Nature Communications (Oct 2016)
Disulfide-activated protein kinase G Iα regulates cardiac diastolic relaxation and fine-tunes the Frank–Starling response
- Jenna Scotcher,
- Oleksandra Prysyazhna,
- Andrii Boguslavskyi,
- Kornel Kistamas,
- Natasha Hadgraft,
- Eva D. Martin,
- Jenny Worthington,
- Olena Rudyk,
- Pedro Rodriguez Cutillas,
- Friederike Cuello,
- Michael J. Shattock,
- Michael S. Marber,
- Maria R. Conte,
- Adam Greenstein,
- David J. Greensmith,
- Luigi Venetucci,
- John F. Timms,
- Philip Eaton
Affiliations
- Jenna Scotcher
- Cardiovascular Division, King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St Thomas’ Hospital
- Oleksandra Prysyazhna
- Cardiovascular Division, King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St Thomas’ Hospital
- Andrii Boguslavskyi
- Cardiovascular Division, King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St Thomas’ Hospital
- Kornel Kistamas
- Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, Core Technology Facility, University of Manchester
- Natasha Hadgraft
- Biomedical Research Centre, University of Salford, Peel Building
- Eva D. Martin
- Cardiovascular Division, King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St Thomas’ Hospital
- Jenny Worthington
- Institute for Women’s Health, University College London
- Olena Rudyk
- Cardiovascular Division, King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St Thomas’ Hospital
- Pedro Rodriguez Cutillas
- Barts Cancer Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square
- Friederike Cuello
- Department of Experimental Pharmacology and Toxicology, Cardiovascular Research Centre, University Medical Center Hamburg-Eppendorf, Hamburg, DZHK (German Centre for Cardiovascular Research), Partner site Hamburg/Kiel/Lübeck
- Michael J. Shattock
- Cardiovascular Division, King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St Thomas’ Hospital
- Michael S. Marber
- Cardiovascular Division, King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St Thomas’ Hospital
- Maria R. Conte
- Randall Division of Cell and Molecular Biophysics, King’s College London, New Hunt’s House, Guy’s Campus
- Adam Greenstein
- Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, Core Technology Facility, University of Manchester
- David J. Greensmith
- Biomedical Research Centre, University of Salford, Peel Building
- Luigi Venetucci
- Institute of Cardiovascular Sciences, Manchester Academic Health Science Centre, Core Technology Facility, University of Manchester
- John F. Timms
- Institute for Women’s Health, University College London
- Philip Eaton
- Cardiovascular Division, King’s College London, The British Heart Foundation Centre of Excellence, The Rayne Institute, St Thomas’ Hospital
- DOI
- https://doi.org/10.1038/ncomms13187
- Journal volume & issue
-
Vol. 7,
no. 1
pp. 1 – 11
Abstract
The stroke volume of the heart increases in response to an increase in the blood volume filling the heart. Here the authors reveal that this coordinated process is mediated in part by oxidative activation of the protein kinase G Iα, which phosphorylates phospholamban to enhance diastolic relaxation in mice.
