Epidermal growth factor inhibits both cholecystokinin octapeptide-induced inositol 1,4,5-trisphosphate production and [Ca2+]i increase in rat pancreatic acinar cells

1991 ◽  
Vol 180 (2) ◽  
pp. 900-906 ◽  
Author(s):  
André Pröfrock ◽  
Albrecht Piiper ◽  
Luise Eckhardt ◽  
Irene Schulz
Pancreas ◽  
1995 ◽  
Vol 10 (3) ◽  
pp. 274-280 ◽  
Author(s):  
Danuta Stryjek-Kaminska ◽  
Albrecht Piiper ◽  
Jürgen Stein ◽  
Wolfgang F. Caspary ◽  
Stefan Zeuzem

1986 ◽  
Vol 116 (7) ◽  
pp. 1306-1315 ◽  
Author(s):  
Patsy M. Brannon ◽  
Alison S. Demarest ◽  
Janet E. Sabb ◽  
Murray Korc

1986 ◽  
Vol 251 (4) ◽  
pp. G487-G494 ◽  
Author(s):  
C. D. Logsdon

Effects of regulatory molecules on growth of mouse pancreatic acinar cells in culture were examined. The cholecystokinin (CCK) analogue caerulein and cholecystokinin octapeptide (CCK-8) each led to threefold increases in incorporation of [3H]thymidine into DNA. Gastrin, which interacts weakly with the CCK receptor, stimulated DNA synthesis, but only at much higher concentrations. In contrast, other secretagogues that utilize Ca2+ as an intracellular messenger, including carbachol, bombesin, substance P, and the ionophore A23187, did not induce trophic responses. Factors that affect intracellular cAMP concentration, such as secretin, somatostatin, VIP, DBcAMP, and forskolin, did not increase DNA synthesis in cultured pancreatic cells. Insulin and epidermal growth factor induced two- and threefold increases in [3H] thymidine incorporation into DNA, respectively. The effects of insulin were mediated via insulin-like growth factor I receptors. Steroid hormones had little effect on pancreatic acinar cell DNA synthesis. The stimulatory effects of CCK, insulin, and EGF were additive. The combination of caerulein, EGF, and insulin in a hormonally defined medium led to a tenfold increase in the incorporation of [3H]thymidine into DNA. These data indicate that CCK, EGF, and insulin directly increase DNA synthesis in pancreatic acinar cells.


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