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Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response

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Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response. / Scotcher, Jenna; Prysyazhna, Oleksandra; Boguslavskyi, Andrii; Kistamas, Kornel; Hadgraft, Natasha; Martin, Eva D; Worthington, Jenny; Rudyk, Olena; Rodriguez Cutillas, Pedro; Cuello, Friederike; Shattock, Michael J; Marber, Michael S; Conte, Maria R; Greenstein, Adam; Greensmith, David J; Venetucci, Luigi; Timms, John F; Eaton, Philip.

in: NAT COMMUN, Jahrgang 7, 26.10.2016, S. 13187.

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

Harvard

Scotcher, J, Prysyazhna, O, Boguslavskyi, A, Kistamas, K, Hadgraft, N, Martin, ED, Worthington, J, Rudyk, O, Rodriguez Cutillas, P, Cuello, F, Shattock, MJ, Marber, MS, Conte, MR, Greenstein, A, Greensmith, DJ, Venetucci, L, Timms, JF & Eaton, P 2016, 'Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response', NAT COMMUN, Jg. 7, S. 13187. https://doi.org/10.1038/ncomms13187

APA

Scotcher, J., Prysyazhna, O., Boguslavskyi, A., Kistamas, K., Hadgraft, N., Martin, E. D., Worthington, J., Rudyk, O., Rodriguez Cutillas, P., Cuello, F., Shattock, M. J., Marber, M. S., Conte, M. R., Greenstein, A., Greensmith, D. J., Venetucci, L., Timms, J. F., & Eaton, P. (2016). Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response. NAT COMMUN, 7, 13187. https://doi.org/10.1038/ncomms13187

Vancouver

Scotcher J, Prysyazhna O, Boguslavskyi A, Kistamas K, Hadgraft N, Martin ED et al. Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response. NAT COMMUN. 2016 Okt 26;7:13187. https://doi.org/10.1038/ncomms13187

Bibtex

@article{a7461ad4ee084f1987fab84f02be935d,
title = "Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response",
abstract = "The Frank-Starling mechanism allows the amount of blood entering the heart from the veins to be precisely matched with the amount pumped out to the arterial circulation. As the heart fills with blood during diastole, the myocardium is stretched and oxidants are produced. Here we show that protein kinase G Iα (PKGIα) is oxidant-activated during stretch and this form of the kinase selectively phosphorylates cardiac phospholamban Ser16-a site important for diastolic relaxation. We find that hearts of Cys42Ser PKGIα knock-in (KI) mice, which are resistant to PKGIα oxidation, have diastolic dysfunction and a diminished ability to couple ventricular filling with cardiac output on a beat-to-beat basis. Intracellular calcium dynamics of ventricular myocytes isolated from KI hearts are altered in a manner consistent with impaired relaxation and contractile function. We conclude that oxidation of PKGIα during myocardial stretch is crucial for diastolic relaxation and fine-tunes the Frank-Starling response.",
author = "Jenna Scotcher and Oleksandra Prysyazhna and Andrii Boguslavskyi and Kornel Kistamas and Natasha Hadgraft and Martin, {Eva D} and Jenny Worthington and Olena Rudyk and {Rodriguez Cutillas}, Pedro and Friederike Cuello and Shattock, {Michael J} and Marber, {Michael S} and Conte, {Maria R} and Adam Greenstein and Greensmith, {David J} and Luigi Venetucci and Timms, {John F} and Philip Eaton",
year = "2016",
month = oct,
day = "26",
doi = "10.1038/ncomms13187",
language = "English",
volume = "7",
pages = "13187",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",

}

RIS

TY - JOUR

T1 - Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank-Starling response

AU - Scotcher, Jenna

AU - Prysyazhna, Oleksandra

AU - Boguslavskyi, Andrii

AU - Kistamas, Kornel

AU - Hadgraft, Natasha

AU - Martin, Eva D

AU - Worthington, Jenny

AU - Rudyk, Olena

AU - Rodriguez Cutillas, Pedro

AU - Cuello, Friederike

AU - Shattock, Michael J

AU - Marber, Michael S

AU - Conte, Maria R

AU - Greenstein, Adam

AU - Greensmith, David J

AU - Venetucci, Luigi

AU - Timms, John F

AU - Eaton, Philip

PY - 2016/10/26

Y1 - 2016/10/26

N2 - The Frank-Starling mechanism allows the amount of blood entering the heart from the veins to be precisely matched with the amount pumped out to the arterial circulation. As the heart fills with blood during diastole, the myocardium is stretched and oxidants are produced. Here we show that protein kinase G Iα (PKGIα) is oxidant-activated during stretch and this form of the kinase selectively phosphorylates cardiac phospholamban Ser16-a site important for diastolic relaxation. We find that hearts of Cys42Ser PKGIα knock-in (KI) mice, which are resistant to PKGIα oxidation, have diastolic dysfunction and a diminished ability to couple ventricular filling with cardiac output on a beat-to-beat basis. Intracellular calcium dynamics of ventricular myocytes isolated from KI hearts are altered in a manner consistent with impaired relaxation and contractile function. We conclude that oxidation of PKGIα during myocardial stretch is crucial for diastolic relaxation and fine-tunes the Frank-Starling response.

AB - The Frank-Starling mechanism allows the amount of blood entering the heart from the veins to be precisely matched with the amount pumped out to the arterial circulation. As the heart fills with blood during diastole, the myocardium is stretched and oxidants are produced. Here we show that protein kinase G Iα (PKGIα) is oxidant-activated during stretch and this form of the kinase selectively phosphorylates cardiac phospholamban Ser16-a site important for diastolic relaxation. We find that hearts of Cys42Ser PKGIα knock-in (KI) mice, which are resistant to PKGIα oxidation, have diastolic dysfunction and a diminished ability to couple ventricular filling with cardiac output on a beat-to-beat basis. Intracellular calcium dynamics of ventricular myocytes isolated from KI hearts are altered in a manner consistent with impaired relaxation and contractile function. We conclude that oxidation of PKGIα during myocardial stretch is crucial for diastolic relaxation and fine-tunes the Frank-Starling response.

U2 - 10.1038/ncomms13187

DO - 10.1038/ncomms13187

M3 - SCORING: Journal article

C2 - 27782102

VL - 7

SP - 13187

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

ER -