ArticleThe Journal of physiology1997
Calcium sparks and excitation-contraction coupling in phospholamban-deficient mouse ventricular myocytes.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 140 citations in OpenAlex.
- Paxilline Prevents the Onset of Myotonic Stiffness in Pharmacologically Induced Myotonia: A Preclinical Investigation.Frontiers in physiology · 2020Article
- Mitochondrial and Sarcoplasmic Reticulum Interconnection in Cardiac Arrhythmia.Frontiers in cell and developmental biology · 2020Review
- Unbalance Between Sarcoplasmic Reticulum CaFrontiers in physiology · 2019Review
- Integrating ER and Mitochondrial Proteostasis in the Healthy and Diseased Heart.Frontiers in cardiovascular medicine · 2019Review
- Unique CaInternational journal of molecular sciences · 2018Review
- Phospholamban ablation rescues the enhanced propensity to arrhythmias of mice with CaMKII-constitutive phosphorylation of RyR2 at site S2814.The Journal of physiology · 2016Article
- Intact Heart Loose Patch Photolysis Reveals Ionic Current Kinetics During Ventricular Action Potentials.Circulation research · 2016Article
- Chasing cardiac physiology and pathology down the CaMKII cascade.American journal of physiology. Heart and circulatory physiology · 2015Review
- Phospholamban phosphorylation, mutation, and structural dynamics: a biophysical approach to understanding and treating cardiomyopathy.Biophysical reviews · 2015Article
- Acute reversal of phospholamban inhibition facilitates the rhythmic whole-cell propagating calcium waves in isolated ventricular myocytes.Journal of molecular and cellular cardiology · 2015Article
- Thin filament incorporation of an engineered cardiac troponin C variant (L48Q) enhances contractility in intact cardiomyocytes from healthy and infarcted hearts.Journal of molecular and cellular cardiology · 2014Article
- Phospholamban knockout breaks arrhythmogenic Ca²⁺ waves and suppresses catecholaminergic polymorphic ventricular tachycardia in mice.Circulation research · 2013Article
- Control of sarcoplasmic reticulum Ca2+ release by stochastic RyR gating within a 3D model of the cardiac dyad and importance of induction decay for CICR termination.Biophysical journal · 2013Article
- Phospholemman is a negative feed-forward regulator of Ca2+ in β-adrenergic signaling, accelerating β-adrenergic inotropy.Journal of molecular and cellular cardiology · 2012Article
- Dynamic local changes in sarcoplasmic reticulum calcium: physiological and pathophysiological roles.Journal of molecular and cellular cardiology · 2012Review
- Article
- Upregulation of cardiomyocyte ribonucleotide reductase increases intracellular 2 deoxy-ATP, contractility, and relaxation.Journal of molecular and cellular cardiology · 2011Article
- Efficacy and potency of class I antiarrhythmic drugs for suppression of Ca2+ waves in permeabilized myocytes lacking calsequestrin.Journal of molecular and cellular cardiology · 2011Article
- Phosphodiesterase 4B in the cardiac L-type Ca²⁺ channel complex regulates Ca²⁺ current and protects against ventricular arrhythmias in mice.The Journal of clinical investigation · 2011Article
- Regulation of gastrointestinal motility by Ca2+/calmodulin-stimulated protein kinase II.Archives of biochemistry and biophysics · 2011Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
1. We examined [Ca2+]i and L-type Ca2+ channel current (ICa) in single cardiac myocytes to determine how the intracellular protein phospholamban (PLB) influences excitation-contraction (E-C) coupling in heart. Wild type (WT) and PLB-deficient (KO) mice were used. Cells were patch clamped in whole-cell mode while [Ca2+]i was imaged simultaneously using the Ca2+ indicator fluo-3 and a confocal microscope. 2. Although ICa was similar in magnitude, the decay of ICa was faster in KO than in WT cells and the [Ca2+]i transient was larger and decayed faster. Furthermore, the E-C coupling 'gain' (measured as delta[Ca2+]i/ICa) was larger in KO cells than in WT cells. 3. Spontaneous Ca2+ sparks were three times more frequent and larger in KO cells than in WT myocytes but, surprisingly, the time constants of decay were similar. 4. SR Ca2+ content was significantly greater in KO than in WT cells. When the SR Ca2+ content in KO cells was reduced to that in WT cells, Ca2+ sparks in these 'modified' (KO') cells decayed faster. E-C coupling gain, [Ca2+]i transient amplitude and the kinetics of decay of ICa were similar in KO' and WT cells. 5. We conclude that SR Ca2+ content influences (1) ICa, (2) the amplitude and kinetics of Ca2+ sparks and [Ca2+]i transients, (3) the sensitivity of the RyRs to triggering by [Ca2+]i, (4) the amount of Ca2+ released, (5) the magnitude of the E-C coupling 'gain' function, and (6) the rate of Ca2+ re-uptake by the SR Ca(2+)-ATPase. In KO cells, the larger [Ca2+]i transients and Ca2+ sparks speed up ICa inactivation. Finally, we conclude that PLB plays an important regulatory role in E-C coupling by modulating SR Ca(2+)-ATPase activity, which establishes the SR Ca2+ content and consequently influences the characteristics of local and global Ca2+ signalling.
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