Restoration of Steroid-Resistant Characters of IBD
Project/Area Number |
12670451
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | Asahikawa Medical College |
Principal Investigator |
ASHIDA Toshifumi Asahikawa Medical College, Third Internal Medicine, INSTRUCTOR, 医学部, 助手 (50261409)
|
Co-Investigator(Kenkyū-buntansha) |
KONGO Yutaka Asahikawa Medical College, Third Internal Medicine, PROFFESSOR, 医学部, 教授 (10133183)
|
Project Period (FY) |
2000 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2000: ¥1,900,000 (Direct Cost: ¥1,900,000)
|
Keywords | UC / IBD / hGR / GC resistant / IL-18 / PBMC / 炎症性腸疾患 / 潰瘍性大腸炎 / Glucocorticoid receptor / ステロイド抵抗性 / glucocorticoid receptor / hGR beta |
Research Abstract |
The aim of this study is to analyze the expressions of human glucocorticoid receptor isoforms in PBMC obtained from IBD patients, in relation to the clinical unresponsiveness to the therapeutic dose of GC We found that, (1)mRNA expression of hGRbeta isoform in PBMC obtained from the UC patients with GC resistant results of the therapeutic intercourses were quite increased in QRT-PCR analysis. (2)Sequential measurement of hGRbeta mRNA in those patients revealed that the induction of hGRbeta isoform occurred during the flare-up of the disease, suggesting the role of inflammatory cytokines. (3)In in vitro examination, hGRbeta mRNA was induced by IL-18 in both T lymphoma cell line CEM and normal PBMC. Through the analysis, we conclude that hGRbeta mRNA expression is strikingly associated with the GC-resistant nature of UC patients, and induced by proinflammatory cytokine of IL-18. These results were published in BBRC,2002.
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Report
(4 results)
Research Products
(8 results)