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Epidermal growth factor inhibits carbachol-stimulated canine parietal cell function via protein kinase C

L Wang1, E J Wilson, J Osburn

  • 1Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, USA.

Gastroenterology
|February 1, 1996
PubMed
Abstract

Insights

Epidermal growth factor (EGF) inhibits gastric acid secretion by activating protein kinase C (PKC) in parietal cells. This study confirms EGF

Area of Science:

  • Gastroenterology
  • Cell Signaling
  • Molecular Biology

Background:

  • Epidermal growth factor (EGF) inhibits gastric acid secretion through receptors on parietal cells.
  • The precise mechanism of EGF-induced inhibition of secretagogue-stimulated acid secretion requires elucidation.

Purpose of the Study:

  • To investigate if epidermal growth factor (EGF) inhibits carbachol-stimulated gastric acid secretion via a protein kinase C (PKC)-dependent pathway.

Main Methods:

  • Studied EGF effects on carbachol-stimulated aminopyrine uptake, inositol trisphosphate formation, and intracellular calcium ([Ca2+]i) in cultured parietal cells.
  • Assessed the impact of protein kinase A (PKA) and C (PKC) inhibitors on EGF's inhibitory action.
  • Determined EGF-mediated translocation and activation of PKC in parietal cells.

Main Results:

  • EGF inhibited carbachol-stimulated aminopyrine uptake in a dose-dependent manner, sensitive to tyrosine kinase inhibitors.
  • EGF did not affect carbachol-stimulated inositol trisphosphate formation or intracellular calcium levels.
  • PKC inhibitors reversed EGF's inhibitory effect, while PKA inhibitors did not.
  • EGF increased PKC translocation and activity in parietal cells.

Conclusions:

  • EGF's inhibition of carbachol-stimulated parietal cell activity is mediated through protein kinase C (PKC).

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