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Updated: Mar 12, 2026

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells

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Calcium Signaling Is Involved in EthanolInduced Volume Decrease and Gap Junction Closure in Cultured Rat Gastric

Harri Mustonen¹, Tuula Kiviluoto¹, Hannu Paimela¹

¹Department of Surgery, Helsinki University Central Hospital, Helsinki, Finland.

Digestive Diseases and Sciences

|November 13, 2016

Summary

Ethanol damages gastric mucosa by increasing intracellular calcium, shrinking cells via potassium channels, and closing gap junctions. These effects are mediated by calcium signaling pathways.

Keywords:

cell membrane integrity cell volume ethyl alcohol gap junctions gastric mucosa intracellular calcium potassium ion channels

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Dissection of Local Ca2+ Signals in Cultured Cells by Membrane-targeted Ca2+ Indicators

Dissection of Local Ca2+ Signals in Cultured Cells by Membrane-targeted Ca2+ Indicators

Published on: March 22, 2019

Area of Science:

Gastroenterology
Cell Biology
Physiology

Background:

Ethanol is a known gastric mucosa irritant.
The precise cellular mechanisms of ethanol's barrier-disrupting effects are not fully understood.
Previous studies indicated ethanol increases intracellular calcium, closes gap junctions, and decreases cell volume.

Purpose of the Study:

To elucidate the cellular mechanisms by which ethanol affects gastric mucosal cells.
To investigate the role of intracellular calcium and ion channels in ethanol-induced gastric mucosal damage.
To determine the impact of ethanol on gastric epithelial cell volume and intercellular communication.

Main Methods:

Primary cultured rat gastric mucosal (RGM) cells were used.
Intracellular calcium levels were measured using fura-2.
Cell volume was assessed using calcein and confocal microscopy.
Gap junctional communication was evaluated by measuring 5-carboxyfluorescein diffusion.
Pharmacological agents (TMB-8, lanthanum, BABTA, quinine) were employed to modulate calcium signaling and ion channel activity.

Main Results:

Ethanol (7.5%) significantly increased intracellular calcium, decreased cell volume, and reduced gap junctional communication.
Inhibition of intracellular calcium release (TMB-8) and calcium influx (lanthanum) partially reduced the calcium increase.
Complete calcium chelation (BABTA) abolished ethanol-induced calcium increase, cell shrinkage, and gap junction closure.
A potassium channel blocker (quinine) largely prevented ethanol-induced cell volume decrease.
Ethanol-induced cellular effects were dependent on intracellular calcium signaling.

Conclusions:

Luminal ethanol triggers a cascade involving increased intracellular calcium.
This calcium increase activates basolateral calcium-dependent potassium channels, leading to cell shrinkage.
Ethanol also inhibits intercellular gap junction communication, mediated by intracellular calcium.
These cellular events contribute to ethanol's barrier-disrupting effects on the gastric mucosa.