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Fibroblast growth factor-2 stimulates interleukin-6 secretion in human pancreatic periacinar myofibroblasts

Akira Andoh1, Shigeki Bamba, Sanae Fujino

  • 1Department of Internal Medicine, Shiga University of Medical Science, Otsu, Japan. andoh@belle.shiga-med.ac.jp

Pancreas
|October 27, 2004
PubMed
Abstract

Insights

Fibroblast growth factor-2 (FGF-2) stimulates interleukin-6 (IL-6) release in pancreatic cells, contributing to inflammation. FGF-2 activates specific signaling pathways, highlighting its role in pancreatitis and acute-phase responses.

Area of Science:

  • Gastroenterology
  • Cell Biology
  • Molecular Medicine

Background:

  • Fibroblast growth factor-2 (FGF-2) is implicated in pancreatitis pathogenesis.
  • Understanding FGF-2's role in pancreatic inflammation is crucial.

Purpose of the Study:

  • To investigate the proinflammatory effects of FGF-2 on IL-6 secretion in human pancreatic periacinar myofibroblasts.
  • To elucidate the signaling pathways involved in FGF-2-induced IL-6 production.

Main Methods:

  • Quantification of IL-6 in supernatants using ELISA.
  • Assessment of IL-6 mRNA expression via Northern blots and qPCR.
  • Evaluation of AP-1 DNA-binding activity using EMSA.
  • Analysis of ERK1/2 and p38 MAP kinase activation.

Main Results:

  • FGF-2 dose- and time-dependently induced IL-6 release, comparable to IL-17.
  • Combined FGF-2 and IL-17 showed additive effects on IL-6 at mRNA and protein levels.
  • FGF-2 activated AP-1, but AP-1 inhibition did not affect FGF-2-induced IL-6 mRNA.
  • FGF-2 rapidly activated ERK1/2 and p38 MAP kinases, crucial for IL-6 release.

Conclusions:

  • FGF-2 acts as an inducer of the acute-phase response by stimulating IL-6 release in the pancreas.
  • Beyond tissue repair, FGF-2 contributes to pancreatic inflammation via IL-6 stimulation.

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