Enhanced vigilin and anionic trypsinogen expression in experimental chronic pancreatitis

Author:

Hilgendorf Inken1,Aßmuth Karen2,Sparmann Gisela3,Emmrich Jörg3,Kruse Charli2

Affiliation:

1. 1Division of Haematology and Oncology, Department of Medicine, Medical Faculty, University Rostock, 18057, Rostock, Germany

2. 2Frauenhofer-Institute of Biomedical Engineering, Group of Cell Differentiation and Cell Technology at the University of Lübeck, 23538, Lübeck, Germany

3. 3Division of Gastroenterology, Department of Medicine, Medical Faculty, University Rostock, 18057, Rostock, Germany

Abstract

AbstractThe molecular principles that lead to chronic pancreatitis are incompletely understood. Trypsin(ogen) plays a key role in the development of pancreatitis. Since the production of trypsin(ogen) by acinary pancreatic cells is paralleled by the expression of vigilin we hypothesised that vigilin may be involved in the onset of pancreatitis. Vigilin is a ubiquitous protein and has apparently high affinity to RNA.In the present study experimental pancreatitis was induced in male rats by a single intravenous application of dibutyltin dichloride (DBTC). Sections of rat pancreas were immunostained with an affinity-purified polyclonal antiserum against vigilin or trypsin(ogen). The changes in vigilin and trypsin(ogen) protein expression were determined by immunoblotting and subsequent sequence analysis of the amino acids.Induction of pancreatitis by DBTC caused alterations in the distribution and the amount of both vigilin and trypsin(ogen) as shown by immunohistochemical and immunoblot analysis.Furthermore we could demonstrate that anionic trypsinogen expression is up-regulated in DBTC-induced chronic pancreatitis. The obtained results suggest that vigilin as well as trypsin(ogen) are involved in the pathogenesis of pancreatitis and that the long-time DBTC-induced pancreatitis is a useful model for study of chronic pancreatitis.

Publisher

Walter de Gruyter GmbH

Subject

General Medicine

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