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A cardiac pathway of cyclic GMP-independent signaling of guanylyl cyclase A, the receptor for atrial natriuretic peptide.

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A cardiac pathway of cyclic GMP-independent signaling of guanylyl cyclase A, the receptor for atrial natriuretic peptide. / Klaiber, Michael; Dankworth, Beatrice; Kruse, Martin; Hartmann, Michael; Nikolaev, Viacheslav O; Yang, Ruey-Bing; Völker, Katharina; Gassner, Birgit; Oberwinkler, Heike; Feil, Robert; Freichel, Marc; Groschner, Klaus; Skryabin, Boris V; Frantz, Stefan; Birnbaumer, Lutz; Pongs, Olaf; Kuhn, Michaela.

in: P NATL ACAD SCI USA, Jahrgang 108, Nr. 45, 45, 2011, S. 18500-18505.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Klaiber, M, Dankworth, B, Kruse, M, Hartmann, M, Nikolaev, VO, Yang, R-B, Völker, K, Gassner, B, Oberwinkler, H, Feil, R, Freichel, M, Groschner, K, Skryabin, BV, Frantz, S, Birnbaumer, L, Pongs, O & Kuhn, M 2011, 'A cardiac pathway of cyclic GMP-independent signaling of guanylyl cyclase A, the receptor for atrial natriuretic peptide.', P NATL ACAD SCI USA, Jg. 108, Nr. 45, 45, S. 18500-18505. <http://www.ncbi.nlm.nih.gov/pubmed/22027011?dopt=Citation>

APA

Klaiber, M., Dankworth, B., Kruse, M., Hartmann, M., Nikolaev, V. O., Yang, R-B., Völker, K., Gassner, B., Oberwinkler, H., Feil, R., Freichel, M., Groschner, K., Skryabin, B. V., Frantz, S., Birnbaumer, L., Pongs, O., & Kuhn, M. (2011). A cardiac pathway of cyclic GMP-independent signaling of guanylyl cyclase A, the receptor for atrial natriuretic peptide. P NATL ACAD SCI USA, 108(45), 18500-18505. [45]. http://www.ncbi.nlm.nih.gov/pubmed/22027011?dopt=Citation

Vancouver

Klaiber M, Dankworth B, Kruse M, Hartmann M, Nikolaev VO, Yang R-B et al. A cardiac pathway of cyclic GMP-independent signaling of guanylyl cyclase A, the receptor for atrial natriuretic peptide. P NATL ACAD SCI USA. 2011;108(45):18500-18505. 45.

Bibtex

@article{24410ff590014d7c9afcdb215bcd0a96,
title = "A cardiac pathway of cyclic GMP-independent signaling of guanylyl cyclase A, the receptor for atrial natriuretic peptide.",
abstract = "Cardiac atrial natriuretic peptide (ANP) regulates arterial blood pressure, moderates cardiomyocyte growth, and stimulates angiogenesis and metabolism. ANP binds to the transmembrane guanylyl cyclase (GC) receptor, GC-A, to exert its diverse functions. This process involves a cGMP-dependent signaling pathway preventing pathological [Ca(2+)](i) increases in myocytes. In chronic cardiac hypertrophy, however, ANP levels are markedly increased and GC-A/cGMP responses to ANP are blunted due to receptor desensitization. Here we show that, in this situation, ANP binding to GC-A stimulates a unique cGMP-independent signaling pathway in cardiac myocytes, resulting in pathologically elevated intracellular Ca(2+) levels. This pathway involves the activation of Ca(2+)-permeable transient receptor potential canonical 3/6 (TRPC3/C6) cation channels by GC-A, which forms a stable complex with TRPC3/C6 channels. Our results indicate that the resulting cation influx activates voltage-dependent L-type Ca(2+) channels and ultimately increases myocyte Ca(2)(+)(i) levels. These observations reveal a dual role of the ANP/GC-A-signaling pathway in the regulation of cardiac myocyte Ca(2+)(i) homeostasis. Under physiological conditions, activation of a cGMP-dependent pathway moderates the Ca(2+)(i)-enhancing action of hypertrophic factors such as angiotensin II. By contrast, a cGMP-independent pathway predominates under pathophysiological conditions when GC-A is desensitized by high ANP levels. The concomitant rise in [Ca(2+)](i) might increase the propensity to cardiac hypertrophy and arrhythmias.",
keywords = "Animals, Humans, Mice, Cell Line, *Signal Transduction, Cyclic GMP/*metabolism, Atrial Natriuretic Factor/*metabolism, Fluorescence Resonance Energy Transfer, Guanylate Cyclase/*metabolism, Myocardium/*metabolism, Receptors, Atrial Natriuretic Factor/*metabolism, Animals, Humans, Mice, Cell Line, *Signal Transduction, Cyclic GMP/*metabolism, Atrial Natriuretic Factor/*metabolism, Fluorescence Resonance Energy Transfer, Guanylate Cyclase/*metabolism, Myocardium/*metabolism, Receptors, Atrial Natriuretic Factor/*metabolism",
author = "Michael Klaiber and Beatrice Dankworth and Martin Kruse and Michael Hartmann and Nikolaev, {Viacheslav O} and Ruey-Bing Yang and Katharina V{\"o}lker and Birgit Gassner and Heike Oberwinkler and Robert Feil and Marc Freichel and Klaus Groschner and Skryabin, {Boris V} and Stefan Frantz and Lutz Birnbaumer and Olaf Pongs and Michaela Kuhn",
year = "2011",
language = "English",
volume = "108",
pages = "18500--18505",
journal = "P NATL ACAD SCI USA",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "45",

}

RIS

TY - JOUR

T1 - A cardiac pathway of cyclic GMP-independent signaling of guanylyl cyclase A, the receptor for atrial natriuretic peptide.

AU - Klaiber, Michael

AU - Dankworth, Beatrice

AU - Kruse, Martin

AU - Hartmann, Michael

AU - Nikolaev, Viacheslav O

AU - Yang, Ruey-Bing

AU - Völker, Katharina

AU - Gassner, Birgit

AU - Oberwinkler, Heike

AU - Feil, Robert

AU - Freichel, Marc

AU - Groschner, Klaus

AU - Skryabin, Boris V

AU - Frantz, Stefan

AU - Birnbaumer, Lutz

AU - Pongs, Olaf

AU - Kuhn, Michaela

PY - 2011

Y1 - 2011

N2 - Cardiac atrial natriuretic peptide (ANP) regulates arterial blood pressure, moderates cardiomyocyte growth, and stimulates angiogenesis and metabolism. ANP binds to the transmembrane guanylyl cyclase (GC) receptor, GC-A, to exert its diverse functions. This process involves a cGMP-dependent signaling pathway preventing pathological [Ca(2+)](i) increases in myocytes. In chronic cardiac hypertrophy, however, ANP levels are markedly increased and GC-A/cGMP responses to ANP are blunted due to receptor desensitization. Here we show that, in this situation, ANP binding to GC-A stimulates a unique cGMP-independent signaling pathway in cardiac myocytes, resulting in pathologically elevated intracellular Ca(2+) levels. This pathway involves the activation of Ca(2+)-permeable transient receptor potential canonical 3/6 (TRPC3/C6) cation channels by GC-A, which forms a stable complex with TRPC3/C6 channels. Our results indicate that the resulting cation influx activates voltage-dependent L-type Ca(2+) channels and ultimately increases myocyte Ca(2)(+)(i) levels. These observations reveal a dual role of the ANP/GC-A-signaling pathway in the regulation of cardiac myocyte Ca(2+)(i) homeostasis. Under physiological conditions, activation of a cGMP-dependent pathway moderates the Ca(2+)(i)-enhancing action of hypertrophic factors such as angiotensin II. By contrast, a cGMP-independent pathway predominates under pathophysiological conditions when GC-A is desensitized by high ANP levels. The concomitant rise in [Ca(2+)](i) might increase the propensity to cardiac hypertrophy and arrhythmias.

AB - Cardiac atrial natriuretic peptide (ANP) regulates arterial blood pressure, moderates cardiomyocyte growth, and stimulates angiogenesis and metabolism. ANP binds to the transmembrane guanylyl cyclase (GC) receptor, GC-A, to exert its diverse functions. This process involves a cGMP-dependent signaling pathway preventing pathological [Ca(2+)](i) increases in myocytes. In chronic cardiac hypertrophy, however, ANP levels are markedly increased and GC-A/cGMP responses to ANP are blunted due to receptor desensitization. Here we show that, in this situation, ANP binding to GC-A stimulates a unique cGMP-independent signaling pathway in cardiac myocytes, resulting in pathologically elevated intracellular Ca(2+) levels. This pathway involves the activation of Ca(2+)-permeable transient receptor potential canonical 3/6 (TRPC3/C6) cation channels by GC-A, which forms a stable complex with TRPC3/C6 channels. Our results indicate that the resulting cation influx activates voltage-dependent L-type Ca(2+) channels and ultimately increases myocyte Ca(2)(+)(i) levels. These observations reveal a dual role of the ANP/GC-A-signaling pathway in the regulation of cardiac myocyte Ca(2+)(i) homeostasis. Under physiological conditions, activation of a cGMP-dependent pathway moderates the Ca(2+)(i)-enhancing action of hypertrophic factors such as angiotensin II. By contrast, a cGMP-independent pathway predominates under pathophysiological conditions when GC-A is desensitized by high ANP levels. The concomitant rise in [Ca(2+)](i) might increase the propensity to cardiac hypertrophy and arrhythmias.

KW - Animals

KW - Humans

KW - Mice

KW - Cell Line

KW - Signal Transduction

KW - Cyclic GMP/metabolism

KW - Atrial Natriuretic Factor/metabolism

KW - Fluorescence Resonance Energy Transfer

KW - Guanylate Cyclase/metabolism

KW - Myocardium/metabolism

KW - Receptors, Atrial Natriuretic Factor/metabolism

KW - Animals

KW - Humans

KW - Mice

KW - Cell Line

KW - Signal Transduction

KW - Cyclic GMP/metabolism

KW - Atrial Natriuretic Factor/metabolism

KW - Fluorescence Resonance Energy Transfer

KW - Guanylate Cyclase/metabolism

KW - Myocardium/metabolism

KW - Receptors, Atrial Natriuretic Factor/metabolism

M3 - SCORING: Journal article

VL - 108

SP - 18500

EP - 18505

JO - P NATL ACAD SCI USA

JF - P NATL ACAD SCI USA

SN - 0027-8424

IS - 45

M1 - 45

ER -