CCK regulation of monitor peptide pene expression in pancreatic acinar AR42J cells.

摘要

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 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. CoCl_2 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.