Enhanced fibroblast growth factor 5 expression in stromal and exocrine elements of the pancreas in chronic pancreatitis

T Ishiwata,^a M Kornmann,^a H G Beger,^b M Korc^a

^a Departments of Medicine, Biological Chemistry and Pharmacology, University of California, Irvine, California, USA, ^b Department of General Surgery, University of Ulm, Ulm, Germany

Correspondence to: Dr M Korc, Division of Endocrinology, Diabetes, and Metabolism, Med. Sci. I C240, University of California, Irvine, California 92697, USA.

Accepted for publication 19 January 1998

BackgroundFibroblast 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.
AimsTo 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 resultsNorthern 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.
ConclusionExocrine and stromal derived FGF-5 has the potential to participate in autocrine and paracrine pathways that may contribute to the pathobiology of chronic pancreatitis.
(GUT 1998;43:134-139)

Keywords: chronic pancreatitis;  fibroblast growth factor;  in situ hybridisation