title: Conversion of gastric mucosa to intestinal metaplasia in Cdx2-expressing transgenic mice.
abstract: Gastric intestinal metaplasia occurs as a pathological condition in the gastric mucosa. To clarify how an intestine-specific homeobox gene, Cdx2, affects the morphogenesis of gastric mucosa, we generated transgenic mice expressing Cdx2 in parietal cells. Until Day 18 after birth, the number of parietal cells inthegastric mucosa of transgenic mice was the same as for their normal littermates. However, at Day 19, we detected several glands in which parietal cells disappeared and the proliferating zone moved from the isthmus to the base of the glands. Thereafter, parietal cells decreased gradually and disappeared at Day 37. All of the gastric mucosal cells, except for enterochromaffin-like (ECL) cells, were completely replaced by intestinal metaplasia, consisting of goblet cells, enteroendocrine cells, and absorptive cells expressing alkaline phosphatase. Pseudopyloric gland metaplasia was also formed. The transgenic mouse is a very useful model for clarifying physiological differentiation of gastric and intestinal cell lineages and analyzing the molecular events from intestinal metaplasia to adenocarcinoma.
authors.affiliation: Department of Gastroenterology, Jichi Medical School, Yakushiji 3311-1, Minamikawachimachi, Kawachigun, Tochigi 329-0498, Japan. muto@jichi.ac.jp
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Mutoh
authors.forename: Yoji
authors.initials: Y
authors.lastname: Hakamata
authors.forename: Kiichi
authors.initials: K
authors.lastname: Sato
authors.forename: Akashi
authors.initials: A
authors.lastname: Eda
authors.forename: Ichiro
authors.initials: I
authors.lastname: Yanaka
authors.forename: Sayaka
authors.initials: S
authors.lastname: Honda
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Osawa
authors.forename: Yoshinari
authors.initials: Y
authors.lastname: Kaneko
authors.forename: Kentaro
authors.initials: K
authors.lastname: Sugano
mesh_terms: D000375:Aging; D000818:Animals; D000071616:CDX2 Transcription Factor; D002454:Cell Differentiation; D002455:Cell Division; D004195:Disease Models, Animal; D018450:Disease Progression; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology*; D017506:H(+)-K(+)-Exchanging ATPase / Q000235:genetics; D018398:Homeodomain Proteins / Q000096:biosynthesis* / Q000235:genetics; D007413:Intestinal Mucosa / Q000473:pathology*; D008679:Metaplasia / Q000473:pathology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D010295:Parietal Cells, Gastric / Q000378:metabolism / Q000473:pathology*; D011401:Promoter Regions, Genetic / Q000235:genetics; D015534:Trans-Activators
chemical_list: D000071616:CDX2 Transcription Factor; D018398:Homeodomain Proteins; D015534:Trans-Activators; D017506:H(+)-K(+)-Exchanging ATPase