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β3-Adrenoceptor redistribution impairs NO/cGMP/PDE2 signalling in failing cardiomyocytes

Standard

β3-Adrenoceptor redistribution impairs NO/cGMP/PDE2 signalling in failing cardiomyocytes. / Schobesberger, Sophie; Wright, Peter T; Poulet, Claire; Sanchez Alonso Mardones, Jose L; Mansfield, Catherine; Friebe, Andreas; Harding, Sian E; Balligand, Jean-Luc; Nikolaev, Viacheslav O; Gorelik, Julia.

In: ELIFE, Vol. 9, 31.03.2020.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Schobesberger, S, Wright, PT, Poulet, C, Sanchez Alonso Mardones, JL, Mansfield, C, Friebe, A, Harding, SE, Balligand, J-L, Nikolaev, VO & Gorelik, J 2020, 'β3-Adrenoceptor redistribution impairs NO/cGMP/PDE2 signalling in failing cardiomyocytes', ELIFE, vol. 9. https://doi.org/10.7554/eLife.52221

APA

Schobesberger, S., Wright, P. T., Poulet, C., Sanchez Alonso Mardones, J. L., Mansfield, C., Friebe, A., Harding, S. E., Balligand, J-L., Nikolaev, V. O., & Gorelik, J. (2020). β3-Adrenoceptor redistribution impairs NO/cGMP/PDE2 signalling in failing cardiomyocytes. ELIFE, 9. https://doi.org/10.7554/eLife.52221

Vancouver

Schobesberger S, Wright PT, Poulet C, Sanchez Alonso Mardones JL, Mansfield C, Friebe A et al. β3-Adrenoceptor redistribution impairs NO/cGMP/PDE2 signalling in failing cardiomyocytes. ELIFE. 2020 Mar 31;9. https://doi.org/10.7554/eLife.52221

Bibtex

@article{e9108de977564544bba0b3ae9f0a5646,
title = "β3-Adrenoceptor redistribution impairs NO/cGMP/PDE2 signalling in failing cardiomyocytes",
abstract = "Cardiomyocyte β3-adrenoceptors (β3-ARs) coupled to soluble guanylyl cyclase (sGC)-dependent production of the second messenger 3',5'-cyclic guanosine monophosphate (cGMP) have been shown to protect from heart failure. However, the exact localization of these receptors to fine membrane structures and subcellular compartmentation of β3-AR/cGMP signals underpinning this protection in health and disease remain elusive. Here, we used a F{\"o}rster Resonance Energy Transfer (FRET)-based cGMP biosensor combined with scanning ion conductance microscopy (SICM) to show that functional β3-ARs are mostly confined to the T-tubules of healthy rat cardiomyocytes. Heart failure, induced via myocardial infarction, causes a decrease of the cGMP levels generated by these receptors and a change of subcellular cGMP compartmentation. Furthermore, attenuated cGMP signals led to impaired phosphodiesterase two dependent negative cGMP-to-cAMP cross-talk. In conclusion, topographic and functional reorganization of the β3-AR/cGMP signalosome happens in heart failure and should be considered when designing new therapies acting via this receptor.",
author = "Sophie Schobesberger and Wright, {Peter T} and Claire Poulet and {Sanchez Alonso Mardones}, {Jose L} and Catherine Mansfield and Andreas Friebe and Harding, {Sian E} and Jean-Luc Balligand and Nikolaev, {Viacheslav O} and Julia Gorelik",
note = "{\textcopyright} 2020, Schobesberger et al.",
year = "2020",
month = mar,
day = "31",
doi = "10.7554/eLife.52221",
language = "English",
volume = "9",
journal = "ELIFE",
issn = "2050-084X",
publisher = "eLife Sciences Publications",

}

RIS

TY - JOUR

T1 - β3-Adrenoceptor redistribution impairs NO/cGMP/PDE2 signalling in failing cardiomyocytes

AU - Schobesberger, Sophie

AU - Wright, Peter T

AU - Poulet, Claire

AU - Sanchez Alonso Mardones, Jose L

AU - Mansfield, Catherine

AU - Friebe, Andreas

AU - Harding, Sian E

AU - Balligand, Jean-Luc

AU - Nikolaev, Viacheslav O

AU - Gorelik, Julia

N1 - © 2020, Schobesberger et al.

PY - 2020/3/31

Y1 - 2020/3/31

N2 - Cardiomyocyte β3-adrenoceptors (β3-ARs) coupled to soluble guanylyl cyclase (sGC)-dependent production of the second messenger 3',5'-cyclic guanosine monophosphate (cGMP) have been shown to protect from heart failure. However, the exact localization of these receptors to fine membrane structures and subcellular compartmentation of β3-AR/cGMP signals underpinning this protection in health and disease remain elusive. Here, we used a Förster Resonance Energy Transfer (FRET)-based cGMP biosensor combined with scanning ion conductance microscopy (SICM) to show that functional β3-ARs are mostly confined to the T-tubules of healthy rat cardiomyocytes. Heart failure, induced via myocardial infarction, causes a decrease of the cGMP levels generated by these receptors and a change of subcellular cGMP compartmentation. Furthermore, attenuated cGMP signals led to impaired phosphodiesterase two dependent negative cGMP-to-cAMP cross-talk. In conclusion, topographic and functional reorganization of the β3-AR/cGMP signalosome happens in heart failure and should be considered when designing new therapies acting via this receptor.

AB - Cardiomyocyte β3-adrenoceptors (β3-ARs) coupled to soluble guanylyl cyclase (sGC)-dependent production of the second messenger 3',5'-cyclic guanosine monophosphate (cGMP) have been shown to protect from heart failure. However, the exact localization of these receptors to fine membrane structures and subcellular compartmentation of β3-AR/cGMP signals underpinning this protection in health and disease remain elusive. Here, we used a Förster Resonance Energy Transfer (FRET)-based cGMP biosensor combined with scanning ion conductance microscopy (SICM) to show that functional β3-ARs are mostly confined to the T-tubules of healthy rat cardiomyocytes. Heart failure, induced via myocardial infarction, causes a decrease of the cGMP levels generated by these receptors and a change of subcellular cGMP compartmentation. Furthermore, attenuated cGMP signals led to impaired phosphodiesterase two dependent negative cGMP-to-cAMP cross-talk. In conclusion, topographic and functional reorganization of the β3-AR/cGMP signalosome happens in heart failure and should be considered when designing new therapies acting via this receptor.

U2 - 10.7554/eLife.52221

DO - 10.7554/eLife.52221

M3 - SCORING: Journal article

C2 - 32228862

VL - 9

JO - ELIFE

JF - ELIFE

SN - 2050-084X

ER -