TXNIP expression and mucosal immunity in the epithelium in patients with inflammatory bowel disease
| Project/Area Number |
16591359
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | Nihon University |
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Principal Investigator |
TAKAHASHI Yasuo Nihon University, School of Medicine, Assistant, 医学部, 助手 (30339329)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Inflammatory bowel disease / TXNIP / Ulcerative colitis / Gene expression |
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| Research Abstract |
Ulcerative colitis (UC) is a form of inflammatory bowel disease associated with chronic inflammation and tissue damage of intestine, specifically the large intestine or colon. It is assumed that the oxidative stress that accompanies chronic inflammation contributes to the development of colorectal cancer (CRC) of UC patients. Thioredoxin interacting protein (TXNIP) is a negative regulator of thioredoxin, which is an important regulator of redox balance. TXNIP expression is induced by various types of stress including oxidative stress, and is downregulated in various types of human cancer including colorectal cancer. Previously, we reported that the TXNIP transcript is abundant in terminal differentiated epithelial cells in the colonic mucosa and in lymphocytes in the lymphoid follicles (14). However, TXNIP expression in clinical specimens of UC remains unclear. In this study, using TaqMan RT-PCR assay, we demonstrated that TXNIP expression in UC and CRC colonic mucosa specimens was significantly lower than that in normal tissues. In addition, in situ hybridization study showed that inflammatory cells expressing the TXNIP transcript were abundant in lymphoid follicles, the lamina propria and submucosa in the colonic mucosa of UC patients, but not in epithelial cells at the flat surface. Our results suggest that downregulation of TXNIP may be involved in the pathogenesis of UC, including inflammation and colitis associated colon carcinogenesis.
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Report
(3 results)
Research Products
(2 results)
