Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Chemical Synapses

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

Chemical Synapses

Chemical Synapses

Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

MRS2339, a cardiac P2X4 receptor nucleotide activator, improves systolic function in heart failure.

Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents·2026

Same author

Emergent RNA targets in cardiovascular disease: likely candidates for treatment development.

Expert opinion on therapeutic targets·2026

Same author

The medium-chain fatty acid octanoate is a beneficial fuel for the failing heart.

American journal of physiology. Heart and circulatory physiology·2026

Same author

A reproducible and physiologically relevant human iPSC-derived platform for in vitro modeling of the neurocardiac junction.

Molecular therapy : the journal of the American Society of Gene Therapy·2026

Same author

Omics medicine: what the clinicians should know.

European journal of internal medicine·2026

Same author

iPSC-Derived Endothelial Cells as Experimental Models for Predictive and Personalized Strategies in Cardiovascular and Cerebrovascular Disease.

International journal of molecular sciences·2026

Search research articles

Related Experiment Video

Updated: Apr 5, 2026

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

Published on: October 4, 2019

Acetylation mediates Cx43 reduction caused by electrical stimulation.

Viviana Meraviglia¹, Valerio Azzimato², Claudia Colussi³

¹Laboratory of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino IRCCS, Milano, Italy; Center for Biomedicine, European Academy Bozen/Bolzano (EURAC), Bolzano Italy.

Journal of Molecular and Cellular Cardiology

|August 13, 2015

Summary

Electrical stimulation alters cardiomyocyte communication by affecting connexin43 (Cx43) acetylation. This study links electrical activity, histone acetylase (HAT) activity, and Cx43 acetylation to regulate cardiac cell-cell communication.

Keywords:

Acetylation Connexin43 Electrical field stimulation Gap junctions

More Related Videos

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Published on: August 15, 2017

Analyzing the Size, Shape, and Directionality of Networks of Coupled Astrocytes

Analyzing the Size, Shape, and Directionality of Networks of Coupled Astrocytes

Published on: October 4, 2018

Related Experiment Videos

Last Updated: Apr 5, 2026

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

Published on: October 4, 2019

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins

Published on: August 15, 2017

Analyzing the Size, Shape, and Directionality of Networks of Coupled Astrocytes

Analyzing the Size, Shape, and Directionality of Networks of Coupled Astrocytes

Published on: October 4, 2018

Area of Science:

Cardiovascular Biology
Molecular Cardiology
Cellular Electrophysiology

Background:

Cardiomyocyte communication relies on gap junctions (GJ), crucial for coordinated heart function.
Electrical stimulation is known to remodel GJs and alter histone acetylase (HAT) and deacetylase (HDAC) activities.
The direct link between electrical stimulation, GJ function, and acetylation-dependent mechanisms remained unclear.

Purpose of the Study:

To investigate if electrical stimulation modulates GJ-mediated cardiac cell-cell communication through acetylation-dependent pathways.
To determine the role of connexin43 (Cx43) acetylation in response to altered electrical activity.

Main Methods:

HL-1 cardiomyocytes were subjected to field electrical stimulation (0.5 Hz for 24 h).
Assessed Cx43 expression, cell-cell communication, HAT/HDAC activities, and Cx43 acetylation.
Utilized proteasomal inhibitor MG132 and HAT inhibitor Anacardic Acid.
Examined Cx43 acetylation in canine left ventricles from a chronic tachypacing model.

Main Results:

Electrical stimulation reduced Cx43 expression and cell-cell communication.
HDAC activity decreased, leading to increased Cx43 acetylation, without altering Cx43 mRNA levels.
Proteasomal inhibition and HAT inhibition preserved Cx43 levels and communication.
Increased Cx43 acetylation was observed in canine hearts with chronic tachypacing.

Conclusions:

Altered electrical activity regulates cardiomyocyte communication via Cx43 acetylation.
Cx43 acetylation represents a key post-translational modification linking electrical activity to GJ function.
Findings suggest acetylation-dependent mechanisms are critical for adapting cardiac cell-cell communication to electrical remodeling.