Load-dependent effects of apelin on murine cardiomyocytes

@article{Peyronnet2017LoaddependentEO,
  title={Load-dependent effects of apelin on murine cardiomyocytes},
  author={R{\'e}mi Peyronnet and Christian Bollensdorff and Rebecca A. Capel and Eva A. Rog-Zielinska and Christopher E. Woods and David N Charo and Oleg N. Lookin and Giovanni Fajardo and Michael Y. Ho and Thomas Quertermous and Euan A. Ashley and Peter Kohl},
  journal={Progress in Biophysics and Molecular Biology},
  year={2017},
  volume={130},
  pages={333 - 343}
}
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17 Citations
Background Citations
4
Methods Citations
5

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17 Citations

Apelin and APJ orchestrate complex tissue-specific control of cardiomyocyte hypertrophy and contractility in the hypertrophy-heart failure transition.
TLDR
The data establish thatAPJ stretch transduction is mediated specifically by myocardial APJ, that APJ is necessary for stretch-induced increases in contractility, and that apelin opposes APJ's stretch-mediated hypertrophy signaling by lowering Ca2+ transients while maintaining contractility through myofilament Ca2- sensitization.
Stimulation of TRPA1 attenuates ischemia-induced cardiomyocyte cell death through an eNOS-mediated mechanism
TLDR
It is demonstrated that TRPA1 stimulation with AITC results in phosphorylation of protein kinase B (Akt) and endothelial NOS (eNOS) concomitantly with NO production in a concentration- and time-dependent manner and the presence and activation ofTRPA1 promotes CM survival and viability following ischemic insult via a mechanism partially dependent upon eNOS.
Cardiac Electrophysiological Effects of Light-Activated Chloride Channels
TLDR
The results show that GtACR1 inhibition of AP generation is caused by cell depolarization, which does not address the need for optogenetic silencing through physiological means, but is a potentially attractive tool for activating cardiomyocytes by transient light-induced depolarizations.
Single cardiomyocytes from papillary muscles show lower preload-dependent activation of force compared to cardiomyocytes from the left ventricular free wall.
Ischemia Enhances the Acute Stretch-Induced Increase in Calcium Spark Rate in Ventricular Myocytes
TLDR
Ischemia enhances the stretch- induced increase of Ca2+ sparks in ventricular myocytes, with an associated enhancement of stretch-induced ROS production, which may be important for premature excitation and/or in the development of an arrhythmogenic substrate in acute regional ischemia.
A novel cyclic biased agonist of the apelin receptor, MM07, is disease modifying in the rat monocrotaline model of pulmonary arterial hypertension
TLDR
It is hypothesised that a G protein‐biased apelin analogue MM07, which is more stable than the endogenous apelin peptide, may be beneficial in this condition with the advantage of reduced β‐arrestin‐mediated receptor internalisation with chronic use.
Consecutive-Day Ventricular and Atrial Cardiomyocyte Isolations from the Same Heart: Shifting the Cost–Benefit Balance of Cardiac Primary Cell Research
TLDR
A method of multi-day CM isolation from one animal heart, yielding calcium-tolerant ventricular and atrial CM and opening the doors to novel experimental designs, including exploring same-heart regional differences.
Myocardial slices come to age: an intermediate complexity in vitro cardiac model for translational research
TLDR
This review examines myocardial slices, a novel model in the translational arena, and interrogates the technological developments that have permitted slices to be cultured chronically in vitro while preserving the functional and structural phenotype.
Beat-by-Beat Cardiomyocyte T-Tubule Deformation Drives Tubular Content Exchange
TLDR
The data confirm the existence of an advective component to TT content exchange, which points toward a novel mechanism of cardiac autoregulation, whereby the previously implied increased propensity for TT luminal concentration imbalances at high electrical stimulation rates would be countered by elevated advection-assisted diffusion at high mechanical beating rates.
Potassium channel-based optogenetic silencing
TLDR
A genetically-encoded two-protein system that enables silencing of excitable cells such as neurons and cardiomyocytes using blue light, and its utility both in vitro and In vivo is introduced.
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TLDR
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