Mechanisms of cck regulation of the monitor peptide mrna expression
in pancreatic acinar ar42j cells.
Kinouchi, Toshi, Satoshi Tsuzuki, Chieko Minami, Yoshihiro Hayashi,
Etsuro Sugimoto, Tohru Fushiki.
Laboratory of Nutritional Chemistry, Department of Food Science and
Technology, Faculty of Agriculture, Kyoto University, Kyoto 606,
Japan
APStracts 3:0267G, 1996.
The mechanism(s) by which the cholecystokinin (CCK) stimulation of
AR42J rat pancreatoma cells results in an increased mRNA expression
of a CCK-releasing peptide (monitor peptide, MP) were explored. Using
a newly established assay system by means of reverse transcription
-polymerase chain reaction, CCK was shown to increase the level of MP
mRNA by about 9-fold. When protein synthesis was blocked by the
addition of cycloheximide, the MP mRNA level remained unchanged in
the presence of CCK. Inhibition of the transcription with actinomycin
D showed a half-life for the MP mRNA of approximately 17 h, and this
rate remained unchanged by CCK treatment, suggesting that CCK may
regulate the MP mRNA level by influencing gene transcription. A23187,
bombesin, substance P and carbachol increased the MP mRNA level.
CoCl2 abolished both the CCK and A23187 actions on the MP mRNA
expression. Neither dibutyryl cAMP and forskolin nor secretin and VIP
had any effect on the MP mRNA expression. Both TPA and PDB failed to
increase the MP mRNA. It was therefore proposed that the CCK
stimulates the MP mRNA expression of AR42J cells in a calcium
-dependent and protein kinase C-independent manner.
Received 6 April 1996; accepted in final form 4 November 1996.
APS Manuscript Number G126-6.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996