Relevant bibliographies by topics / Calcium exchanger (NCX)

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  2. Dissertations / Theses
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  4. Conference papers

Academic literature on the topic 'Calcium exchanger (NCX)'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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

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 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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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 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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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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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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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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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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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 altered the activities of SERCA and NCX in human embryonic stem cell-derived ventricular cardiomyocytes (hESC-VCMs) and their engineered microtissues, followed by examining the resultant phenotypic consequences. SERCA overexpression in hESC-VCMs shortened the decay of Ca2+ transient at low frequencies (0.5 Hz) without affecting the amplitude, SR Ca2+ content and Ca2+ baseline. Interestingly, short hairpin RNA-based NCX suppression did not prolong the transient decay, indicating a compensatory response for Ca2+ removal. Although hESC-VCMs and their derived microtissues exhibited negative frequency-transient/force responses, SERCA overexpression rendered them less negative at high frequencies (>2 Hz) by accelerating Ca2+ sequestration. We conclude that for hESC-VCMs and their microtissues, SERCA, rather than NCX, is the main Ca2+ remover during diastole; poor SERCA expression is the leading cause for immature negative-frequency/force responses, which can be partially reverted by forced expression. Combinatorial approach to mature calcium handling in hESC-VCMs may help shed further mechanistic insights. NEW & NOTEWORTHY In this study of human pluripotent stem cell-derived cardiomyocytes, we studied the role of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) and Na+-Ca2+ exchanger (NCX) in Ca2+ handling. Our data support the notion that SERCA is more effective in cytosolic calcium removal than the NCX.
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Dissertations / Theses on the topic "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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Nguidjoe, Evrard. "Etude de la fonction de la cellule bêta pancréatique dans un modèle de souris présentant une mutation nulle partielle de l'échangeur sodium/calcium." Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209833.

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Précédemment, nous avons montré que la surexpression de l'échangeur Na/Ca NCX1), une protéine responsable de la sortie de calcium (Ca2+) des cellules, augmentait la mort cellulaire programmée ou « apoptose » et réduisait la prolifération des cellules β. Afin d’étudier plus en profondeur le rôle de l’échangeur dans les cellules β in vivo, nous avons développé et caractérisé des souris présentant une inactivation de NCX1.

Des méthodes biologiques et morphologiques (imagerie du Ca2+, capture de Ca2+, métabolisme du glucose, sécrétion d'insuline et morphométrie par comptage de points) ont été utilisées pour évaluer la fonction de la cellule β in vitro. Les taux de glucose et d'insuline dans le sang ont été mesurés afin de déterminer le métabolisme du glucose et la sensibilité à l’insuline in vivo. Des îlots ont été transplantés sous la capsule rénale pour évaluer leur capacité à corriger le diabète chez les souris rendues diabétiques par l’alloxane.

L'inactivation hétérozygote de Ncx1 chez les souris provoque une augmentation de la sécrétion d’insuline induite par le glucose avec un renforcement important à la fois de la première et de la deuxième phase. Ces résultats s’accompagnent d’une augmentation de la masse et de la prolifération des cellules β. La mutation augmente également le contenu en insuline, l’immunomarquage de la proinsuline, la capture de Ca2+ induite par le glucose et la résistance à l'hypoxie des cellules β. En outre, les îlots de souris Ncx1+/- montrent une capacité à compenser le diabète 2 à 4 fois plus élevé que les îlots de souris Ncx1+/+ lorsque transplantés chez des souris diabétiques.

En conclusion, l’inactivation de l'échangeur Na/Ca conduit à une augmentation de la fonction de la cellule β, de sa prolifération, de sa masse et de sa résistance au stress physiologique, à savoir à divers changements de fonction des cellules β opposés aux principales anomalies rencontrées dans le diabète de type 2 (Type 2 Diabetes Mellitus,T2DM). Ceci nous procure un modèle unique pour la prévention et le traitement du dysfonctionnement des cellules β dans le T2DM et pour la transplantation d'îlots.


Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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de, Moissac Danielle. "Structure-function studies of the sodium-calcium exchanger isoforms, NCX1 and NCX2." 2009. http://hdl.handle.net/1993/3158.

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The sodium-calcium exchanger (NCX) is a countertransporter of Na+ and Ca2+ across most cell membranes. It has been identified as an essential component of Ca2+ homeostasis in physiological and disease conditions in both cardiovascular and neurological settings. The exchanger not only transports Na+ and Ca2+, but is also regulated by these ions. Although ionic regulatory profiles differ between NCX isoforms, similar regulatory domains have been identified. Previous structure-function studies have determined key residues within these domains, particularly in the eXchanger Inhibitory Peptide region (XIP) and the Ca2+ binding domains (CBD1/2), which have a direct impact on ionic regulation of the outward exchange currents. Recent structural studies of the Ca2+ binding domains of NCX1 suggest a mechanism by which Ca2+ binding would not only be essential for activation of current but may also influence Na+-dependent inactivation. The alternative splice region is located within the Ca2+ binding domain and may play a role in mediating these regulatory phenotypes. Previous studies have demonstrated that specific combinations of the mutually-exclusive and cassette exons are associated with profound effects on ionic regulation in NCX1. This study focuses on examining the mechanisms by which the alternative splice region, in combination with specific regulatory domains, modulates exchange activity in two isoforms, NCX1 and NCX2. Chimaeric and mutant constructs in the alternative splice region were expressed in Xenopus oocytes and outward Na+-Ca2+ exchange activity was assessed using the giant, excised patch clamp technique. Substitution of the region corresponding to the mutually exclusive exon in either exchanger greatly reduced the extent of Na+-dependent inactivation, independently of intracellular Ca2+ concentrations. However, replacement of both the region corresponding to the mutually exclusive exon A and the XIP region reestablishes a wild-type profile in NCX2. The first mutually exclusive exon is therefore critical in determining Na+ and Ca2+-dependent regulatory properties. Furthermore, non-conserved residues within the XIP region may be essential in maintaining the structural stability of the Na+-dependent inactive state of NCX1, and by interacting with the mutually exclusive exon, may contribute to the structure-function relationship and the distinct regulatory phenotype of each Na+-Ca2+ exchanger variant and isoform.
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Chen, Shao-Hong, and 陳紹弘. "A Study of the Sodium Calcium Ion Exchange Mechanism in NCX." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/06903241036428583046.

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碩士
國立新竹教育大學
應用數學系碩士班
103
Biological sodium calcium ion exchange channel (NCX) removes calcium ions very rapidly from cell inside in exchange with sodium ions from outside. The Poisson-Fermi theory is used to analyze the binding potentials of NCX. It allows us to mathematically investigate the sodium-calcium ion exchange mechanism in NCX. Numerical results have been shown to agree with the experimental results of the sodium-calcium ion exchange.
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Book chapters on the topic "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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Annunziato, Lucio, and Pasquale Molinaro. "NCX, Sodium-Calcium Exchanger." In xPharm: The Comprehensive Pharmacology Reference, 1–17. Elsevier, 2009. http://dx.doi.org/10.1016/b978-008055232-3.63805-x.

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Fajmut, Aleš. "Molecular Mechanisms and Targets of Cyclic Guanosine Monophosphate (cGMP) in Vascular Smooth Muscles." In Muscle Cell and Tissue - Novel Molecular Targets and Current Advances [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97708.

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Molecular mechanisms and targets of cyclic guanosine monophosphate (cGMP) accounting for vascular smooth muscles (VSM) contractility are reviewed. Mathematical models of five published mechanisms are presented, and four novel mechanisms are proposed. cGMP, which is primarily produced by the nitric oxide (NO) dependent soluble guanylate cyclase (sGC), activates cGMP-dependent protein kinase (PKG). The NO/cGMP/PKG signaling pathway targets are the mechanisms that regulate cytosolic calcium ([Ca2+]i) signaling and those implicated in the Ca2+-desensitization of the contractile apparatus. In addition to previous mathematical models of cGMP-mediated molecular mechanisms targeting [Ca2+]i regulation, such as large-conductance Ca2+-activated K+ channels (BKCa), Ca2+-dependent Cl− channels (ClCa), Na+/Ca2+ exchanger (NCX), Na+/K+/Cl− cotransport (NKCC), and Na+/K+-ATPase (NKA), other four novel mechanisms are proposed here based on the existing but perhaps overlooked experimental results. These are the effects of cGMP on the sarco−/endo- plasmic reticulum Ca2+-ATPase (SERCA), the plasma membrane Ca2+-ATPase (PMCA), the inositol 1,4,5-trisphosphate (IP3) receptor channels type 1 (IP3R1), and on the myosin light chain phosphatase (MLCP), which is implicated in the Ca2+-desensitization. Different modeling approaches are presented and discussed, and novel model descriptions are proposed.
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Conference papers on the topic "Calcium exchanger (NCX)"

1

Ågren, Niklas D., Mats O. Westermark, Michael A. Bartlett, and Torbjörn Lindquist. "First Experiments on an Evaporative Gas Turbine Pilot Power Plant: Water Circuit Chemistry and Humidification Evaluation." In ASME Turbo Expo 2000: Power for Land, Sea, and Air. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/2000-gt-0168.

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The evaporative gas turbine (EvGT), also known as the humid air turbine (HAT) cycle, is a novel advanced gas turbine cycle that has attracted considerable interest for the last decade. This high efficiency cycle shows the potential to be competitive with Diesel engines or combined cycles in small and intermediate scale plants for power production — and/or cogeneration. A 0.6 MW natural gas fired EvGT pilot plant has been constructed by a Swedish national research group in cooperation between universities and industry. The plant is located at the Lund Institute of Technology, Lund, Sweden. The pilot plant uses a humidification tower with metallic packing in which heated water from the flue gas economizer is brought into direct counter current contact with the pressurized air from the compressor. This gives an efficient heat recovery and thereby a thermodynamically sound cycle. As the hot sections in high temperature gas turbines are sensitive to particles and alkali compounds, water quality issues need to be carefully considered. As such, apart from evaluating the thermodynamic and part load performance characteristics of the plant, and verifying the operation of the high pressure humidifier, much attention is focused on the water chemistry issues associated with the recovery and reuse of condensate water from the flue gas. A water treatment system has been designed and integrated into the pilot plant. This paper presents the first water quality results from the plant. The experimental results show that the condensate contains low levels of alkali and calcium, around 2 mg/l Σ(K,Na,Ca), probably originating from the unfiltered compressor intake. About 14 mg/l NO2− + NO3− comes from condensate absorption of flue gas NOx. Some Cu is noted, 16 mg/l, which originates from copper corrosion of the condenser tubes. After CO2-stripping, condensate filtration and a mixed bed ion exchanger, the condensate is of suitable quality for reuse as humidification water. The need for large quantities of demineralized water has by many authors been identified as a drawback for the evaporative cycle. However, by cooling the humid flue gas, the recovery of condensed water cuts the need of water feed. A self supporting water circuit can be achieved, with no need for any net addition of water to the system. In the pilot plant, this was achieved by cooling the flue gas to around 35°C.
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