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

T. Ishiwata, M. Kornmann, H. G. Beger, Murray Korc

Research output: Contribution to journalArticle

29 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)134-139
Number of pages6
JournalGut
Volume43
Issue number1
StatePublished - 1998
Externally publishedYes

Fingerprint

Fibroblast Growth Factor 5
Exocrine Pancreas
Chronic Pancreatitis
Pancreas
Islets of Langerhans
Northern Blotting
Acinar Cells
Pancreatic Ducts
Mesocricetus
Immunoblotting
In Situ Hybridization
Heparin
Intercellular Signaling Peptides and Proteins
Fibroblasts

Keywords

  • Chronic pancreatitis
  • Fibroblast growth factor
  • In situ hybridisation

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Enhanced fibroblast growth factor 5 expression in stromal and exocrine elements of the pancreas in chronic pancreatitis. / Ishiwata, T.; Kornmann, M.; Beger, H. G.; Korc, Murray.

In: Gut, Vol. 43, No. 1, 1998, p. 134-139.

Research output: Contribution to journalArticle

Ishiwata, T, Kornmann, M, Beger, HG & Korc, M 1998, 'Enhanced fibroblast growth factor 5 expression in stromal and exocrine elements of the pancreas in chronic pancreatitis', Gut, vol. 43, no. 1, pp. 134-139.
Ishiwata, T. ; Kornmann, M. ; Beger, H. G. ; Korc, Murray. / Enhanced fibroblast growth factor 5 expression in stromal and exocrine elements of the pancreas in chronic pancreatitis. In: Gut. 1998 ; Vol. 43, No. 1. pp. 134-139.
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AB - 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.

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