title: Effects of dexamethasone on antral mucosal protein and gastric development in postnatal rats.
abstract: BACKGROUND
  The rat stomach undergoes major developmental changes postnatally. An antral mucosal protein (AMP-18) with in vitro mitogenic activity has recently been found in the mammalian stomach.
  
  
  METHODS
  To evaluate the role of AMP-18 in gastric development in postnatal rats, the AMP-18 content of glandular stomach extracts from postnatal rats at different ages were measured by Western blots using anti-AMP-18 specific serum. Dexamethasone administration was used to evaluate the corticosteroid regulation of AMP-18 expression.
  
  
  RESULTS
  AMP-18 was detected only in glandular stomach homogenate and gastric mucus. AMP-18 and pepsin levels were high at birth. Both decreased postnatally to low levels at 7 days of age, then increased at 10-15 days of age and reached peak levels around weaning (18-21 days of age). The glandular stomach showed stepwise growth relative to body weight, with a significant increase at 18-20 days of age. The forestomach showed a decrease in growth relative to body weight during the same period. Dexamethasone given to pups before 7 days of age induced the accumulation of AMP-18 and pepsin. Induction of AMP-18 by dexamethasone was evident by 7 hours with a delayed increase in glandular stomach mass 30 hours after dexamethasone injection. Induction of AMP-18 by dexamethasone was attenuated by RU-486 but not by spironolactone.
  
  
  CONCLUSIONS
  Increases in AMP-18, pepsin and glandular stomach mass during normal postnatal development suggest that AMP-18 might be involved in gastric maturation, at least in the glandular portion. Dexamethasone induction of pepsin and AMP-18 and the subsequent increase in glandular stomach mass also suggest a possible role for AMP-18 in glandular stomach maturation. Dexamethasone apparently acts through the type II corticosteroid receptor to induce AMP-18.
authors.affiliation: Department of Pediatrics and Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.
authors.forename: Michael K
authors.initials: MK
authors.lastname: Petri
authors.forename: Ping C
authors.initials: PC
authors.lastname: Lee
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D003907:Dexamethasone / Q000494:pharmacology*; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects / Q000254:growth & development; D018507:Gene Expression Regulation, Developmental; D005938:Glucocorticoids / Q000494:pharmacology*; D007150:Immunohistochemistry; D008297:Male; D008934:Mitogens / Q000378:metabolism*; D010434:Pepsin A / Q000378:metabolism; D036361:Peptide Hormones; D010455:Peptides; D051381:Rats; D017207:Rats, Sprague-Dawley; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism; D013270:Stomach / Q000187:drug effects* / Q000254:growth & development*
chemical_list: C477000:GKN1 protein, human; D005938:Glucocorticoids; D008934:Mitogens; D036361:Peptide Hormones; D010455:Peptides; D011965:Receptors, Glucocorticoid; D003907:Dexamethasone; D010434:Pepsin A