ArticleAmerican journal of physiology. Heart and circulatory physiology2008
Regulation of cardiac myocyte contractility by phospholemman: Na+/Ca2+ exchange versus Na+ -K+ -ATPase.
Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 45 citations in OpenAlex.
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- Carvedilol Selectively Stimulates βArrestin2-Dependent SERCA2a Activity in Cardiomyocytes to Augment Contractility.International journal of molecular sciences · 2022Article
- Novel BAG3 Variants in African American Patients With Cardiomyopathy: Reduced β-Adrenergic Responsiveness in Excitation-Contraction.Journal of cardiac failure · 2020Article
- Antidotal effects of methylene blue against cyanide neurological toxicity: in vivo and in vitro studies.Annals of the New York Academy of Sciences · 2020Article
- Trpm2 enhances physiological bioenergetics and protects against pathological oxidative cardiac injury: Role of Pyk2 phosphorylation.Journal of cellular physiology · 2019Article
- Mitochondrial dysfunction in human immunodeficiency virus-1 transgenic mouse cardiac myocytes.Journal of cellular physiology · 2019Article
- Methylene Blue Counteracts HCardiovascular toxicology · 2018Article
- Haplo-insufficiency of Bcl2-associated athanogene 3 in mice results in progressive left ventricular dysfunction, β-adrenergic insensitivity, and increased apoptosis.Journal of cellular physiology · 2018Article
- Methylene blue counteracts cyanide cardiotoxicity: cellular mechanisms.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Compartmentalized cAMP Signaling Associated With Lipid Raft and Non-raft Membrane Domains in Adult Ventricular Myocytes.Frontiers in pharmacology · 2018Article
- Structural Determinants Influencing the Potency and Selectivity of Indazole-Paroxetine Hybrid G Protein-Coupled Receptor Kinase 2 Inhibitors.Molecular pharmacology · 2017Article
- Structure-Based Design of Highly Selective and Potent G Protein-Coupled Receptor Kinase 2 Inhibitors Based on Paroxetine.Journal of medicinal chemistry · 2017Article
- Adeno-associated Virus Serotype 9 - Driven Expression of BAG3 Improves Left Ventricular Function in Murine Hearts with Left Ventricular Dysfunction Secondary to a Myocardial Infarction.JACC. Basic to translational science · 2016Article
- Bcl-2-associated athanogene 3 protects the heart from ischemia/reperfusion injury.JCI insight · 2016Article
- Methylene blue counteracts H2S toxicity-induced cardiac depression by restoring L-type Ca channel activity.American journal of physiology. Regulatory, integrative and comparative physiology · 2016Article
- Structure-Based Design, Synthesis, and Biological Evaluation of Highly Selective and Potent G Protein-Coupled Receptor Kinase 2 Inhibitors.Journal of medicinal chemistry · 2016Article
- BAG3 regulates contractility and Ca(2+) homeostasis in adult mouse ventricular myocytes.Journal of molecular and cellular cardiology · 2016Article
- Enhanced Cardiac Regenerative Ability of Stem Cells After Ischemia-Reperfusion Injury: Role of Human CD34+ Cells Deficient in MicroRNA-377.Journal of the American College of Cardiology · 2015Article
- Cardiac Dysfunction in HIV-1 Transgenic Mouse: Role of Stress and BAG3.Clinical and translational science · 2015Article
- Regulation of L-type calcium channel by phospholemman in cardiac myocytes.Journal of molecular and cellular cardiology · 2015Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Phospholemman (PLM) regulates cardiac Na(+)/Ca(2+) exchanger (NCX1) and Na(+)-K(+)-ATPase in cardiac myocytes. PLM, when phosphorylated at Ser(68), disinhibits Na(+)-K(+)-ATPase but inhibits NCX1. PLM regulates cardiac contractility by modulating Na(+)-K(+)-ATPase and/or NCX1. In this study, we first demonstrated that adult mouse cardiac myocytes cultured for 48 h had normal surface membrane areas, t-tubules, and NCX1 and sarco(endo)plasmic reticulum Ca(2+)-ATPase levels, and retained near normal contractility, but alpha(1)-subunit of Na(+)-K(+)-ATPase was slightly decreased. Differences in contractility between myocytes isolated from wild-type (WT) and PLM knockout (KO) hearts were preserved after 48 h of culture. Infection with adenovirus expressing green fluorescent protein (GFP) did not affect contractility at 48 h. When WT PLM was overexpressed in PLM KO myocytes, contractility and cytosolic Ca(2+) concentration ([Ca(2+)](i)) transients reverted back to those observed in cultured WT myocytes. Both Na(+)-K(+)-ATPase current (I(pump)) and Na(+)/Ca(2+) exchange current (I(NaCa)) in PLM KO myocytes rescued with WT PLM were depressed compared with PLM KO myocytes. Overexpressing the PLMS68E mutant (phosphomimetic) in PLM KO myocytes resulted in the suppression of I(NaCa) but had no effect on I(pump). Contractility, [Ca(2+)](i) transient amplitudes, and sarcoplasmic reticulum Ca(2+) contents in PLM KO myocytes overexpressing the PLMS68E mutant were depressed compared with PLM KO myocytes overexpressing GFP. Overexpressing the PLMS68A mutant (mimicking unphosphorylated PLM) in PLM KO myocytes had no effect on I(NaCa) but decreased I(pump). Contractility, [Ca(2+)](i) transient amplitudes, and sarcoplasmic reticulum Ca(2+) contents in PLM KO myocytes overexpressing the S68A mutant were similar to PLM KO myocytes overexpressing GFP. We conclude that at the single-myocyte level, PLM affects cardiac contractility and [Ca(2+)](i) homeostasis primarily by its direct inhibitory effects on Na(+)/Ca(2+) exchange.
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