Direct modulation of epidermal growth factor binding by cholecystokinin

Murray Korc; Lynn M. Matrisian; Bruce E. Magun

doi:10.1016/0024-3205(83)90131-5

Direct modulation of epidermal growth factor binding by cholecystokinin

Murray Korc, Lynn M. Matrisian, Bruce E. Magun

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

13 Scopus citations

Abstract

The effects of cholecystokinin-octapeptide (CCK₈), the biologically active C-terminal moiety of cholecystokinin (CCK), on the binding of epidermal growth factor (EGF) were studied in isolated rat pancreatic acini. CCK₈ inhibited ¹²⁵I-EGF binding in a dose-dependent manner. One-half maximal inhibition occurred at 5 × 10^-10M, and maximal inhibition at 10^-8M CCK₈. This inhibitory effect was detectable within 5 minutes of addition of CCK₈, and was not associated with enhanced degradation of ¹²⁵I-EGF in incubation media. Unlabeled EGF exerted only a slightly greater inhibitory effect than CCK₈ on ¹²⁵I-EGF binding at equivalent molar concentrations. In contrast to CCK₈, the gastrointestinal hormone vasoactive intestinal polypeptide (VIP) did not significantly alter EGF binding. CCK₈ also inhibited EGF binding in mouse pancreatic acini, but did not alter binding in A-431 human carcinoma cells. These findings suggest that physiological levels of CCK may regulate EGF binding in the pancreas and other tissues with receptors for both hormones. They thus point to a previously unrecognized mechanism for hormonal interaction.

Original language	English (US)
Pages (from-to)	561-568
Number of pages	8
Journal	Life Sciences
Volume	33
Issue number	6
DOIs	https://doi.org/10.1016/0024-3205(83)90131-5
State	Published - Aug 8 1983
Externally published	Yes

ASJC Scopus subject areas

General Pharmacology, Toxicology and Pharmaceutics
General Biochemistry, Genetics and Molecular Biology

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@article{c224cac98c424679b5b16ded296870f3,

title = "Direct modulation of epidermal growth factor binding by cholecystokinin",

abstract = "The effects of cholecystokinin-octapeptide (CCK8), the biologically active C-terminal moiety of cholecystokinin (CCK), on the binding of epidermal growth factor (EGF) were studied in isolated rat pancreatic acini. CCK8 inhibited 125I-EGF binding in a dose-dependent manner. One-half maximal inhibition occurred at 5 × 10-10M, and maximal inhibition at 10-8M CCK8. This inhibitory effect was detectable within 5 minutes of addition of CCK8, and was not associated with enhanced degradation of 125I-EGF in incubation media. Unlabeled EGF exerted only a slightly greater inhibitory effect than CCK8 on 125I-EGF binding at equivalent molar concentrations. In contrast to CCK8, the gastrointestinal hormone vasoactive intestinal polypeptide (VIP) did not significantly alter EGF binding. CCK8 also inhibited EGF binding in mouse pancreatic acini, but did not alter binding in A-431 human carcinoma cells. These findings suggest that physiological levels of CCK may regulate EGF binding in the pancreas and other tissues with receptors for both hormones. They thus point to a previously unrecognized mechanism for hormonal interaction.",

author = "Murray Korc and Matrisian, {Lynn M.} and Magun, {Bruce E.}",

note = "Funding Information: This investigation was supported by NIH grant grant CA-29290 to B.M. To whom reprint requests should be addressed.",

year = "1983",

month = aug,

day = "8",

doi = "10.1016/0024-3205(83)90131-5",

language = "English (US)",

volume = "33",

pages = "561--568",

journal = "Life Sciences",

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T1 - Direct modulation of epidermal growth factor binding by cholecystokinin

AU - Korc, Murray

AU - Matrisian, Lynn M.

AU - Magun, Bruce E.

N1 - Funding Information: This investigation was supported by NIH grant grant CA-29290 to B.M. To whom reprint requests should be addressed.

PY - 1983/8/8

Y1 - 1983/8/8

N2 - The effects of cholecystokinin-octapeptide (CCK8), the biologically active C-terminal moiety of cholecystokinin (CCK), on the binding of epidermal growth factor (EGF) were studied in isolated rat pancreatic acini. CCK8 inhibited 125I-EGF binding in a dose-dependent manner. One-half maximal inhibition occurred at 5 × 10-10M, and maximal inhibition at 10-8M CCK8. This inhibitory effect was detectable within 5 minutes of addition of CCK8, and was not associated with enhanced degradation of 125I-EGF in incubation media. Unlabeled EGF exerted only a slightly greater inhibitory effect than CCK8 on 125I-EGF binding at equivalent molar concentrations. In contrast to CCK8, the gastrointestinal hormone vasoactive intestinal polypeptide (VIP) did not significantly alter EGF binding. CCK8 also inhibited EGF binding in mouse pancreatic acini, but did not alter binding in A-431 human carcinoma cells. These findings suggest that physiological levels of CCK may regulate EGF binding in the pancreas and other tissues with receptors for both hormones. They thus point to a previously unrecognized mechanism for hormonal interaction.

AB - The effects of cholecystokinin-octapeptide (CCK8), the biologically active C-terminal moiety of cholecystokinin (CCK), on the binding of epidermal growth factor (EGF) were studied in isolated rat pancreatic acini. CCK8 inhibited 125I-EGF binding in a dose-dependent manner. One-half maximal inhibition occurred at 5 × 10-10M, and maximal inhibition at 10-8M CCK8. This inhibitory effect was detectable within 5 minutes of addition of CCK8, and was not associated with enhanced degradation of 125I-EGF in incubation media. Unlabeled EGF exerted only a slightly greater inhibitory effect than CCK8 on 125I-EGF binding at equivalent molar concentrations. In contrast to CCK8, the gastrointestinal hormone vasoactive intestinal polypeptide (VIP) did not significantly alter EGF binding. CCK8 also inhibited EGF binding in mouse pancreatic acini, but did not alter binding in A-431 human carcinoma cells. These findings suggest that physiological levels of CCK may regulate EGF binding in the pancreas and other tissues with receptors for both hormones. They thus point to a previously unrecognized mechanism for hormonal interaction.

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DO - 10.1016/0024-3205(83)90131-5

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VL - 33

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JO - Life Sciences

JF - Life Sciences

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ER -

Direct modulation of epidermal growth factor binding by cholecystokinin

Abstract

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