Aarhus Universitet

Birgitte Mønster Christensen

Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Standard

Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure. / Sheikh-Hamad, David; Bick, Roger; Wu, Gang-Yi; Christensen, Birgitte Mønster; Razeghi, Peter; Poindexter, Brian; Taegtmeyer, Heinrich; Wamsley, Ann; Padda, Ranjit; Entman, Mark; Nielsen, Søren; Youker, Keith.

I: American Journal of Physiology: Heart and Circulatory Physiology, Bind 285, Nr. 1, 2003, s. H442-8.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Sheikh-Hamad, D, Bick, R, Wu, G-Y, Christensen, BM, Razeghi, P, Poindexter, B, Taegtmeyer, H, Wamsley, A, Padda, R, Entman, M, Nielsen, S & Youker, K 2003, 'Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure', American Journal of Physiology: Heart and Circulatory Physiology, bind 285, nr. 1, s. H442-8. https://doi.org/10.1152/ajpheart.01071.2002

APA

Sheikh-Hamad, D., Bick, R., Wu, G-Y., Christensen, B. M., Razeghi, P., Poindexter, B., ... Youker, K. (2003). Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure. American Journal of Physiology: Heart and Circulatory Physiology, 285(1), H442-8. https://doi.org/10.1152/ajpheart.01071.2002

CBE

Sheikh-Hamad D, Bick R, Wu G-Y, Christensen BM, Razeghi P, Poindexter B, Taegtmeyer H, Wamsley A, Padda R, Entman M, Nielsen S, Youker K. 2003. Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure. American Journal of Physiology: Heart and Circulatory Physiology. 285(1):H442-8. https://doi.org/10.1152/ajpheart.01071.2002

MLA

Sheikh-Hamad, David o.a.. "Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure". American Journal of Physiology: Heart and Circulatory Physiology. 2003, 285(1). H442-8. https://doi.org/10.1152/ajpheart.01071.2002

Vancouver

Sheikh-Hamad D, Bick R, Wu G-Y, Christensen BM, Razeghi P, Poindexter B o.a. Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure. American Journal of Physiology: Heart and Circulatory Physiology. 2003;285(1):H442-8. https://doi.org/10.1152/ajpheart.01071.2002

Author

Sheikh-Hamad, David ; Bick, Roger ; Wu, Gang-Yi ; Christensen, Birgitte Mønster ; Razeghi, Peter ; Poindexter, Brian ; Taegtmeyer, Heinrich ; Wamsley, Ann ; Padda, Ranjit ; Entman, Mark ; Nielsen, Søren ; Youker, Keith. / Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure. I: American Journal of Physiology: Heart and Circulatory Physiology. 2003 ; Bind 285, Nr. 1. s. H442-8.

Bibtex

@article{485219a0cc4611dd9710000ea68e967b,
title = "Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure",
abstract = "Cardiomyocytes of the failing heart undergo profound phenotypic and structural changes that are accompanied by variations in the genetic program and profile of calcium homeostatic proteins. The underlying mechanisms for these changes remain unclear. Because the mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) is expressed in the heart, we reasoned that STC1 might play a role in the adaptive-maladaptive processes that lead to the heart failure phenotype. We examined the expression and localization of STC1 in cardiac tissue of patients with advanced heart failure before and after mechanical unloading using a left ventricular assist device (LVAD), and we compared the results with those of normal heart tissue. STC1 protein is markedly upregulated in cardiomyocytes and arterial walls of failing hearts pre-LVAD and is strikingly reduced after LVAD treatment. STC1 is diffusely expressed in cardiomyocytes, although nuclear predominance is apparent. Addition of recombinant STC1 to the medium of cultured rat cardiomyocytes slows their endogenous beating rate and diminishes the rise in intracellular calcium with each contraction. Furthermore, using whole cell patch-clamp studies in cultured rat cardiomyocytes, we find that addition of STC1 to the bath causes reversible inhibition of transmembrane calcium currents through L-channels. Our data suggest differential regulation of myocardial STC1 protein expression in heart failure. In addition, STC1 may regulate calcium currents in cardiomyocytes and may contribute to the alterations in calcium homeostasis of the failing heart.",
keywords = "Animals, Calcium, Calcium Channel Blockers, Calcium Channels, L-Type, Cells, Cultured, Coronary Vessels, Glycoproteins, Heart Failure, Homeostasis, Hormones, Humans, Immunohistochemistry, In Situ Hybridization, Muscle, Smooth, Vascular, Myocardium, Myocytes, Cardiac, Nimodipine, Rats, Reverse Transcriptase Polymerase Chain Reaction, Spectrometry, Fluorescence, Ventricular Function, Left",
author = "David Sheikh-Hamad and Roger Bick and Gang-Yi Wu and Christensen, {Birgitte M{\o}nster} and Peter Razeghi and Brian Poindexter and Heinrich Taegtmeyer and Ann Wamsley and Ranjit Padda and Mark Entman and S{\o}ren Nielsen and Keith Youker",
year = "2003",
doi = "10.1152/ajpheart.01071.2002",
language = "English",
volume = "285",
pages = "H442--8",
journal = "American Journal of Physiology: Heart and Circulatory Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "1",

}

RIS

TY - JOUR

T1 - Stanniocalcin-1 is a naturally occurring L-channel inhibitor in cardiomyocytes: relevance to human heart failure

AU - Sheikh-Hamad, David

AU - Bick, Roger

AU - Wu, Gang-Yi

AU - Christensen, Birgitte Mønster

AU - Razeghi, Peter

AU - Poindexter, Brian

AU - Taegtmeyer, Heinrich

AU - Wamsley, Ann

AU - Padda, Ranjit

AU - Entman, Mark

AU - Nielsen, Søren

AU - Youker, Keith

PY - 2003

Y1 - 2003

N2 - Cardiomyocytes of the failing heart undergo profound phenotypic and structural changes that are accompanied by variations in the genetic program and profile of calcium homeostatic proteins. The underlying mechanisms for these changes remain unclear. Because the mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) is expressed in the heart, we reasoned that STC1 might play a role in the adaptive-maladaptive processes that lead to the heart failure phenotype. We examined the expression and localization of STC1 in cardiac tissue of patients with advanced heart failure before and after mechanical unloading using a left ventricular assist device (LVAD), and we compared the results with those of normal heart tissue. STC1 protein is markedly upregulated in cardiomyocytes and arterial walls of failing hearts pre-LVAD and is strikingly reduced after LVAD treatment. STC1 is diffusely expressed in cardiomyocytes, although nuclear predominance is apparent. Addition of recombinant STC1 to the medium of cultured rat cardiomyocytes slows their endogenous beating rate and diminishes the rise in intracellular calcium with each contraction. Furthermore, using whole cell patch-clamp studies in cultured rat cardiomyocytes, we find that addition of STC1 to the bath causes reversible inhibition of transmembrane calcium currents through L-channels. Our data suggest differential regulation of myocardial STC1 protein expression in heart failure. In addition, STC1 may regulate calcium currents in cardiomyocytes and may contribute to the alterations in calcium homeostasis of the failing heart.

AB - Cardiomyocytes of the failing heart undergo profound phenotypic and structural changes that are accompanied by variations in the genetic program and profile of calcium homeostatic proteins. The underlying mechanisms for these changes remain unclear. Because the mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) is expressed in the heart, we reasoned that STC1 might play a role in the adaptive-maladaptive processes that lead to the heart failure phenotype. We examined the expression and localization of STC1 in cardiac tissue of patients with advanced heart failure before and after mechanical unloading using a left ventricular assist device (LVAD), and we compared the results with those of normal heart tissue. STC1 protein is markedly upregulated in cardiomyocytes and arterial walls of failing hearts pre-LVAD and is strikingly reduced after LVAD treatment. STC1 is diffusely expressed in cardiomyocytes, although nuclear predominance is apparent. Addition of recombinant STC1 to the medium of cultured rat cardiomyocytes slows their endogenous beating rate and diminishes the rise in intracellular calcium with each contraction. Furthermore, using whole cell patch-clamp studies in cultured rat cardiomyocytes, we find that addition of STC1 to the bath causes reversible inhibition of transmembrane calcium currents through L-channels. Our data suggest differential regulation of myocardial STC1 protein expression in heart failure. In addition, STC1 may regulate calcium currents in cardiomyocytes and may contribute to the alterations in calcium homeostasis of the failing heart.

KW - Animals

KW - Calcium

KW - Calcium Channel Blockers

KW - Calcium Channels, L-Type

KW - Cells, Cultured

KW - Coronary Vessels

KW - Glycoproteins

KW - Heart Failure

KW - Homeostasis

KW - Hormones

KW - Humans

KW - Immunohistochemistry

KW - In Situ Hybridization

KW - Muscle, Smooth, Vascular

KW - Myocardium

KW - Myocytes, Cardiac

KW - Nimodipine

KW - Rats

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Spectrometry, Fluorescence

KW - Ventricular Function, Left

U2 - 10.1152/ajpheart.01071.2002

DO - 10.1152/ajpheart.01071.2002

M3 - Journal article

VL - 285

SP - H442-8

JO - American Journal of Physiology: Heart and Circulatory Physiology

JF - American Journal of Physiology: Heart and Circulatory Physiology

SN - 0363-6135

IS - 1

ER -