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Epithelial cells fire voltage spikes
1Department of Polymer Science and Engineering, University of Massachusetts, Amherst, MA 01003.
Summary
Epithelial cells exhibit bioelectric signaling, generating voltage spikes in response to mechanical stress. This electrical excitability, mediated by mechanosensitive channels, challenges the notion that only neurons and muscles possess such signaling capabilities.
Area of Science:
- Cellular biology
- Bioelectricity
- Tissue engineering
Background:
- Bioelectric signaling is established in neurons and cardiomyocytes.
- Its role in epithelial tissues is largely unexplored.
- Epithelia were traditionally not considered electrically excitable.
Purpose of the Study:
- To investigate bioelectric signaling in epithelial cells.
- To determine the mechanisms underlying epithelial electrical excitability.
- To explore the role of mechanical stress in epithelial bioelectricity.
Main Methods:
- Utilized multielectrode arrays to record electrical activity in epithelial monolayers (primary human keratinocytes and MDCK cells).
- Induced localized laser injury to trigger bioelectric responses.
- Employed calcium chelation (EDTA), myosin II inhibition (blebbistatin), and mechanosensitive channel modulators (GsMTx4, TRPV4, Piezo1 agonists).
Main Results:
- Localized epithelial injury triggered slow voltage spikes (1-2s duration, 4-12/min).
- Spike generation required calcium influx and actomyosin contractility.
- Mechanosensitive channels (TRPV4, Piezo1) were sufficient to induce spiking, even without injury.
- Electrical signals propagated non-monotonically over distances up to 740 μm.
Conclusions:
- Epithelia possess intrinsic bioelectric excitability regulated by mechanical stress.
- This challenges the exclusive role of electrical signaling in neurons and muscles.
- Epithelial bioelectricity may coordinate collective cellular responses across tissues.
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