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Articles in PresS, published online ahead of print September 21, 2001
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00117.2001
Submitted on March 21, 2001
Accepted on September 16, 2001
1 Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine, Kyoto, Kyoto, Japan
2 Molecular Medicine, Gunma University, Institute for Molecular and Cellular Regulation, Maebashi, Gunma, Japan
* To whom correspondence should be addressed. E-mail: tstake{at}showa.gunma-u.ac.jp.
Gastrin/CCK-B receptors (CCKB-Rs) are present on parietal and enterochromaffin-like cells in the gastric mucosa, but not on pit cells in the proliferative zone. Because serum gastrin levels are well correlated with the growth of the gastric pit, we examined whether pit precursor cells express CCKB-Rs, using hypergastrinemic transgenic mice and a mouse pit precursor cell line, GSM06. In situ hybridization indicated that CCKB-R mRNA was limited to the lower one-third of the mucosa in control mice, whereas it was faintly distributed along the mid- to low-glandular region in the hypergastrinemic transgenic mouse mucosa. CCKB-R-positive mid-glandular cells appear to have a pit cell lineage, therefore GSM06 cells were used for an I-gastrin binding study. I-gastrin bound to the membrane fraction of the GSM06 cells when precultured with gastrin. Gastrin dose-dependently induced CCKB-R expression in GSM06 cells and stimulated their growth. Thus, these findings suggest that gastrin directly stimulate the growth of the pit cell lineage by inducing its own receptor in pit cell precursors.
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