Regular ArticlesEffects of Na+/Ca2+-exchanger Overexpression on Excitation–contraction Coupling in Adult Rabbit Ventricular Myocytes
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Histone modifications in cardiovascular disease initiation and progression
2021, Epigenetics in Cardiovascular DiseaseNew experimental evidence for mechanism of arrhythmogenic membrane potential alternans based on balance of electrogenic I<inf>NCX</inf>/I <inf>Ca</inf> currents
2012, Heart RhythmCitation Excerpt :INCX predominance was achieved by in vivo NCX gene transfer by using a modified cross-clamping method.9 Western blot from in vitro NCX overexpression showed that NCX protein expression was indeed increased by (3.8 ± 2.9)-fold compared with control (n = 3), and previously Ranu et al10 demonstrated that the overexpression of NCX increases INCX, with no change in ICa. ICa predominance was achieved by INCX inhibition or ICa enhancement.
Systematic characterization of the ionic basis of rabbit cellular electrophysiology using two ventricular models
2011, Progress in Biophysics and Molecular BiologyCitation Excerpt :The influence of ICaL on the frequency dependence of systolic [Ca2+]i is also consistent with experiments performed in rabbit ventricular preparations (McCans et al., 1974). The increase in the frequency dependence of systolic [Ca2+]i with INaCa overexpression is in accordance with some experiments reported in adult rabbit myocytes (Ranu et al., 2002). Others however report the opposite effect (Schillinger et al., 2000).
Targeted GLUT-4 deficiency in the heart induces cardiomyocyte hypertrophy and impaired contractility linked with Ca<sup>2+</sup> and proton flux dysregulation
2010, Journal of Molecular and Cellular CardiologyCitation Excerpt :The basis for the delayed latency in the GLUT4-KO is not clear, but the possibility that myofilament access is less immediate for activator Ca2+ supplied via the reverse mode NCX is suggested. Overexpression of cardiomyocyte NCX has previously been linked with decreased SR Ca2+ stores and reduced contractility [36]. While this may be an energetically advantageous adaptation in the GLUT4-KO, the shift from SR to trans-sarcolemmal Ca2+ cycling would have the undesirable effect of depleting the systolic functional reserve [37] and increasing the propensity for generation of arrhythmogenic currents in early relaxation (by forward NCX).
β-Adrenergic receptor stimulated Ncx1 upregulation is mediated via a CaMKII/AP-1 signaling pathway in adult cardiomyocytes
2010, Journal of Molecular and Cellular CardiologyCitation Excerpt :More importantly, both Ncx1 mRNA and protein levels are significantly upregulated in human end-stage heart failure [13–16]. The diastolic performance of failing human myocardium correlates inversely with protein levels of NCX1 [17] and upregulation of Ncx1 alone contributes directly to limiting SR loading and contractile dysfunction [18,19]. In addition, Ncx1 gene upregulation results in greater potential for delayed after depolarizations (DADs), which are major initiators of ventricular tachycardia [9,20].
Chronic administration of KB-R7943 induces up-regulation of cardiac NCX1
2009, Journal of Biological Chemistry
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Please address all correspondence to: Dr Sian E. Harding, Cardiac Medicine, National Heart and Lung Institute, Imperial College School of Medicine, Dovehouse StLondon SW3 6LY, UK. Tel: 0044 207 351 8146. Fax: 0044 207 823 3392. E-mail: [email protected]