The role of trypsin, trypsin inhibitor, and trypsin receptor in the onset and aggravation of pancreatitis

Trypsin activity is properly suppressed in the pancreatic acinar cells under normal conditions. A small amount of trypsinogen is converted to active trypsin and inactivated by pancreatic secretory trypsin inhibitor (PSTI), thereby preventing damage to pancreatic acinar cells as a first line of defen...

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Bibliographic Details
Published in:Journal of gastroenterology 2006-09, Vol.41 (9), p.832-836
Main Authors: Hirota, Masahiko, Ohmuraya, Masaki, Baba, Hideo
Format: Article
Language:English
Subjects:
Animals
Carrier Proteins - genetics
Carrier Proteins - metabolism
DNA - genetics
Humans
Mutation
Pancreatitis - genetics
Pancreatitis - metabolism
Receptor, PAR-2 - metabolism
Trypsin - metabolism
Trypsin Inhibitor, Kazal Pancreatic
Trypsin Inhibitors - metabolism
Trypsinogen - genetics
Trypsinogen - metabolism
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Summary:Trypsin activity is properly suppressed in the pancreatic acinar cells under normal conditions. A small amount of trypsinogen is converted to active trypsin and inactivated by pancreatic secretory trypsin inhibitor (PSTI), thereby preventing damage to pancreatic acinar cells as a first line of defense. However, if trypsin activation (due to excessive stimulation of pancreatic acinar cells) exceeds the capacity of PSTI, a subsequent cascade of events leads to the activation of various proteases that damage cells. This can be interpreted as the main causative event of pancreatitis onset. Trypsin produced in and secreted from the pancreatic acinar cells activates protease activated receptor-2 (PAR-2), which is present at high densities on the luminal surfaces of pancreatic acinar cells and duct cells. Results of PAR-2 activation are the production of cytokines and the regulation of exocrine function via a negative feedback loop. Thus, the actions of trypsin, trypsin inhibitor (PSTI), and trypsin receptor (PAR-2) in the pancreas are strongly interconnected.
ISSN:0944-1174
1435-5922
DOI:10.1007/s00535-006-1874-2