Comparative effects of epidermal growth factor and carbachol on phosphoinositide synthesis and breakdown in pancreatic acinar cells

Bruce R. Conway; Suzanne G. Laychock; Ronald P. Rubin

doi:10.1016/0006-291X(91)90176-8

Comparative effects of epidermal growth factor and carbachol on phosphoinositide synthesis and breakdown in pancreatic acinar cells

Bruce R. Conway
, Suzanne G. Laychock
, Ronald P. Rubin

Pharmacology and Toxicology

Virginia Commonwealth University
SUNY Buffalo

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

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.

Original language	English
Pages (from-to)	780-785
Number of pages	6
Journal	Biochemical and Biophysical Research Communications
Volume	178
Issue number	2
DOIs	https://doi.org/10.1016/0006-291X(91)90176-8
State	Published - Jul 31 1991

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title = "Comparative effects of epidermal growth factor and carbachol on phosphoinositide synthesis and breakdown in pancreatic acinar cells",

abstract = "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.",

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AU - Conway, Bruce R.

AU - Laychock, Suzanne G.

AU - Rubin, Ronald P.

PY - 1991/7/31

Y1 - 1991/7/31

N2 - 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.

AB - 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.

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JO - Biochemical and Biophysical Research Communications

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IS - 2

ER -

Comparative effects of epidermal growth factor and carbachol on phosphoinositide synthesis and breakdown in pancreatic acinar cells

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