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Electrotonic modulation of cardiac impulse conduction by myofibroblasts
Michele Miragoli1, Giedrius Gaudesius, Stephan Rohr
1Department of Physiology, University of Bern, Bern, Switzerland.
Circulation Research
|February 18, 2006
Summary
Cardiac myofibroblasts can alter heart electrical signals by forming gap junctions with cardiomyocytes. This interaction, influencing impulse propagation, may contribute to arrhythmias and suggests myofibroblasts as an antiarrhythmic target.
Area of Science:
- Cardiovascular Biology
- Cardiac Electrophysiology
- Cellular Biology
Background:
- Myofibroblasts, characterized by alpha-smooth muscle actin (alphaSMA), emerge during cardiac remodeling.
- These cells express connexins in non-cardiac tissues, but their role in cardiac electrophysiology is unclear.
Purpose of the Study:
- To investigate heterocellular gap junctional coupling between cardiac myofibroblasts and cardiomyocytes.
- To determine the impact of electrotonic interactions on cardiac impulse propagation.
Main Methods:
- Cultured cardiac fibroblasts were induced to differentiate into myofibroblasts.
- Immunocytochemistry confirmed alphaSMA expression and connexin presence.
- Optical mapping assessed impulse conduction velocity (theta) and maximal upstroke velocity (dV/dtmax) in cardiomyocyte strands co-cultured with myofibroblasts.
- Microelectrode recordings measured cardiomyocyte membrane potential.
Main Results:
- Cardiac fibroblasts differentiated into alphaSMA-positive myofibroblasts expressing connexins 43 and 45.
- Myofibroblast density exhibited a biphasic effect on theta and dV/dtmax, initially increasing then decreasing conduction.
- Higher myofibroblast ratios led to significant cardiomyocyte depolarization and slowed conduction velocity.
Conclusions:
- Cardiac myofibroblasts form functional gap junctions with cardiomyocytes, modulating impulse propagation.
- These electrotonic interactions can contribute to arrhythmogenesis.
- Preventing myofibroblast formation may be a novel antiarrhythmic strategy.
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