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Mechanism of gastric mucosal proliferation induced by gastrin
Author(s) -
Kinoshita Yoshikazu,
Ishihara Shunji
Publication year - 2000
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2000.02145.x
Subject(s) - enterochromaffin like cell , gastrin , amphiregulin , g cell , medicine , foveolar cell , endocrinology , epidermal growth factor , gastric mucosa , progenitor cell , gastric chief cell , microbiology and biotechnology , secretion , biology , cell growth , receptor , cancer research , stem cell , stomach , genetics
Gastrin has a potent trophic effect on gastric fundic mucosa. When serum concentrations of gastrin are elevated, proliferation of both the progenitor cells in the glandular neck zone and enterochromaffin‐like (ECL) cells in the bottom of the glands is stimulated. Because ECL cells have gastrin receptors, their proliferation is directly stimulated by gastrin. However, because the proliferation of progenitor cells cannot be directly stimulated (so far there has been no gastrin receptor demonstrated on these proliferating cells), some indirect mechanisms must be involved. Enterochromaffin‐like and parietal cells are only two types of cells that have demonstrated a strong gene expression of the gastrin receptor. Furthermore, they secrete several growth factors, such as Reg protein, heparin‐binding epidermal growth factor‐like growth factor (HB‐EGF) and amphiregulin (AR). Reg protein production by ECL cells, as well as HB‐EGF and AR production by parietal cells, is stimulated by gastrin and these growth factors are potent trophic agents of progenitor cells in the neck zone of the gastric fundic mucosa. Accordingly, gastrin may stimulate the proliferation of gastric mucosal cells indirectly via these growth factors in addition to its direct trophic effect on ECL cells.