NA-K+-ATPASE ALPHA(1)-MESSENGER-RNA AND BETA(1)-MESSENGER-RNA AND PROTEIN-LEVELS IN RAT SMALL-INTESTINE IN EXPERIMENTAL ILEITIS()

Citation
Ge. Wild et Abr. Thomson, NA-K+-ATPASE ALPHA(1)-MESSENGER-RNA AND BETA(1)-MESSENGER-RNA AND PROTEIN-LEVELS IN RAT SMALL-INTESTINE IN EXPERIMENTAL ILEITIS(), American journal of physiology: Gastrointestinal and liver physiology, 32(5), 1995, pp. 666-675
Citations number
53
Categorie Soggetti
Physiology
ISSN journal
01931857
Volume
32
Issue
5
Year of publication
1995
Pages
666 - 675
Database
ISI
SICI code
0193-1857(1995)32:5<666:NAABAP>2.0.ZU;2-S
Abstract
Na+-K+-adenosinetriphosphatase (ATPase) plays a key role in the absorp tion of electrolytes, water, and nutrients from the small intestine. T he expression of Na+-K+-ATPase was examined in isolated enterocytes du ring the course of the ileal inflammatory response elicited by intralu minal administration of 2,4,6-trinitrobenzenesulfonic acid. The ileal inflammatory response was characterized by a marked cellular infiltrat e, villous atrophy, and crypt hyperplasia along with fibrosis and smoo th muscle hypertrophy. Peak levels of myeloperoxidase were observed at day 7, and ileal mucosal injury was paralleled by increases in ileal mucosal permeability. Ileal enterocytes were harvested from days 3 to 30 after the induction of ileitis. Decreases in Na+-K+-ATPase function al activity were observed from days 3 to 21 and were accompanied by co rresponding decreases in Na+-K+-ATPase pump abundance, alpha(1)- and b eta(1)-protein expression, and mRNA abundance, whereas Na+-K+-ATPase t urnover, Michaelis-Menten constant values, and inhibition constant val ues for Na+ and ouabain, respectively, were unaltered. Alterations in transcriptional and posttran scriptional events may determine the chan ges in Na+-K+-ATPase activity in this particular model. Additionally o bserved increases in thymidine kinase and ornithine decarboxylase acti vities appear to signify alterations in the state of differentiation o f the ileal epithelium and may determine the phenotypic expression of enterocyte transporters and permeability in the setting of inflammatio n.