title: Expression of a specific mucin type recognized by monoclonal antibodies in the rat gastric mucosa regenerating from acetic acid-induced ulcer.
abstract: BACKGROUND
  Detailed research on the healing process of gastric mucosa from injury due to various necrotizing agents is important for regenerating medicine as well as for estimating the quality of ulcer healing. To elucidate this issue, we prepared monoclonal antibodies reacting with mucin molecules present in the specific region and layer of the gastrointestinal mucosa.
  
  
  METHODS
  Acetic acid-induced gastric ulcers were prepared in 8-week-old male Wistar rats. Following 24-h fasting, the animals were killed at 20, 30 and 50 days after acid insult and their stomachs were removed immediately. Serial paraffin sections of the ulcer area were made and immunostained with three distinct monoclonal antibodies. RGM21 and HIK1083 react with mucins derived from the surface mucous cells of the corpus and the gland mucous cells of corpus and antrum, respectively. HCM31 stains sialomucin present in the small intestine and colonic mucosa of rat, but does not react with the intact gastric mucosa, except in the very narrow cardiac gland area.
  
  
  RESULTS
  On the 20th day after ulcer preparation, the cells stained with RGM21 and HIK1083 were restricted only to the surface layer and the bottom layer of regenerating epithelia, respectively. HCN31 staining covered most of the regenerating epithelia. On the 30th day, the staining of HCM31 was enhanced in the regenerating area. Staining of RGM21 did not change, but the HIK1083 stained area increased in the lower part of the regenerating epithelia. On the 50th day, the staining with HCM31 weakened markedly in the lower part, and this area was occupied with HIK1083 positive cells.
  
  
  CONCLUSIONS
  A notable but temporary expression of a kind of sialomucin specifically stained with HCM31 was observed in the regenerating epithelia during the healing stage of acetic acid-induced gastric damage.
authors.affiliation: Dept. of Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Hayashida
authors.forename: K
authors.initials: K
authors.lastname: Ishihara
authors.forename: T
authors.initials: T
authors.lastname: Ichikawa
authors.forename: I
authors.initials: I
authors.lastname: Okayasu
authors.forename: M
authors.initials: M
authors.lastname: Kurihara
authors.forename: K
authors.initials: K
authors.lastname: Saigenji
authors.forename: K
authors.initials: K
authors.lastname: Hotta
mesh_terms: D019342:Acetic Acid / Q000009:adverse effects*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000502:physiology*; D004195:Disease Models, Animal; D005752:Gastric Mucins / Q000502:physiology*; D005753:Gastric Mucosa / Q000276:immunology / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012038:Regeneration / Q000502:physiology*; D013276:Stomach Ulcer / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology*
chemical_list: D000911:Antibodies, Monoclonal; D005752:Gastric Mucins; D019342:Acetic Acid