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Cholinergic signaling impairs cardiomyocyte cohesion.

Sunil Yeruva1, Lars Körber1, Matthias Hiermaier1

  • 1Chair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, Ludwig-Maximilian-University (LMU) Munich, Munich, Germany.

Acta Physiologica (Oxford, England)
|August 30, 2022
PubMed
Summary

Cholinergic signaling, using carbachol, reduces cardiomyocyte cohesion by affecting desmoglein 2, independent of plakoglobin phosphorylation. This reveals a new mechanism for autonomic nervous system dysregulation in heart disease.

Keywords:
adrenergic signalingcardiomyocyte cohesioncholinergic signalingdesmoglein 2desmoplakinglycogen synthase kinase-3β

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Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Signaling
  • Cellular Adhesion Mechanisms

Background:

  • Cardiac autonomic nervous system (ANS) dysregulation is linked to cardiovascular diseases.
  • Adrenergic signaling enhances cardiomyocyte cohesion via PKA-mediated plakoglobin phosphorylation (positive adhesiotropy).

Purpose of the Study:

  • To investigate cholinergic regulation of cardiomyocyte cohesion.
  • To determine the role of muscarinic receptor agonist carbachol (CCH) in cardiomyocyte cohesion.

Main Methods:

  • Experiments conducted in HL-1 cells and plakoglobin (PG) wild type and knockout mice.
  • Techniques included dissociation assays, Western blot, immunostaining, atomic force microscopy (AFM), immunoprecipitation, transmission electron microscopy (TEM), and siRNA knockdown.

Main Results:

  • Carbachol (CCH) impaired cardiomyocyte cohesion and reduced desmoglein 2 (DSG2) at cell borders.
  • CCH decreased intercalated disc plaque thickness and inhibited adrenergic-stimulated ERK phosphorylation.
  • Cholinergic signaling activated the AKT/GSK-3β axis, independent of plakoglobin phosphorylation.

Conclusions:

  • Cholinergic signaling antagonizes adrenergic effects on cardiomyocyte cohesion, causing negative adhesiotropy.
  • This effect is independent of plakoglobin phosphorylation and highlights a novel mechanism in cardiac autonomic dysregulation.