Gastrin stimulates epithelial cell proliferation in the oesophagus of rats

Abstract

Gastrin can induce mitotic stimulation in the oxyntic mucosa of the stomach, sometimes leading to abnormal growth. We examined whether gastrin was able to influence cell proliferation in the oesophageal epithelium. Rats were treated with gastrin, omeprazole or saline for 3 days, or were subjected to fundectomy or sham operation. Bromodeoxyuridine labelling (LI) and mitotic (MI) indices were counted in the proliferative zone of the squamous epithelium. Infusion of exogenous gastrin, treatment with omeprazole or fundectomy raised the LI and the MI values in the oesophageal epithelium, indicating that gastrin stimulates cell proliferation in the oesophageal mucosa in the rat.

Gastrin Stimulates β-Cell Neogenesis and Increases Islet Mass From Transdifferentiated but Not From Normal Exocrine Pancreas Tissue

“…Therefore, in vitro experiments that try to reproduce this phenomenon seem to be promising. By infusing 2.5 nmol ⅐ kg -1 ⅐ h -1 , it was reported that a level of ϳ0.15 nmol/l gastrin is reached in the serum (14), which is in a range similar to the concentrations we used in culture experiments. Experiments in vitro showed that gastrin exerts a strong mitogenic effect on ductlike cells, obtained by culturing acinar cells, as described previously (8).…”

“…In our model of PDL (3), an internal control is present: the unligated part, which remains unaffected histologically and allows us to discriminate between effects of gastrin on normal exocrine tissue and on transdifferentiated cells. We evaluated the effect of intravenously administered gastrin (8,14) from day 7 postligation; this treatment lasted for 72 h. saline treatment. The treatment lasted for 72 h, and rats were fasted for 2 h before being killed on day 10 after duct ligation.…”

Immunohistochemical Examination of Gastrin, Gastrin Precursors, and Gastrin/CCK-2 Receptor in Human Esophageal Squamous Cell Carcinomas

“…Given the finding of potential roles of gastrin precursors in stimulating human cancer growth in vitro [25,43,44] and animal cancer models in vivo [26, 28, It is well known that the effect of amidated gastrin on stimulating gastrointestinal cancer cell growth was mediated by gastrin/CCK2 receptors [15,17,18], a gastringastrin/CCK2 receptor loop was found in some human cancers [15,16,20,24] and targeting of gastrin/CCK2 receptor by peptide or antibody exhibited a therapeutic potential in colonic, pancreatic and hepatocellular carcinoma cell lines in vitro [46]. In animals, gastrin has been found to stimulate normal esophageal epithelium proliferation [31,47,48] and promote carcinogenesis [32]. In Barett's esophagus, gastrin induces proliferation [33], metaplasia [33], and reduced apoptosis [21], which were mediated by upregulated gastrin/CCK2 receptors [21,33].…”

“…In animals, amidated gastrin was previously shown to stimulate the proliferation of esophageal epithelium in rats by either omeprazole (a potent gastric acid inhibitor) induced hypergastrinemia or infused gastrin-17 [30,31]. Karaki et al [32] reported that hypergastrinemia in rats enhances chemical carcinogen induced esophageal carcinoma.…”

Detection and localization of MIP‐3α/LARC/exodus, a macrophage proinflammatory chemokine, and its CCR6 receptor in human pancreatic cancer

“…Activation of some members of the G-protein linked 7-transmembrane receptor family, such as the bombesin or gastrin receptors, is known to enhance the proliferation of some cells (Chu et al, 1996;Van Nieuwenhove et al, 1998;Shulkes and Baldwin, 1997;Rozengurt, 1998). Therefore, we next sought to determine whether Mip-3␣ also modulated pancreatic cancer cell growth.…”