Genomes and Genes
Joshua I Goldhaber
Affiliation: Cedars-Sinai Medical Center
- Cardiac sodium-calcium exchange and efficient excitation-contraction coupling: implications for heart diseaseJoshua I Goldhaber
Cedars Sinai Heart Institute, Los Angeles, CA 90048, USA
Adv Exp Med Biol 961:355-64. 2013..Thus, our data support the conclusion that NCX is an important regulator of cardiac contractility. These findings suggest that manipulation of NCX may be beneficial in the treatment of heart failure...
- Functional adult myocardium in the absence of Na+-Ca2+ exchange: cardiac-specific knockout of NCX1Scott A Henderson
Department of Physiology and Medicine, David Geffen School of Medicine at the University of California, Los Angeles, CA 90095 1760, USA
Circ Res 95:604-11. 2004..The magnitude of Ca2+ transients appears to be maintained by an increased gain of sarcoplasmic reticular Ca2+ release. The myocardium of the NCX1 knockout mice undergoes a remarkable adaptation to maintain near normal cardiac function...
- Cardiac excitation-contraction coupling in the absence of Na(+) - Ca2+ exchangeHannes Reuter
Departments of Physiology and Medicine and the Cardiovascular Research Laboratory, MRL 3 645, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095 1760, USA
Cell Calcium 34:19-26. 2003..Expression of the sarcolemmal Ca(2+) pump was not upregulated. The sarcolemmal Ca(2+) pump, however, was able to compensate surprisingly well for the absence of Na(+) - Ca(2+) exchange under basal conditions...
- Effect of metabolic inhibition on couplon behavior in rabbit ventricular myocytesChana Chantawansri
Division of Cardiology, Cardiovascular Research Laboratories, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Biophys J 94:1656-66. 2008..In addition, the results are consistent with loss of RyR activity, which can be mitigated under conditions likely to enlarge the trigger...
- Mechanism of shortened action potential duration in Na+-Ca2+ exchanger knockout miceChristian Pott
Cardiovascular Research Laboratory, MRL 3 645, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095 1760, USA
Am J Physiol Cell Physiol 292:C968-73. 2007..The upregulation of I(to) may comprise an important regulatory mechanism to limit Ca(2+) influx via a reduction of AP duration, thus preventing Ca(2+) overload in situations of reduced myocyte Ca(2+) extrusion capacity...
- Regulation of cardiac L-type Ca2+ current in Na+-Ca2+ exchanger knockout mice: functional coupling of the Ca2+ channel and the Na+-Ca2+ exchangerChristian Pott
Department of Physiology, David Geffen School of Medicine at the University of California, Los Angeles, California 90095, USA
Biophys J 92:1431-7. 2007..Modulation of subsarcolemmal Ca2+ by the Na+-Ca2+ exchanger may be an important regulator of excitation-contraction coupling...
- Mice overexpressing the cardiac sodium-calcium exchanger: defects in excitation-contraction couplingHannes Reuter
Department of Physiology, Division of Cardiology, David Geffen School of Medicine at UCLA, 47 123 CHS, 10833 LeConte Avenue, Los Angeles, CA 90095 1679, USA
J Physiol 554:779-89. 2004..0005) and substantially reduced gain of excitation-contraction coupling. These alterations in excitation-contraction coupling may underlie the tendency for these animals to develop heart failure following haemodynamic stress...
- Action potential duration restitution and alternans in rabbit ventricular myocytes: the key role of intracellular calcium cyclingJoshua I Goldhaber
UCLA Cardiovascular Research Laboratory, Department of Medicine Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, Calif 90095 1679, USA
Circ Res 96:459-66. 2005..Ca2+i cycling may contribute to differences between APD restitution curves measured by S1S2 versus dynamic pacing protocols by inducing short-term memory effects related to pacing-dependent Ca2+i accumulation...
- Sodium-calcium exchange is essential for effective triggering of calcium release in mouse heartPatricia Neco
Departments of Medicine Cardiology and Physiology and the Cardiovascular Research Laboratories, David Geffen School of Medicine at UCLA, Los Angeles, California, USA
Biophys J 99:755-64. 2010..Thus, reducing subsarcolemmal Ca2+ with EGTA in NCX KO mice reveals the dependence of Ca2+ release on NCX...
- Excitation-contraction coupling in Na+-Ca2+ exchanger knockout mice: reduced transsarcolemmal Ca2+ fluxChristian Pott
Department of Physiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095 1760, USA
Circ Res 97:1288-95. 2005..Contractility is maintained by an increase in the gain of excitation-contraction coupling resulting from both a more rapid repolarization of the AP and an as yet unidentified AP-independent mechanism...
- Metabolic inhibition alters subcellular calcium release patterns in rat ventricular myocytes: implications for defective excitation-contraction coupling during cardiac ischemia and failureGary H Fukumoto
Department of Medicine, Cardiovascular Research Laboratories, Geffen School of Medicine at UCLA, Los Angeles, Calif 90095 1679, USA
Circ Res 96:551-7. 2005..We conclude that metabolic inhibition interferes with E-C coupling by (1) reducing trigger Ca2+, and (2) directly inhibiting sarcoplasmic reticulum Ca2+ release site open probability...
- Knockout mice for pharmacological screening: testing the specificity of Na+-Ca2+ exchange inhibitorsHannes Reuter
Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, Calif 90095 1760, USA
Circ Res 91:90-2. 2002..Both drugs depress the Ca2+ transients at low concentrations even in the absence of any Na+-Ca2+ exchanger. KB-R7943 and SEA0400 are not completely specific and should be used with caution as Na+-Ca2+ exchange inhibitors...
- Effects of Na+-Ca2+ exchange expression on excitation-contraction coupling in genetically modified miceJoshua I Goldhaber
Cardiovascular Research Laboratories, David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA
Ann N Y Acad Sci 1047:122-6. 2005..Cardiac function is surprisingly normal in seven-week-old mice, but E-C coupling gain is apparently increased. Thus, genetic modification of exchanger expression has a major influence on E-C coupling...
- Spontaneously beating cardiomyocytes derived from white mature adipocytesMedet Jumabay
David Geffen School of Medicine at UCLA, Los Angeles, CA 90095 1679, USA
Cardiovasc Res 85:17-27. 2010..The objective of this study was to examine if white adipocytes would be able to supply cardiomyocytes...
- Homozygous overexpression of the Na+-Ca2+ exchanger in mice: evidence for increased transsarcolemmal Ca2+ fluxesChristian Pott
Department of Physiology, David Geffen School of Medicine at UCLA, 675 Charles E Young Dr South, Los Angeles, CA 90095, USA
Ann N Y Acad Sci 1099:310-4. 2007..We conclude that transsarcolemmal Ca2+ fluxes in NCX-overexpressing myocytes are balanced by an increase in Ca2+ influx via (a) slowed inactivation of I(Ca) and (b) a prolongation of the AP to compensate for increased Ca2+ efflux...
- Na+/Ca2+ exchanger knockout mice: plasticity of cardiac excitation-contraction couplingChristian Pott
Department of Physiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
Ann N Y Acad Sci 1099:270-5. 2007..These adaptations may comprise important feedback mechanisms by which cardiomyocytes may be able to limit Ca2+ influx in situations of compromised Ca2+ extrusion capacity...
- Gi alpha 1-mediated cardiac electrophysiological remodeling and arrhythmia in hypertrophic cardiomyopathyHongmei Ruan
Department of Anesthesiology, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90095, USA
Circulation 116:596-605. 2007..However, the underlying signaling mechanisms involved in the induction of arrhythmia and electrophysiological remodeling in cardiac hypertrophy are unclear...
- Genetic manipulation of cardiac Na+/Ca2+ exchange expressionChristian Pott
Departments of Physiology and Medicine, The Cardiovascular Research Laboratories, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
Biochem Biophys Res Commun 322:1336-40. 2004..Ca2+ influx in these animals is limited by a decrease of peak L-type Ca2+ current. An alternative Ca2+ efflux mechanism, presumably the plasma membrane Ca2+-ATPase, is sufficient to maintain Ca2+-homeostasis in the NCX knockout mice...
- Activation of reverse Na+-Ca2+ exchange by the Na+ current augments the cardiac Ca2+ transient: evidence from NCX knockout miceRobert Larbig
Cardiovascular Research Laboratories, MRL 3 645, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095 1760, USA
J Physiol 588:3267-76. 2010..This is an important mechanism for regulation of Ca(2+) release and contractility in murine heart...
- 20 years from NCX purification and cloning: milestonesDebora A Nicoll
Department of Physiology and Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095 1760, USA
Adv Exp Med Biol 961:17-23. 2013..Of special interest are mice with atrial- or ventricular-specific KO of NCX that reveal new information on the role of NCX in excitation-contraction coupling and in cardiac pacemaker activity...
- Mutation in sodium-calcium exchanger 1 (NCX1) causes cardiac fibrillation in zebrafishAdam D Langenbacher
Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 102:17699-704. 2005..These data signify the essential role of calcium homeostasis and NCX1h in establishing rhythmic contraction in the embryonic zebrafish heart...
- Na/Ca exchange and contraction of the heartMichela Ottolia
Heart Institute, Cedars Sinai Medical Center, Los Angeles, CA, USA
J Mol Cell Cardiol 61:28-33. 2013..This article is part of a Special Issue entitled "Na(+) Regulation in Cardiac Myocytes". ..
- The role of E2F-1 and downstream target genes in mediating ischemia/reperfusion injury in vivoEkaterini Angelis
Cardiovascular Research Laboratory, Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA
J Mol Cell Cardiol 51:919-26. 2011..These results suggest that E2F-1 and FoxO-1a belong to a complex transcriptional network that may modulate myocardial cell death during I/R injury...
- The Na+-Ca2+ exchanger is essential for the action of cardiac glycosidesHannes Reuter
Department of Physiology, UCLA School of Medicine, Los Angeles, Calif 90095 1760, USA
Circ Res 90:305-8. 2002..We conclude that in embryonic mouse myocytes the Na+-Ca2+ exchanger is absolutely required for the effect of cardiac glycosides on Ca2+(i)...
- Reprogrammed mouse fibroblasts differentiate into cells of the cardiovascular and hematopoietic lineagesKatja Schenke-Layland
Department of Medicine and Physiology, Cardiovascular Research Laboratory, University of California Los Angeles School of Medicine, Los Angeles, California 90095 1760, USA
Stem Cells 26:1537-46. 2008..Disclosure of potential conflicts of interest is found at the end of this article...
- Return of calcium: manipulating intracellular calcium to prevent cardiac pathologiesYibin Wang
Department of Anesthesiology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA
Proc Natl Acad Sci U S A 101:5697-8. 2004
- Calcium Signaling, Metabolism, and EC Coupling in HeartJoshua I Goldhaber; Fiscal Year: 2010..This will lead to new therapeutic strategies for preserving heart muscle function, thereby reducing the incidence of heart failure. ..