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Growth of mouse hepatocytes is stimulated by gastrin
Author(s) -
Yao Chong Zheng,
Bold Richard J.,
Ishizuka Jin,
Townsend Courtney M.,
Thompson James C.
Publication year - 1995
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041630313
Subject(s) - gastrin , medicine , endocrinology , epidermal growth factor , hepatocyte , receptor , growth factor , biology , peptide hormone , cell culture , cell growth , gastrointestinal hormone , bromodeoxyuridine , g cell , hormone , chemistry , secretion , in vitro , biochemistry , genetics
Abstract Hepatocyte growth is regulated by various growth factors, including epidermal growth factor (EGF) and insulin. Recently, several additional peptide hormones have been shown to stimulate growth of hepatocyte only in the presence of EGF or insulin and are thus termed secondary mitogens. Gastrin regulates growth of normal and neoplastic gastrointestinal tissues, but the effect on growth of hepatocyte is unknown. We examined the effect of gastrin on growth of a normal mouse hepatocyte (NMH) line established in our laboratory. Effect of gastrin‐17 (G‐17) (10 −8 to 10 −6 M) on growth of NMH cells was examined in either the presence or absence of EGF in the culture medium. Growth of NMH cells was evaluated by incorporation of either bromodeoxyuridine (BrdU) or 3 H‐thymidine and by counting cells. Presence of a cell‐surface receptor for G‐17 was determined by Scatchard analysis using 125 I‐G‐17. In the presence of EGF, gastrin stimulated growth of NMH cells; in the absence of EGF, gastrin did not affect growth. The stimulatory effect of gastrin on NMH cells was blocked by JMV 320, a CCK‐B type receptor antagonist. NMH cells possess a single, high affinity binding site for gastrin (K d = 1.2 nM); EGF increased the gastrin binding capacity compared to non‐treated cells (3.5 ± 0.4 vs. 2.2 ± 0.6 fmol/10 6 cells). G‐17 stimulated growth of NMH cells through a single high affinity receptor for G‐17 which pharmcologically appears to be the CCK‐B type only in the presence of EGF and thus can be considered a secondary mitogen. © 1995 Wiley‐Liss, Inc.