ArticleCardiovascular research2008
Targeting of phospholamban by peroxynitrite decreases beta-adrenergic stimulation in cardiomyocytes.
Article in Cardiovascular research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 41 citations in OpenAlex.
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- Nitric oxide: what's new to NO?American journal of physiology. Cell physiology · 2017Review
- Ischemic postconditioning protects the heart against ischemia-reperfusion injury via neuronal nitric oxide synthase in the sarcoplasmic reticulum and mitochondria.Cell death & disease · 2016Article
- Should we treat heart failure with phosphatase inhibitors? Better to start at the end.Journal of molecular and cellular cardiology · 2015Article
- Tri-modal regulation of cardiac muscle relaxation; intracellular calcium decline, thin filament deactivation, and cross-bridge cycling kinetics.Biophysical reviews · 2014Article
- Abnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balance.Antioxidants & redox signaling · 2014Review
- The NO/ONOO-cycle as the central cause of heart failure.International journal of molecular sciences · 2013Review
- Influence of phosphodiesterases and cGMP on cAMP generation and on phosphorylation of phospholamban and troponin I by 5-HT4 receptor activation in porcine left atrium.Naunyn-Schmiedeberg's archives of pharmacology · 2013Article
- Differential effects of the peroxynitrite donor, SIN-1, on atrial and ventricular myocyte electrophysiology.Journal of cardiovascular pharmacology · 2013Article
- Neuronal nitric oxide synthase is indispensable for the cardiac adaptive effects of exercise.Basic research in cardiology · 2013Article
- Hydralazine and organic nitrates restore impaired excitation-contraction coupling by reducing calcium leak associated with nitroso-redox imbalance.The Journal of biological chemistry · 2013Article
- Effects of increased systolic Ca(2+) and β-adrenergic stimulation on Ca(2+) transient decline in NOS1 knockout cardiac myocytes.Nitric oxide : biology and chemistry · 2012Article
- Modulation of myocardial contraction by peroxynitrite.Frontiers in physiology · 2012Article
- Effects of increased systolic Ca²⁺ and phospholamban phosphorylation during β-adrenergic stimulation on Ca²⁺ transient kinetics in cardiac myocytes.American journal of physiology. Heart and circulatory physiology · 2011Article
- Regulation of myocyte contraction via neuronal nitric oxide synthase: role of ryanodine receptor S-nitrosylation.The Journal of physiology · 2010Article
- cAMP-independent activation of protein kinase A by the peroxynitrite generator SIN-1 elicits positive inotropic effects in cardiomyocytes.Journal of molecular and cellular cardiology · 2010Article
- CB1 cannabinoid receptors promote oxidative stress and cell death in murine models of doxorubicin-induced cardiomyopathy and in human cardiomyocytes.Cardiovascular research · 2010Article
- Nitroxyl enhances myocyte Ca2+ transients by exclusively targeting SR Ca2+-cycling.Frontiers in bioscience (Elite edition) · 2010Article
- Transnitrosylating nitric oxide species directly activate type I protein kinase A, providing a novel adenylate cyclase-independent cross-talk to beta-adrenergic-like signaling.The Journal of biological chemistry · 2009Article
- Phosphodiesterase 5 restricts NOS3/Soluble guanylate cyclase signaling to L-type Ca2+ current in cardiac myocytes.Journal of molecular and cellular cardiology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
aimsPeroxynitrite production increases during the pathogenesis of numerous cardiac disorders (e.g. heart failure). However, limited studies have investigated the mechanism through which peroxynitrite exerts anti-adrenergic effects. Thus, the purpose of this study is to investigate the contribution of phospholamban (PLB), a critical excitation-contraction coupling protein, to the peroxynitrite-induced dysfunction. METHODS AND
resultsIsolated myocytes from wild-type (WT, CF-1) and PLB knockout (PLB(-/-)) mice were stimulated at 1 Hz, and myocyte shortening and Ca(2+) transients were simultaneously recorded. PLB phosphorylation was measured via western blot. Myocytes were superfused with isoproterenol, a beta-adrenergic agonist, and SIN-1, a peroxynitrite donor. SIN-1 superfusion dramatically decreased isoproterenol-stimulated Ca(2+) transients and myocyte shortening in WT myocytes. These effects were inhibited upon addition of the peroxynitrite decomposition catalyst, FeTPPS. Surprisingly, SIN-1 had no functional effect on beta-adrenergic-stimulated PLB(-/-) myocytes. Western blot analyses revealed that SIN-1 significantly decreased isoproterenol-stimulated PLB(Ser16) phosphorylation. Experiments with the protein phosphatase inhibitor, okadaic acid, alleviated the SIN-1-induced functional effects and the decrease in PLB phosphorylation.
conclusionsThe peroxynitrite donor SIN-1 decreases beta-adrenergic stimulation by reducing PLB(Ser16) phosphorylation via protein phosphatase activation. This peroxynitrite-induced decrease in PLB phosphorylation may be a key mechanism in the beta-adrenergic dysfunction observed in many cardiomyopathies.
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