Epithelial expression of caveolin-2, but not caveolin-1, is enhanced in the inflamed mucosa of patients with ulcerative colitis

Citation
A. Andoh et al., Epithelial expression of caveolin-2, but not caveolin-1, is enhanced in the inflamed mucosa of patients with ulcerative colitis, INFLAMM B D, 7(3), 2001, pp. 210-214
Citations number
22
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
INFLAMMATORY BOWEL DISEASES
ISSN journal
10780998 → ACNP
Volume
7
Issue
3
Year of publication
2001
Pages
210 - 214
Database
ISI
SICI code
1078-0998(200108)7:3<210:EEOCBN>2.0.ZU;2-8
Abstract
Caveolae are vesicular invaginations of the plasma membrane that act as a s caffold of the assembly of many classes of signaling molecules, Caveolins a re the principal structural component of caveolae membranes, and three dist inct forms of caveolins have been identified: caveolin-1, caveolin-2, and c aveolin-3. In this study, we evaluated the changes in the caveolin-1 and ca veolin-2 expression in the inflamed mucosa of patients with IBD. Tissue sam ples were obtained endoscopically from patients with ulcerative colitis (UC ) (n = 18), Crohn's disease (n = 10) and ischemic colitis (n = 8). Normal c olorectal tissues were also obtained (n = 15). The caveolin expression was evaluated by standard immunohistochemical procedure. In normal colonic muco sa, caveolin-1 expression was detected in the smooth-muscle cells of the mu scularis mucosae and the endothelial cells, but caveolin-2 expression was n ot detected. In the inflamed mucosa of patients with active UC, caveolin-2 expression was clearly detectable as small scattered foci on the luminal su rfaces of epithelial cells, but caveolin-1 expression was similar to that i n normal mucosa. Caveolin-2 expression increased in accordance with the dis ease activity of UC. This enhanced caveolin-2 expression was not detected i n active Crohn's disease or ischemic colitis. In conclusion, we demonstrate d that the epithelial expression of caveolin-2 is markedly enhanced in the inflamed mucosa of patients with UC. It is likely that the enhanced caveoli n-2 expression in patients with UC was associated with the altered signal t ransductions in the intestinal epithelial cells. Furthermore, our results s uggest that there are differences in the phenotypic features of epithelial cells between UC and Crohn's disease.