Bax is downregulated in inflamed colonic mucosa of ulcerative colitis. (1st August 2000)

• Record Type: Journal Article
• Authors: Iimura, M; Nakamura, T; Shinozaki, S; Iizuka, B; Inoue, Y; Suzuki, S; Hayashi, N
• Is Part Of: Gut. Volume 47(2000)Supplement 2
• Page Start: 228
• Page End: 235
• Publication Date: 2000-08-01
• Subjects: ulcerative colitis -- apoptosis -- Bax -- Bcl-2 -- Bcl-xL -- CD95; Gastroenterology -- Periodicals; 616.33
• DOI: 10.1136/gut.47.2.228
• Languages: English
• ISSNs: 0017-5749

Abstract

Abstract : BACKGROUND AND AIMS: One form of epithelial cell injury in inflamed colonic mucosa in ulcerative colitis (UC) is reported to involve apoptosis of these cells. Bcl-2 family proteins Bax and Bcl-2 are the major regulators of apoptosis. The aim of this study was to elucidate the involvement of the Bax/Bcl-2 system in induction of apoptosis of the inflamed colonic epithelium in UC. METHODS: Colonic epithelium was isolated from colonic biopsy specimens. Expression of CD95, Bax, Bcl-xL, and Bcl-2 proteins was determined by western blotting. Bax gene expression was assessed by both reverse transcription-polymerase chain reaction (RT-PCR) followed by Southern hybridisation and a real time PCR assay. RESULTS: Equal levels of expression of CD95, Bcl-xL, and Bcl-2 proteins were noted in normal and UC colonic epithelia. Equal levels of expression of Bax protein and mRNA were noted in epithelia of normal colon and inactive UC. Levels of expression of Bax protein and mRNA were markedly reduced in inflamed UC colonic epithelium. CONCLUSIONS: Our study showed for the first time downregulation of Bax in inflamed colonic epithelium of UC. The Bax/Bcl-2 system did not seem to be involved in induction of apoptosis of epithelial cells in the inflamed colonic mucosa of UC.