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Preparation of Pancreatic Acinar Cells for the Purpose of Calcium Imaging, Cell Injury Measurements, and Adenoviral Infection
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Pertussis toxin-sensitive G-proteins inhibit fibroblast growth factor-induced signaling in pancreatic acini

A Piiper1, D Stryjek-Kaminska, R Gebhardt

  • 1Medical Department, University of Frankfurt, Germany.

Journal of Cellular Physiology
|April 1, 1996
PubMed

Insights

Fibroblast growth factor (FGF) receptors interact with inhibitory Gi-proteins in rat pancreatic acini. These Gi-proteins regulate FGF-induced phospholipase C activation and amylase release, clarifying FGF signaling pathways.

Area of Science:

  • Cellular Biology
  • Molecular Signaling
  • Gastroenterology

Background:

  • Fibroblast growth factor (FGF) receptor signaling involves tyrosine phosphorylation but the role of G-proteins remains debated.
  • Previous studies indicate diverse substrates for FGF receptors, including Grb2 and phospholipase C-gamma (PLCγ).

Purpose of the Study:

  • To investigate the role of G-proteins in fibroblast growth factor receptor (FGFR) signaling in rat pancreatic acini.
  • To elucidate the interaction between FGFRs and G-proteins in regulating cellular responses.

Main Methods:

  • Immunological analysis to detect FGFR and PLCγ1 in pancreatic acini.
  • Stimulation assays using basic FGF (FGF-2) and guanosine 5'-(γ-thio)triphosphate (GTPγS) to measure inositol 1,4,5-trisphosphate (1,4,5-IP3) production and amylase release.
  • Pertussis toxin-mediated ADP-ribosylation to assess Gi-protein activity and functional interaction with FGFRs.

Main Results:

  • Both FGF-2 and GTPγS increased 1,4,5-IP3 production and amylase release.
  • Combined FGF-2 and GTPγS stimulation resulted in diminished responses compared to single stimulations.
  • FGF-2 pre-treatment reduced pertussis toxin ADP-ribosylation of Gi-proteins, indicating functional interaction.
  • Pertussis toxin pretreatment abolished GTPγS's inhibitory effect on FGF-2-induced responses, while stimulatory effects remained.

Conclusions:

  • FGFRs communicate with Gi-type G-proteins in pancreatic acinar cells.
  • Gi-type G-proteins exert an inhibitory influence on FGF-induced activation of phosphoinositide-specific phospholipase C.
  • This study clarifies a novel inhibitory role for Gi-proteins in FGF receptor signaling pathways.

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