- Author:
Min MIN
;
Jing YANG
;
Yun-Sheng YANG
1
;
Yan LIU
;
Li-Mei LIU
;
Yang XU
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Blotting, Western; Colitis, Ulcerative; immunology; metabolism; pathology; Enzyme-Linked Immunosorbent Assay; Female; Forkhead Box Protein O3; genetics; metabolism; HT29 Cells; Humans; Inflammation; immunology; metabolism; pathology; Interleukin-8; metabolism; Intestines; immunology; metabolism; pathology; Male; Middle Aged; Real-Time Polymerase Chain Reaction; Tumor Necrosis Factor-alpha; metabolism
- From: Chinese Medical Journal 2015;128(20):2759-2763
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDUlcerative colitis (UC) is associated with differential expression of genes involved in inflammation and tissue remodeling, including FOXO3a, which encodes a transcription factor known to promote inflammation in several tissues. However, FOXO3a expression in tissues affected by UC has not been examined. This study investigated the effects of FOXO3a on UC pathogenesis.
METHODSFOXO3a expression, in 23 patients with UC and in HT29 cells treated with tumor necrosis factor-α (TNF-α) for various durations, was detected by quantitative real-time polymerase chain reaction and Western blotting analysis. Enzyme-linked immunosorbent assay was used to quantify interleukin (IL)-8 expression in FOXO3a-silenced HT29 cells treated with TNF-α for various durations.
RESULTSThe messenger RNA and protein expression of FOXO3a were significantly lower in UC tissues than those in normal subjects (P < 0.01). TNF-α treatment for 0, 0.5, 1, 6, and 24 h induced FOXO3 degradation in HT29 cells. FOXO3a silencing increased IL-8 levels in HT29 cells treated with TNF-α for 6 h (P < 0.05).
CONCLUSIONFOXO3a may play an important role in the intestinal inflammation of patients with UC.