ArticleAmerican journal of physiology. Heart and circulatory physiology2006
Altered contractility and [Ca2+]i homeostasis in phospholemman-deficient murine myocytes: role of Na+/Ca2+ exchange.
Article in American journal of physiology. Heart and circulatory physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
- Bag3 Regulates Mitochondrial Function and the Inflammasome Through Canonical and Noncanonical Pathways in the Heart.JACC. Basic to translational science · 2023Article
- 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
- 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
- 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
- BAG3 regulates contractility and Ca(2+) homeostasis in adult mouse ventricular myocytes.Journal of molecular and cellular cardiology · 2016Article
- Phospholemman is not required for the acute stimulation of Na⁺-K⁺-ATPase α₂-activity during skeletal muscle fatigue.American journal of physiology. Cell physiology · 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
- Ca²⁺ entry via Trpm2 is essential for cardiac myocyte bioenergetics maintenance.American journal of physiology. Heart and circulatory physiology · 2015Article
- Induced overexpression of phospholemman S68E mutant improves cardiac contractility and mortality after ischemia-reperfusion.American journal of physiology. Heart and circulatory physiology · 2014Article
- TRPM2 channels protect against cardiac ischemia-reperfusion injury: role of mitochondria.The Journal of biological chemistry · 2014Article
- The second member of transient receptor potential-melastatin channel family protects hearts from ischemia-reperfusion injury.American journal of physiology. Heart and circulatory physiology · 2013Article
- Induced overexpression of Na(+)/Ca(2+) exchanger does not aggravate myocardial dysfunction induced by transverse aortic constriction.Journal of cardiac failure · 2013Article
- Phospholemman deficiency in postinfarct hearts: enhanced contractility but increased mortality.Clinical and translational science · 2012Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Phospholemman (PLM) regulates contractility and Ca(2+) homeostasis in cardiac myocytes. We characterized excitation-contraction coupling in myocytes isolated from PLM-deficient mice backbred to a pure congenic C57BL/6 background. Cell length, cell width, and whole cell capacitance were not different between wild-type and PLM-null myocytes. Compared with wild-type myocytes, Western blots indicated total absence of PLM but no changes in Na(+)/Ca(2+) exchanger, sarcoplasmic reticulum (SR) Ca(2+)-ATPase, alpha(1)-subunit of Na(+)-K(+)-ATPase, and calsequestrin levels in PLM-null myocytes. At 5 mM extracellular Ca(2+) concentration ([Ca(2+)](o)), contraction and cytosolic [Ca(2+)] ([Ca(2+)](i)) transient amplitudes and SR Ca(2+) contents in PLM-null myocytes were significantly (P < 0.0004) higher than wild-type myocytes, whereas the converse was true at 0.6 mM [Ca(2+)](o). This pattern of contractile and [Ca(2+)](i) transient abnormalities in PLM-null myocytes mimics that observed in adult rat myocytes overexpressing the cardiac Na(+)/Ca(2+) exchanger. Indeed, we have previously reported that Na(+)/Ca(2+) exchange currents were higher in PLM-null myocytes. Activation of protein kinase A resulted in increased inotropy such that there were no longer any contractility differences between the stimulated wild-type and PLM-null myocytes. Protein kinase C stimulation resulted in decreased contractility in both wild-type and PLM-null myocytes. Resting membrane potential and action potential amplitudes were similar, but action potential duration was much prolonged (P < 0.04) in PLM-null myocytes. Whole cell Ca(2+) current densities were similar between wild-type and PLM-null myocytes, as were the fast- and slow-inactivation time constants. We conclude that a major function of PLM is regulation of cardiac contractility and Ca(2+) fluxes, likely by modulating Na(+)/Ca(2+) exchange activity.
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