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Multicellular organisms employ a variety of ways for cells to communicate with each other. Gap junctions are specialized proteins that form pores between neighboring cells in animals, connecting the cytoplasm between the two, and allowing for the exchange of molecules and ions. They are found in a wide range of invertebrate and vertebrate species, mediate numerous functions including cell differentiation and development, and are associated with numerous human diseases, including cardiac and...

Gap Junctions

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Adrenergic control of cardiac gap junction function and expression.

Aida Salameh¹, Stefan Dhein

¹Clinic for Paediatric Cardiology, Heart Centre, University of Leipzig, Strümpellstraße. 39, 04289, Leipzig, Germany. aida.salameh@med.uni-leipzig.de

Naunyn-Schmiedeberg'S Archives of Pharmacology

|February 15, 2011

Summary

Cardiac adrenoceptors regulate electrical communication via connexins (Cx). Chronic adrenergic stimulation alters Cx43 expression, impacting cardiac function and potentially contributing to arrhythmias and hypertrophy.

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Published on: May 22, 2018

Area of Science:

Cardiovascular Physiology
Molecular Cardiology
Cellular Electrophysiology

Background:

Electrical intercellular communication in the heart relies on gap junction channels, formed by connexins (Cx).
Cx43 is the most abundant connexin isoform in the heart, crucial for electrical signal propagation.
Intercellular communication is dynamically regulated by gap junction conductance and connexin expression levels.

Purpose of the Study:

To investigate the role of adrenoceptors in regulating cardiac intercellular communication.
To elucidate the signaling pathways involved in adrenoceptor-mediated control of connexin expression.
To understand the implications of altered connexin expression in cardiac diseases like hypertrophy and arrhythmia.

Main Methods:

Analysis of connexin isoform expression and phosphorylation.
Investigation of signaling cascades activated by β- and α-adrenoceptor stimulation.
Assessment of adrenoceptor density across species.
Correlation of Cx43 expression patterns with cardiac hypertrophy and arrhythmogenesis.

Main Results:

Chronic β-adrenergic stimulation enhances Cx43 expression via protein kinase A and MAPK pathways.
α-Adrenergic stimulation acutely uncouples cells and chronically upregulates Cx43 expression via protein kinase C and other signaling molecules.
Cx43 expression is specifically regulated by α(1D)-adrenoceptors, while general protein synthesis is via α(1A)-adrenoceptors.
Abnormal Cx43 incorporation in lateral membranes during hypertrophy may lead to gap junction disarray and arrhythmogenesis.

Conclusions:

Cardiac adrenoceptors are critical regulators of intercellular electrical communication and Cx43 expression.
Adrenergic modulation of Cx43 plays a significant role in maintaining normal cardiac electrical networking.
Dysregulation of Cx43 expression and localization by adrenoceptors can contribute to arrhythmogenic substrates in heart diseases.