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Related Experiment Videos

Calcium signaling is involved in ethanol-induced volume decrease and gap junction closure in cultured rat gastric

Harri Mustonen1, Tuula Kiviluoto, Hannu Paimela

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

Digestive Diseases and Sciences
|February 17, 2005
PubMed
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Ethanol exposure increases intracellular calcium and causes gastric epithelial cells to shrink and close gap junctions. These effects are mediated by calcium signaling and opening of potassium channels.

Area of Science:

  • Cell Biology
  • Gastroenterology
  • Pharmacology

Background:

  • Ethanol is a known gastric mucosa barrier breaker.
  • Its precise cellular mechanisms are not fully understood.
  • Previous studies indicated increased intracellular calcium, closed gap junctions, and decreased cell volume.

Purpose of the Study:

  • To elucidate the cellular mechanisms of ethanol's effects on gastric mucosal cells.
  • To investigate the role of intracellular calcium and ion channels in ethanol-induced cellular changes.
  • To determine how ethanol affects gap junction communication and cell volume.

Main Methods:

  • Primary cultured rat gastric mucosal (RGM) cells were used.
  • Intracellular calcium was measured using fura-2.

Related Experiment Videos

  • Cell volume was assessed using calcein and confocal microscopy.
  • Gap junctional diffusion was measured using 5-carboxyfluorescein and confocal microscopy.
  • Pharmacological agents (TMB-8, lanthanum, BABTA, quinine) were used to probe signaling pathways.

    • Main Results:

    • Ethanol (7.5%) increased intracellular calcium, decreased cell volume, and closed gap junctions.
    • Quinine prevented ethanol-induced cell volume decrease, suggesting potassium channel involvement.
    • BABTA and TMB-8 + lanthanum inhibited ethanol-induced calcium increase.
    • BABTA abolished ethanol-induced cell shrinkage and gap junction closure.
    • TMB-8 + lanthanum partially inhibited cell shrinkage and abolished gap junction closure.

    Conclusions:

    • Luminal ethanol triggers intracellular calcium signaling.
    • This signaling opens basolateral calcium-dependent potassium channels, leading to cell shrinkage.
    • Ethanol also blocks intercellular gap junctions via intracellular calcium.
    • These cellular events contribute to ethanol's barrier-breaking effects on the gastric mucosa.