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Enhanced fibroblast growth factor 5 expression in stromal and exocrine elements of the pancreas in chronic pancreatitis
  1. T Ishiwataa,
  2. M Kornmanna,
  3. H G Begerb,
  4. M Korca
  1. aDepartments of Medicine, Biological Chemistry and Pharmacology, University of California, Irvine, California, USA, bDepartment of General Surgery, University of Ulm, Ulm, Germany
  1. Dr M Korc, Division of Endocrinology, Diabetes, and Metabolism, Med. Sci. I C240, University of California, Irvine, California 92697, USA.

Abstract

Background—Fibroblast growth factor 5 (FGF-5) belongs to a group of mitogenic and angiogenic heparin binding growth factors but its potential role in chronic inflammatory conditions is not known.

Aims—To compare FGF-5 expression in the normal pancreas and in the pancreas of patients with chronic pancreatitis (CP) and to characterise FGF-5 expression and secretion in TAKA-1 cells, an immortalised Syrian hamster pancreatic duct cell line.

Methods and results—Northern blotting revealed the presence of a 4.0 kb FGF-5 mRNA transcript in both normal and CP tissue samples. Densitometric analysis indicated that the transcript levels were increased by a factor of 1.44 in CP tissue samples compared with normal tissue samples (p=0.039). By immunohistochemisty and in situ hybridisation, FGF-5 was faintly expressed in ductal and islet cells in the normal pancreas. In contrast, in CP tissue samples, there was abundant expression of FGF-5 in ductal, acinar, and islet cells, as well as in periductal fibroblasts. FGF-5 was also expressed in TAKA-1 cells as determined by Northern blotting. By immunoblotting of heparin-sepharose precipitates, TAKA-1 cells were shown to secrete FGF-5 into the medium.

Conclusion—Exocrine and stromal derived FGF-5 has the potential to participate in autocrine and paracrine pathways that may contribute to the pathobiology of chronic pancreatitis.

  • chronic pancreatitis
  • fibroblast growth factor
  • in situ hybridisation

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