Nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated calcium signaling and arrhythmias in the heart evoked by β-adrenergic stimulation

Standard

Nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated calcium signaling and arrhythmias in the heart evoked by β-adrenergic stimulation. / Nebel, Merle; Schwoerer, Alexander P; Warszta, Dominik; Siebrands, Cornelia C; Limbrock, Ann-Christin; Swarbrick, Joanna M; Fliegert, Ralf; Weber, Karin; Bruhn, Sören; Hohenegger, Martin; Geisler, Anne; Herich, Lena; Schlegel, Susan; Carrier, Lucie; Eschenhagen, Thomas; Potter, Barry V L; Ehmke, Heimo; Guse, Andreas H.

in: J BIOL CHEM, Jahrgang 288, Nr. 22, 31.05.2013, S. 16017-30.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Nebel, M, Schwoerer, AP, Warszta, D, Siebrands, CC, Limbrock, A-C, Swarbrick, JM, Fliegert, R, Weber, K, Bruhn, S, Hohenegger, M, Geisler, A, Herich, L, Schlegel, S, Carrier, L, Eschenhagen, T, Potter, BVL, Ehmke, H & Guse, AH 2013, 'Nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated calcium signaling and arrhythmias in the heart evoked by β-adrenergic stimulation', J BIOL CHEM, Jg. 288, Nr. 22, S. 16017-30. https://doi.org/10.1074/jbc.M112.441246

APA

Nebel, M., Schwoerer, A. P., Warszta, D., Siebrands, C. C., Limbrock, A-C., Swarbrick, J. M., Fliegert, R., Weber, K., Bruhn, S., Hohenegger, M., Geisler, A., Herich, L., Schlegel, S., Carrier, L., Eschenhagen, T., Potter, B. V. L., Ehmke, H., & Guse, A. H. (2013). Nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated calcium signaling and arrhythmias in the heart evoked by β-adrenergic stimulation. J BIOL CHEM, 288(22), 16017-30. https://doi.org/10.1074/jbc.M112.441246

Vancouver

Bibtex

@article{f61992ed69c541ca8257e89ed8cc2c47,
title = "Nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated calcium signaling and arrhythmias in the heart evoked by β-adrenergic stimulation",
abstract = "Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most potent Ca(2+)-releasing second messenger known to date. Here, we report a new role for NAADP in arrhythmogenic Ca(2+) release in cardiac myocytes evoked by β-adrenergic stimulation. Infusion of NAADP into intact cardiac myocytes induced global Ca(2+) signals sensitive to inhibitors of both acidic Ca(2+) stores and ryanodine receptors and to NAADP antagonist BZ194. Furthermore, in electrically paced cardiac myocytes BZ194 blocked spontaneous diastolic Ca(2+) transients caused by high concentrations of the β-adrenergic agonist isoproterenol. Ca(2+) transients were recorded both as increases of the free cytosolic Ca(2+) concentration and as decreases of the sarcoplasmic luminal Ca(2+) concentration. Importantly, NAADP antagonist BZ194 largely ameliorated isoproterenol-induced arrhythmias in awake mice. We provide strong evidence that NAADP-mediated modulation of couplon activity plays a role for triggering spontaneous diastolic Ca(2+) transients in isolated cardiac myocytes and arrhythmias in the intact animal. Thus, NAADP signaling appears an attractive novel target for antiarrhythmic therapy.",
keywords = "Adrenergic beta-Agonists, Animals, Arrhythmias, Cardiac, Calcium Signaling, Cells, Cultured, Isoproterenol, Mice, Myocardium, Myocytes, Cardiac, NADP, Nicotinic Acids, Ryanodine Receptor Calcium Release Channel, Sarcoplasmic Reticulum",
author = "Merle Nebel and Schwoerer, {Alexander P} and Dominik Warszta and Siebrands, {Cornelia C} and Ann-Christin Limbrock and Swarbrick, {Joanna M} and Ralf Fliegert and Karin Weber and S{\"o}ren Bruhn and Martin Hohenegger and Anne Geisler and Lena Herich and Susan Schlegel and Lucie Carrier and Thomas Eschenhagen and Potter, {Barry V L} and Heimo Ehmke and Guse, {Andreas H}",
year = "2013",
month = may,
day = "31",
doi = "10.1074/jbc.M112.441246",
language = "English",
volume = "288",
pages = "16017--30",
journal = "J BIOL CHEM",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "22",

}

RIS

TY - JOUR

T1 - Nicotinic acid adenine dinucleotide phosphate (NAADP)-mediated calcium signaling and arrhythmias in the heart evoked by β-adrenergic stimulation

AU - Nebel, Merle

AU - Schwoerer, Alexander P

AU - Warszta, Dominik

AU - Siebrands, Cornelia C

AU - Limbrock, Ann-Christin

AU - Swarbrick, Joanna M

AU - Fliegert, Ralf

AU - Weber, Karin

AU - Bruhn, Sören

AU - Hohenegger, Martin

AU - Geisler, Anne

AU - Herich, Lena

AU - Schlegel, Susan

AU - Carrier, Lucie

AU - Eschenhagen, Thomas

AU - Potter, Barry V L

AU - Ehmke, Heimo

AU - Guse, Andreas H

PY - 2013/5/31

Y1 - 2013/5/31

N2 - Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most potent Ca(2+)-releasing second messenger known to date. Here, we report a new role for NAADP in arrhythmogenic Ca(2+) release in cardiac myocytes evoked by β-adrenergic stimulation. Infusion of NAADP into intact cardiac myocytes induced global Ca(2+) signals sensitive to inhibitors of both acidic Ca(2+) stores and ryanodine receptors and to NAADP antagonist BZ194. Furthermore, in electrically paced cardiac myocytes BZ194 blocked spontaneous diastolic Ca(2+) transients caused by high concentrations of the β-adrenergic agonist isoproterenol. Ca(2+) transients were recorded both as increases of the free cytosolic Ca(2+) concentration and as decreases of the sarcoplasmic luminal Ca(2+) concentration. Importantly, NAADP antagonist BZ194 largely ameliorated isoproterenol-induced arrhythmias in awake mice. We provide strong evidence that NAADP-mediated modulation of couplon activity plays a role for triggering spontaneous diastolic Ca(2+) transients in isolated cardiac myocytes and arrhythmias in the intact animal. Thus, NAADP signaling appears an attractive novel target for antiarrhythmic therapy.

AB - Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most potent Ca(2+)-releasing second messenger known to date. Here, we report a new role for NAADP in arrhythmogenic Ca(2+) release in cardiac myocytes evoked by β-adrenergic stimulation. Infusion of NAADP into intact cardiac myocytes induced global Ca(2+) signals sensitive to inhibitors of both acidic Ca(2+) stores and ryanodine receptors and to NAADP antagonist BZ194. Furthermore, in electrically paced cardiac myocytes BZ194 blocked spontaneous diastolic Ca(2+) transients caused by high concentrations of the β-adrenergic agonist isoproterenol. Ca(2+) transients were recorded both as increases of the free cytosolic Ca(2+) concentration and as decreases of the sarcoplasmic luminal Ca(2+) concentration. Importantly, NAADP antagonist BZ194 largely ameliorated isoproterenol-induced arrhythmias in awake mice. We provide strong evidence that NAADP-mediated modulation of couplon activity plays a role for triggering spontaneous diastolic Ca(2+) transients in isolated cardiac myocytes and arrhythmias in the intact animal. Thus, NAADP signaling appears an attractive novel target for antiarrhythmic therapy.

KW - Adrenergic beta-Agonists

KW - Animals

KW - Arrhythmias, Cardiac

KW - Calcium Signaling

KW - Cells, Cultured

KW - Isoproterenol

KW - Mice

KW - Myocardium

KW - Myocytes, Cardiac

KW - NADP

KW - Nicotinic Acids

KW - Ryanodine Receptor Calcium Release Channel

KW - Sarcoplasmic Reticulum

U2 - 10.1074/jbc.M112.441246

DO - 10.1074/jbc.M112.441246

M3 - SCORING: Journal article

C2 - 23564460

VL - 288

SP - 16017

EP - 16030

JO - J BIOL CHEM

JF - J BIOL CHEM

SN - 0021-9258

IS - 22

ER -