes. In nonfailing rabbits in vivo, basal systolic contractility (fractional shortening and dP/d tmax) and maximum rate of LV relaxation (−dP/d tmax) in vivo were largely unaffected after NCX overexpression. However, during heart failure, long-term NCX overexpression over 2 wk significantly improved fractional shortening and dP/d tmax compared with AdGFP-infected rabbits, both without inotropic stimulation and after β-adrenergic stimulation with isoproterenol. −dP/d tmax was also improved after NCX overexpression in the failing rabbits group. These results indicate that short-term effects of NCX overexpression impair contractility of isolated failing and nonfailing rabbit cardiomyocytes. NCX overexpression over 2 wk in vivo does not seem to affect myocardial contractility in nonfailing rabbits. Interestingly, in vivo overexpression of NCX decreased the progression of systolic and diastolic contractile dysfunction and improved β-adrenoceptor-mediated contractile reserve in heart failure in rabbits in vivo.
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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 disorganized and arrhythmic depolarizations within the NCX KO SAN that failed to propagate into the atria. LSCM revealed intermittent bursts of Ca transients. Bursts were accompanied by rising diastolic Ca, culminating in long pauses dominated by Ca waves. The L-type Ca channel agonist BayK8644 reduced the rate of Ca transients and inhibited burst generation in the NCX KO SAN whereas the Ca buffer 1,2-Bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (acetoxymethyl ester) (BAPTA AM) did the opposite. These results suggest that cellular Ca accumulation hinders spontaneous depolarization in the NCX KO SAN, possibly by inhibiting L-type Ca currents. The funny current (If) blocker ivabradine also suppressed NCX KO SAN automaticity. We conclude that pacemaker activity is present in the NCX KO SAN, generated by a mechanism that depends upon If. However, the absence of NCX-mediated depolarization in combination with impaired Ca efflux results in intermittent bursts of pacemaker activity, reminiscent of human sinus node dysfunction and “tachy-brady” syndrome.
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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/calcium exchanger, and is not only expressed in adult neurons as was expected, but is also expressed during ventral nerve cord development in the embryo and in larval imaginal discs. Nckx30C is expressed in a dorsal–ventral pattern in the eye-antennal disc in a pattern that is similar to, but broader than that of wingless, suggesting that large fluxes of calcium may be occurring during imaginal disc development. Nckx30C may not only function in the removal of calcium and maintenance of calcium homeostasis during signaling in the adult, but may also play a critical role in signaling during development.
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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 used to study changes in the activity of the reverse mode of the NCX by propofol. Results The effect of propofol on steady state peak force depended on pacing frequency and calcium concentration. A negative inotropic effect was observed at pacing frequencies greater than 0.5 Hz, but a positive inotropic effect was observed at 0.1 Hz and low calcium, which cannot be explained by an effect on the L-type calcium channel. Propofol enhanced postrest potentiation in a calcium-dependent manner. Sodium withdrawal during quiescence and the use of the specific NCX inhibitor KB-R7943 provided evidence for an enhancement of calcium influx by propofol the reverse mode of the NCX. Conclusions The effects of propofol on the myocardium depend on pacing frequency and calcium concentration. The positive inotropic effect of propofol is associated with increased calcium influx the reverse mode of the NCX. The authors conclude that the net inotropic effect of propofol is the result of its counteracting influence on the functioning of the L-type calcium channel and the NCX.
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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: 1) no effects on ICa; 2) reduction of the [Ca2+]c transient amplitude and slowing down of its rate of clearance; 3) blockade of the K+-elicited quantal release of catecholamine; 4) blockade of burst catecholamine release elicited by K+; 5) no effect on catecholamine release elicited by short K+ pulses (1–2 s) and blockade of the responses produced by longer K+ pulses (3–5 s); and 6) potentiation of secretion elicited by histamine or caffeine. Furthermore, the more selective NCX blocker SEA0400 also potentiated the secretory responses to caffeine. The results suggest that at physiological temperature the NCX substantially contributes to shaping the kinetics of [Ca2+]c transients and the exocytotic responses elicited by Ca2+ entry through Ca2+ channels as well as by Ca2+ release from the endoplasmic reticulum.
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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+-extruding proteins [Na+/Ca2+ exchanger (NCX), plasma membrane Ca2+-ATPase (PCMA)] and the cytoplasmic Ca2+-binding protein calbindin D28K (CB) were found at very low levels, whereas the cytoplasmic Ca2+/Mg2+-binding protein parvalbumin was highly abundant. NCX, PMCA, and CB prevailed in DCT2 and CNT, where we located the apical epithelial Ca2+ channel (ECaC1). Its subcellular localization changed from apical in DCT2 to exclusively cytoplasmic at the end of CNT. NCX and PMCA decreased in parallel with the fading of ECaC1 in the apical membrane. All three of them were undetectable in CD. These findings disclose DCT2 and CNT as major sites for transcellular Ca2+ transport in the mouse distal nephron. Cellular colocalization of Ca2+ and Na+ transport pathways suggests their mutual interactions in transport regulation.
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Dissertations / Theses on the topic "Sodium/calcium exchanger (NCX)"

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Jeffs, Graham J. "The effect of sodium/calcium exchanger 3 (NCX3) knockout on neuronal survival following global cerebral ischaemia in mice." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2007. http://theses.library.uwa.edu.au/adt-WU2008.0063.

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Cerebral ischaemia is a leading cause of disability and death world-wide. The only effective treatments are thrombolytic therapy (plasminogen activator; tPA) and hypothermia (33?C). However, tPA has limited clinical application due to its short therapeutic time window and its specific application in thrombo-embolic stroke. Moderate hypothermia (33?C) is only being used following cardiac arrest in comatose survivors. Hence more treatments are urgently required. The first step in developing new treatments is the identification and characterisation of a potential therapeutic target. Since brain damage following cerebral ischaemia is associated with disturbances in intracellular calcium homeostasis, the sodium-calcium exchanger (NCX) is a potential therapeutic target due to its ability to regulate intracellular calcium. Currently, however there is uncertainty as to whether the plasma membrane NCX has a neuroprotective or neurodamaging role following cerebral ischemia. To address this issue I compared hippocampal neuronal injury in NCX3 knockout mice (Ncx3-/-) and wild-type mice (Ncx3+/+) following global cerebral ischaemia. In order to perform this study I first established a bilateral common carotid occlusion (BCCAO) model of global ischaemia in wild-type C57/BlHsnD mice using controlled ventilation. After trials of several ischaemic time points, 17 minutes was established as the optimum duration of ischaemia to produce selective hippocampal CA1 neuronal loss in the wild-type mice. I then subjected NCX3 knockout and wild-type mice to 17 minutes of ischaemia. Following the 17 minute period of ischaemia, wild-type mice exhibited 80% CA1 neuronal loss and 40% CA2 neuronal loss. In contrast, NCX3 knockout mice displayed > 95% CA1 neuronal loss and 95% CA2 neuronal loss. Following experiments using a 17 minute duration of global ischaemia, a 15 minute duration of ischaemia was also evaluated. Wild-type mice exposed to a 15 minute period of ischaemia, did not exhibit any significant hippocampal neuronal loss. In contrast, NCX3 knockout mice displayed 45% CA1 neuronal loss and 25% CA2 neuronal loss. The results clearly demonstrate that mice deficient for the NCX3 protein are more susceptible to global cerebral ischaemia than wild-type mice. My findings showing a neuroprotective role for NCX3 following ischaemia, suggest that the exchanger has a positive role in maintaining neuronal intracellular calcium homeostasis. When this function is disrupted, neurons are more susceptible to calcium deregulation, with resultant cell death via calcium mediated pathways. Therefore, improving NCX activity following cerebral ischaemia may provide a therapeutic strategy to reduce neuronal death.
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Reilly, Louise. "Palmitoylation of the cardiac sodium-calcium exchanger." Thesis, University of Dundee, 2014. https://discovery.dundee.ac.uk/en/studentTheses/37d8a92d-1536-4a05-85f6-a45f9c41a489.

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Sher, Anna. "Modelling local calcium dynamics and the sodium/calcium exchanger in ventricular myocytes." Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670114.

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Bossuyt, Julie. "Sodium-calcium exchange and caveolins." MU has:, 2002. http://wwwlib.umi.com/cr/mo/fulltext?p3052149.

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Han, C. (Chunlei). "Intracellular calcium stores and sodium-calcium exchanger in cardiac myocytes:experimental and computer simulation study." Doctoral thesis, University of Oulu, 2001. http://urn.fi/urn:isbn:9514265912.

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Abstract Cytosolic Ca2+, [Ca2+]I , has a key role in intracellular signalling during excitation-contraction coupling (E-C coupling) in cardiac myocytes. The sarcoplasmic reticulum (SR) is a main intracellular Ca2+ store and the Na+-Ca2+ exchanger (NaCaX) is a major mechanism to extrude Ca2+ for balancing the Ca2+ influx via L-type Ca2+ channels during excitation. Furthermore, [Ca2+]I also affects the configuration of the action potential (AP). The present study, by combination of animal experiments and computer simulations, investigated the roles of [Ca2+]I, SR and NaCaX in cardiac myocytes, in Ca2+-induced Ca2+ release (CICR) and in modulation of APs. The following were studied: (I) the stretch-induced effects on rat atrium and the role of [Ca2+]I in modulation of AP; (II) the role of the SR in modulation in rat atrium by stretch; (III) the role of NaCaX; (IV) the role of [Ca2+]I in modulation of action potential duration (APD) in myocytes with short and long action potential duration. In isolated rat atrial preparations, the physiological or moderate stretch stimulus caused two- phasic rise of developed contraction, rapid and slow phases, accompanied with slow increments of [Ca2+]I and prolongations of action potentials durations in continuous recordings. In sustained stretch, the APD and [Ca2+]I were all increased significantly when intra-atrial pressure increased from 1 to 3 mmHg. In computer simulations, employing a rat atrial model (RA model), it was found that stretch-activated channels and increased Tn C affinity for Ca2+ alone could not produce the changes in the experiments. Only after both mechanisms applied to model cells, the main experimental findings could be mimicked (I). The prolongation of APD induced by stretch in rat atrial preparations was reversed after depleting the Ca2+ content of the SR by application of the SR functional inhibitors, ryanodine, thapsigargin and caffeine (II). In the computer simulation using modified guinea pig ventricular model, the Ca2+ entry via the reversal of NaCaX was found to be accounting 25% of the total activator Ca2+ for triggering Ca2+ release from the SR during normal excitation. This contribution increases with elevated [Na+]i (III). In a guinea pig ventricular model (GPV model) and a RA model were employed for investigating the regulation of APD by [Ca2+]I-dependent membrane currents. Increased SR Ca2+ content produced an elevated [Ca2+]I in both model cells, leading to prolongation of APD in the RA model but shortening in the GPV model. Increased [Ca2+]I enhances the NaCaX current in the same scale in both models, but inhibits L-type Ca current much more in the GPV model than the RA model (IV). In conclusion, (I) Stretch-induced [Ca2+]I increase prolongs the rat atrial AP by enhancing the NaCaX inward current. Stretch-activated channels (SACs) and increased affinity of TnC for Ca2+ are main general factors responsible for the variety of changes of cardiac muscles induced by stretch. (II) The SR plays a crucial role in the modulation of myocytes by accumulating the additional Ca2+ influx via sarcolemma during stretch. (III) The NaCaX contributes a small part for activator Ca2+ for calcium release from the SR during normal cardiac E-C coupling. However, this contribution is [Na]i-dependent, and in some pathological conditions, it may be a potential factor for cardiac arrhythmogenesis. (IV) Different effects on the NaCaX and L-type channels induced by increased [Ca2+]I leads to the dispersion of the change of APD in myocytes with long and short AP during inotropic interventions that increase the [Ca2+]I.
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Hung, Hsiao-Yu. "Spatial organization of sodium calcium exchanger and caveolin-3 in developing mammalian ventricular cardiomyocytes." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/791.

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In adult cardiomyocytes, the established mechanism of excitation-contraction coupling is calcium-induced calcium release (CICR) mediated by L-type Ca2+ channels (Cav1.2). Briefly, membrane depolarization opens voltage-gated Cav1.2 to allow for the influx of extracellular Ca2+ into the cytosol. This small sarcolemmal (SL) Ca2+ influx is necessary for triggering a larger release of Ca2+ from the intracellular Ca2+ storage site, the sarcoplasmic reticulum (SR), through the SR Ca2+ release channel also known as the ryanodine receptor (RyR). RyR-mediated release of SR Ca2+ effectively raises the cytosolic free Ca2+ concentration, allowing for Ca2+ binding to troponin C on the troponin-tropomysin complex, leading to cross-bridge formation and cell contraction. However, previous functional data suggests an additional CICR modality involving reverse mode Na+-Ca2+ exchanger (NCX) activity also exists in neonate cardiomyocytes. To further our understanding of how CICR changes occur during development, we investigated the spatial arrangement of caveolin-3 (cav-3), the principle structural protein of small membrane invaginations named caveolae, and NCX in developing rabbit ventricular myocytes. Using traditional as well as novel image processing and analysis techniques, both qualitative and quantitative findings firmly establish the highly robust and organized nature of NCX and cav-3 distributions during development. Specifically, our results show that NCX and cav-3 are distributed on the peripheral membrane as discrete clusters and are not highly colocalized throughout development. 3D distance analysis revealed that NCX and cav-3 clusters are organized with a distinct longitudinal and transverse periodicity of 1-1.5 μm and that NCX and cav-3 cluster have a pronounced tendency to be mutually exclusive on the cell periphery. Although these findings do not support the original hypothesis that caveolae is the structuring element for a restricted microdomain facilitating NCX-CICR, our results cannot rule out the existence of such microdomain organized by other anchoring proteins. The developmentally stable distributions of NCX and cav-3 imply that the observed developmental CICR changes are achieved by the spatial re-organization of other protein partners of NCX or non-spatial modifications. In addition, the newly developed image processing and analysis techniques can have wide applicability to the investigations on the spatial distribution of other proteins and cellular structures.
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Modgi, Amol Polo-Parada Luis. "The role of sodium-calcium exchanger in the electrical activity of embryonic chicken heart." Diss., Columbia, Mo. : University of Missouri--Columbia, 2008. http://hdl.handle.net/10355/6671.

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The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file. Title from PDF of title page (University of Missouri--Columbia, viewed on September 25, 2009). Thesis advisor: Dr. Luis Polo Parada. Includes bibliographical references.
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Elliott, Elspeth B. A. "Investigation of factors affecting the sodium/calcium exchanger in a rabbit model of left ventricular dysfunction." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433518.

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Guan, Yinzheng. "Blebbistatin Protects Rodent Myocytes from Death in Primary Culture via Inhibiting the Sodium/ Calcium Exchanger and the L-type Calcium Channel." Master's thesis, Temple University Libraries, 2011. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/150014.

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Physiology
M.S.
Introduction: Cardiac disease is a leading cause of mortabity and morbidity in the developed countries. Cultured cardiac myocytes are widely used for exploring the underlying pathophysiology of cardiac disease. Rodents, especially mice with transgenes or gene ablation, have become popular animal models for heart disease research. However, it has been long recognized that rodent myoyctes die during long-term primary culture, which limits the use of genetically altered myocytes for signaling studies. Blebbistatin (BLB), a myosin II ATPase inhibitor, has been used to protect rodent myocytes. The mechanisms underlying the protective effects of this drug are not clear and are the topics of this study. Materials & methods: Adult rat ventricular myocytes (ARVM) were isolated and cultured with or without BLB (10 µM) for 72 hours in comparison with another protective chemical, BDM (10mM). Myocyte death was evaluated by morphology changes and trypan blue staining. The effects of these two drugs on myocyte contraction, intracellular Ca2+ transient ([Ca2+]i, indo-1,410/480), SR Ca2+ content, L-type calcium and Na+ /Ca2+exchanger currents were studied acutely. Neonatal rat ventricular myocytes (NRVM) were isolated from 1-3 days old neonatal rat hearts and cultured. The effect of BDM (10mM BDM) and BLB (10 µM) in the medium on NRVM growth and hypertrophy induced by norepinephrine (NE, 10µM) were determined. Results: 1. Both BDM and BLB promoted myocyte survival in culture at 72 hours but BLB protected more myocytes (Control: 7.0±1.8% vs. BDM: 61.5±6.4% vs. BLB: 74.0±3.2%); 2. ARVM fractional shortening was reduced by BLB to 1.7±0.4% and by BDM to 0.5±0.1% from the baseline of 6.5±0.7%; 3. Acutely, the amplitude of [Ca2+]i (∆ [Ca2+]i) evaluated with indo-1 AM (F410/F480) was depressed by both BDM (0.04±0.01) and BLB (0.07±0.01) compared to control (0.13±0.01). 4. Diastolic Ca2+ was significantly increased by BLB (0.90±0.06) but not by BDM (0.73±0.06) compared to pre-treat values (0.70±0.05); 5. BLB and BDM significantly reduced the SR Ca2+ content, as indicated by the reduced amplitudes of caffeine-induced Ca2+ transients in BLB- and BDM-treated ARVMs (∆[Ca2+]i in BLB vs. BDM vs. baseline: 0.20±0.03, 0.19±0.04, 0.30±0.03). 6. The mechanisms of the protective effects of BDM and BLB were similar but quantitatively different in that BDM reduced more Ca influx through the L-type Ca2+ channel (ICa-L) than BLB (the reduction in BDM-treated cells vs. BLB-treated cells: 70% vs. 40%) while BLB inhibited more Na+/Ca2+exchanger current (75% inhibition) than BDM (40% reduction); 7. Both BDM and BLB inhibited normal NRVM growth and NE-induced hypertrophy and NFAT translocation in NRVMs. Conclusion: These results suggest both BDM and BLB protect rodent myocytes in culture by preventing cytosolic and SR Ca2+ overload by similar mechanisms: inhibiting NCX and reducing the LTCC. The application of BLB to whole-heart studies and myocyte hypertrophy should be extremely cautioned because BLB does alter myocyte Ca2+ handling.
Temple University--Theses
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Yuan, Jiaqi. "Investigations of macromolecules and small biomolecules by solution NMR: applications to the intracellular loop structure of the sodium-calcium exchanger and metabolite identification methods." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1542630633935356.

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Books on the topic "Sodium/calcium exchanger (NCX)"

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(Editor), Jonathan Lytton, Paul P. M. Schnetkamp (Editor), Larry V. Hryshko (Editor), and M. P. Blaustein (Editor), eds. Cellular and Molecular Physiology of Sodium-Calcium Exchange: Proceedings of the Fourth International Conference (Annals of the New York Academy of Sciences). New York Academy of Sciences, 2002.

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Cellular and Molecular Physiology of Sodium-Calcium Exchange: Proceedings of the Fourth International Conference (Annals of the New York Academy of Sciences, V. 976). New York Academy of Sciences, 2002.

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Andre, Herchuelz, and New York Academy of Sciences, eds. Sodium-calcium exchange and the plasma membrane Ca2+-ATPase in cell function: Fifth international conference. Boston, Mass: Blackwell Pub. on behalf of the New York Academy of Sciences, 2007.

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Herchulez, Mordecai P. Blaustein, Jonathan Lytton, and Kenneth D. Philipson. Sodium-Calcium Exchange and the Plasma Membrane Ca2+-ATPase in Cell Function: Fifth International Conference (Annals of the New York Academy of Sciences). Blackwell Publishing Limited, 2007.

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Book chapters on the topic "Sodium/calcium exchanger (NCX)"

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Wang, Jian, Andrew Lindsley, Tony Creazzo, Srinagesh V. Koushik, and Simon J. Conway. "Role of the Sodium-calcium Exchanger (NCX-1) within Splotch (Sp2h) Myocardial Failure." In Cardiovascular Development and Congenital Malformations, 193–95. Malden, Massachusetts, USA: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch48.

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Roome, Chris J., and Ruth M. Empson. "The Contribution of the Sodium-Calcium Exchanger (NCX) and Plasma Membrane Ca2+ ATPase (PMCA) to Cerebellar Synapse Function." In Advances in Experimental Medicine and Biology, 251–63. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_21.

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Yang, Hyun, Kyung-Chul Choi, Eui-Man Jung, Beum-Soo An, Sang-Hwan Hyun, and Eui-Bae Jeung. "Expression and Regulation of Sodium/Calcium Exchangers, NCX and NCKX, in Reproductive Tissues: Do They Play a Critical Role in Calcium Transport for Reproduction and Development?" In Advances in Experimental Medicine and Biology, 109–21. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_10.

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Hurtado, Cecilia, Thane G. Maddaford, and Grant N. Pierce. "Cardiac Sodium–Calcium Exchanger Expression." In Genes and Cardiovascular Function, 43–56. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4419-7207-1_5.

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Scorziello, Antonella, Claudia Savoia, Agnese Secondo, Francesca Boscia, Maria Josè Sisalli, Alba Esposito, Annalisa Carlucci, et al. "New Insights in Mitochondrial Calcium Handling by Sodium/Calcium Exchanger." In Advances in Experimental Medicine and Biology, 203–9. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_17.

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Yang, Ya-Chi, and Lung-Sen Kao. "Regulation of Sodium-Calcium Exchanger Activity by Creatine Kinase." In Advances in Experimental Medicine and Biology, 163–73. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_14.

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Scorziello, Antonella, Claudia Savoia, Agnese Secondo, Francesca Boscia, Maria Josè Sisalli, Alba Esposito, Annalisa Carlucci, et al. "Erratum To: Chapter 17 New Insights in Mitochondrial Calcium Handling by Sodium/Calcium Exchanger." In Advances in Experimental Medicine and Biology, E1. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_38.

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Rojas, Héctor, Claudia Colina, Magaly Ramos, Gustavo Benaim, Erica Jaffe, Carlo Caputo, and Reinaldo Di Polo. "Sodium-Calcium Exchanger Modulates the L-Glutamate Cai 2+ Signalling in Type-1 Cerebellar Astrocytes." In Advances in Experimental Medicine and Biology, 267–74. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_22.

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Levitsky, Dmitri O., and Masayuki Takahashi. "Interplay of Ca2+ and Mg2+ in Sodium-Calcium Exchanger and in Other Ca2+-Binding Proteins: Magnesium, Watchdog That Blocks Each Turn if Able." In Advances in Experimental Medicine and Biology, 65–78. Boston, MA: Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-4756-6_7.

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Millour, Marie, Laurent Lescaudron, Alexander Kraev, and Dmitri O. Levitsky. "Expression of Sodium-Calcium Exchanger Genes in Heart and Skeletal Muscle Development. Evidence for a Role of Adjacent Cells in Regulation of Transcription and Splicing." In Signal Transduction and Cardiac Hypertrophy, 105–23. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0347-7_9.

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Conference papers on the topic "Sodium/calcium exchanger (NCX)"

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Zheng, Yun-Min, Lin Mei, Ling Dong, and Yong-Xiao Wang. "Genetic Evidence For Essential Role Of Sodium-Calcium Exchanger In Development Of Pulmonary Hypertension." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4750.

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Balasubramaniam, Sona Lakshme, Anilkumar Gopalakrishnapillai, Nicholas J. Petrelli, and Sonali P. Barwe. "Abstract 3931: Sodium-calcium exchanger-1 regulates the epithelial phenotype and is lost in renal cancers." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3931.

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Zou, Yong, Liang Zhao, Gongming Xin, and Lin Cheng. "Effect of Metallic Ion on the Formation of Calcium Carbonate Fouling." In 2010 14th International Heat Transfer Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/ihtc14-22312.

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Calcium carbonate (CaCO3) is the most common fouling adhering on the surface of heat exchanger. But metallic ion in natural water could affect the crystalline type of calcium carbonate. In this study, the effect of sodium ion, magnesium ion and aluminum ion on crystalline type and morphology of CaCO3 were reported. The experimental results indicate that the addition of sodium ion has no obvious role for changing the crystalline type of CaCO3, only calcite was obtained and the lattice parameter of calcite has a little variation depending on the concentration of sodium ion. However, the addition of magnesium and aluminum ion prompts obviously the formation of aragonite. In order to clarify the mechanism about the effect of metallic ion on lattice stability of calcium carbonate, the energies and electronic structures for the calcite with sodium, magnesium or aluminum inclusion have been determined from first-principle calculations. The calculated results indicate magnesium and aluminum inclusion has more effects on the stability of calcite than that of sodium inclusion.
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Shestakova, N. N., and D. A. Belinskaia. "Structure of the Cation- And Ligand-Binding Sites of Human Sodium-Calcium Exchanger According to Homology Modeling." In Mathematical Biology and Bioinformatics. Pushchino: IMPB RAS - Branch of KIAM RAS, 2020. http://dx.doi.org/10.17537/icmbb20.2.

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Izadi, M., D. K. Aidun, P. Marzocca, and H. Lee. "The Experimental Investigation of Fouling Phenomenon in Heat Exchangers by Heat Transfer Resistance Monitoring (HTRM) Method." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-12524.

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The aim of this paper is to describe a monitoring system for fouling phenomenon in tubular heat exchangers. This system is based on a physical model of the fouling resistance. A mathematical model of the fouling resistance is developed based on the applied thermal heat, the inside heat transfer coefficient, and geometrical characteristics of the heat exchanger under consideration. The resulting model is a function of measured quantities such as water and tube wall temperatures, fluid flow velocities, and some physical properties of the fluid flowing inside the tubes such as viscosity, conductivity, and density. An on-line fouling evaluation system was prepared and the heat transfer resistance for selected solutions was measured in real time by this system. The effect of concentration and chemical reactions on fouling is studied experimentally by using different contaminants such as sodium bicarbonate, calcium chloride, and their mixture. Accelerated corrosion was observed for the calcium chloride-0.4g/l solution due to the presence of chlorine ions. This corrosion-fouling can be mitigated by adding sodium bicarbonate. However, calcium carbonate is formed as the result of the chemical reaction between calcium chloride and sodium bicarbonate which activates two other fouling categories, particulate fouling and crystallization. The inside surface of the tube is analyzed by analytical microscopy after the experiment to investigate different fouling categories. Experimental results provide quantitative information of liquid-side fouling on heat transfer surfaces, and its effects on the thermal efficiency. Experimental data is significantly important for the design, and for formulating operating, and cleaning schedules of the equipment.
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Izadi, M., D. K. Aidun, P. Marzocca, and H. Lee. "Effect of Surface Roughness on Fouling of Calcium Carbonate: An Experimental Investigation." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-40623.

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The effect of surface roughness on the fouling behavior of calcium carbonate is experimentally investigated. The real operating conditions of a tubular heat exchanger are simulated by performing prolonged experiments with duration of 3 to 7 days. The solution used is a mixture of sodium bicarbonate and calcium chloride in de-ionized water with the concentration of 0.4 g/l of each. An on-line fouling evaluation system was developed such that the fouling resistance for a selected solution could be measured in real time. The experiments are repeated with the same procedure for 90/10 Cu/Ni tubes with different internal surface roughness. After the experiment the surface is analyzed by analytical microscopy to investigate the morphology of the deposit layer. Comparison of the experimental results of smooth and rough surfaces shows that a combination of aragonite and calcite polymorphs are formed on rough surface while only dendritic porous aragonite crystals are formed on smooth surface. Accordingly, the deposit layer formed on rough surface is denser and has a higher thermal resistance comparing to that formed on smooth surface. The fouling factor-time curves of smooth and rough surfaces obtained by the current experimental study agree with the results found by the analytical microscopy of the surface and show higher fouling resistances for rough surface. Experimental data is significantly important for the design, and formulating operating, and cleaning schedules of the equipment.
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