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ID 30955
file
creator
subject
X-irradiation
rat
glandular stomach
intestinal metaplasia
gastric cancer
NDC
Medical sciences
abstract
This review concerns stem cells and their relation to intestinal metaplasia. When gastric regions of mice, Mongolian gerbils or several strains of rats were irradiated with a total dose of 20 Gy of X-rays given in two fractions, intestinal metaplasia was only induced in rats. In addition, it was greatly influenced by rat strain and sex. Alkaline phosphatase (ALP) positive metaplastic foci were increased by administration of ranitidine (H2 receptor antagonist), crude stomach antigens or subtotal resection of the fundus and decreased by cysteamine (gastric acid secretion stimulator), histamine or removal of the submandibular glands. Recent studies have shown that Cdx2 transgenic mice with gastric achlorhydria develop intestinal metaplasia and that in men and animals, Helicobacter pylori (H. pyrlori) infection can cause intestinal metaplasias that are reversible on eradication. Our results combined with findings for H. pylori infection or eradication and transgenic mice suggest that an elevation in the pH of the gastric juice due to disappearance of parietal cells is one of the principal factors for development of reversible intestinal metaplasia. When different organs were transplanted into the stomach or duodenum, they were found to transdifferentiate into gastric or duodenal mucosae, respectively. Organ-specific stem cells in normal non-liver tissues (heart, kidney, brain and skin) also differentiate into hepatocytes when transplanted into an injured liver. Therefore, stem cells have a multipotential ability, transdifferentiating into different organs when transplanted into different environments. Finally, intestinal metaplasia has been found to possibly increase sensitivity to the induction of tumors by colon carcinogens of the 1,2-dimethylhydrazine (DMH), azoxymethane (AOM) or 2-amino-1-methyl-6-phenylimidazo[4.5-b]pyridine (PhIP) type. This carcinogenic process, however, may be relatively minor compared with the main gastric carcinogenesis process induced by N-methy1-N'-nitro-N-nitrosoguanidine (MMNG) or N-met
journal title
Journal of toxicologic pathology
volume
Volume 23
issue
Issue 3
start page
115
end page
123
date of issued
2010
publisher
日本毒性病理学会
issn
0914-9198
ncid
publisher doi
language
eng
nii type
Journal Article
HU type
Journal Articles
DCMI type
text
format
application/pdf
text version
publisher
rights
Copyright (c) 2010 The Japanese Society of Toxicologic Pathology
relation url
department
Research Institute for Radiation Biology and Medicine