Comparative effects of epidermal growth factor and carbachol on phosphoinositide synthesis and breakdown in pancreatic acinar cells.
Carbachol (CCh) and epidermal growth factor (EGF) elicited a concentration-dependent increase in [32P]phosphatidyl-inositol-4-phosphate (PtdIns-4P) formation in homogenates derived from agonist-stimulated rat pancreatic acini. The combination of CCh and EGF produced a response which was not synergistic or additive. EGF, unlike CCh, failed to cause [32P]PtdIns-4,5P2 breakdown, suggesting different mechanisms involved in the stimulation of [32P]PtdIns-4P formation induced by EGF and CCh. We conclude that PtdIns kinase represents a key component of the signaling pathways utilized by EGF and CCh in exocrine pancreas.
Conway
B R
BR
Department of Pharmacology and Toxicology, Medical College of Virginia, Richmond 23298.
Laychock
S G
SG
Rubin
R P
RP
D000818:Animals; D002217:Carbachol / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004815:Epidermal Growth Factor / Q000494:pharmacology*; D066298:In Vitro Techniques; D007700:Kinetics; D010179:Pancreas / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D018129:Phosphatidylinositol Phosphates; D010716:Phosphatidylinositols / Q000096:biosynthesis / Q000378:metabolism*; D051381:Rats
D018129:Phosphatidylinositol Phosphates; D010716:Phosphatidylinositols; C037178:phosphatidylinositol 4-phosphate; D004815:Epidermal Growth Factor; D002217:Carbachol