Expression of proteinase-activated receptor 2 during taurocholate-induced acute pancreatic lesion development in Wistar rats.
BACKGROUND
Proteinase-activated receptor 2 (PAR-2) is a G-protein coupled transmembrane receptor activated by trypsin by site-specific cleavage. Its presence on pancreatic structures was demonstrated in the past. PAR-2 physiologically involves in duct/acinary cells secretion, arterial tonus regulation or capillary liquid turnover. During development of acute pancreatitis/acute pancreatic lesion (APL) these mentioned structures are influenced by very high concentration of trypsin due to its increased basolateral secretion into the interstitium. The aim of our study as presented was to investigate whether PAR-2 is also involved in APL following changes of PAR-2 expression.


METHODS
APL was investigated in Wistar rats after injection of 0.1 mL taurocholate into the ductus choledochus. Anatomy, histology, reverse transcriptase polymerase chain reaction (RT PCR) as well as immunohistochemistry and Western-blot analysis of pancreatic tissue were performed using antibody mapping of the new NH2 terminal of PAR-2 after trypsin cleavage. Results from control rats and d 1 or d 4 rats after taurocholate injection were compared.


RESULTS
Much higher positivity on acinary/duct cells was observed in APL induced animals than in controls. Similar findings were noticed on arterial smooth muscle cells. Surprisingly, parallel to the exocrine pancreas and vessel findings, enhanced Langerhans' islet cell positivity was observed in experimental animals.


CONCLUSIONS
Based on these results, we have demonstrated that during APL development PAR-2 expression increases. This effect is caused by conformational changes after PAR-2 activation, and the new NH2 terminal of activated receptor presentation. We suggest that PAR-2 physiological functions are enhanced during APL development.
Olejár
T
T
Institute of Biophysics, 1st Medical School, Charles University, Prague, Czech Republic. 1159@post.cz
Matej
R
R
Zadinová
M
M
Poucková
P
P
D000208:Acute Disease; D000818:Animals; D015153:Blotting, Western; D007150:Immunohistochemistry; D007515:Islets of Langerhans / Q000378:metabolism; D023421:Models, Animal; D010179:Pancreas / Q000166:cytology / Q000378:metabolism*; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D044464:Receptor, PAR-2; D018179:Receptors, Thrombin / Q000096:biosynthesis* / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013656:Taurocholic Acid
D044464:Receptor, PAR-2; D018179:Receptors, Thrombin; D013656:Taurocholic Acid