Gene Therapy of Rheumatoid Arthritis
| Project/Area Number |
08557037
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
内科学一般
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KOHSAKA Hitoshi First Department of Intemal Medicine, School of Medicine, Tokyo Medical and Dental University, Assistant, 医学部, 助手 (00251554)
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| Co-Investigator(Kenkyū-buntansha) |
MIYASAKA Nobuyuki First Department of Intemal Medicine, School of Medicine, Tokyo Medical and Dent, 医学部, 教授 (30157622)
SASANO Minoru Research and Development Santen Pharmaceuticals, 開発研究本部, 主任研究員
TERADA Yoshio Second Department of Intemal Medicine, School of Medicine , Tokyo Medical and De, 医学部, 助手 (30251531)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥11,700,000 (Direct Cost: ¥11,700,000)
Fiscal Year 1998: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1997: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 1996: ¥6,300,000 (Direct Cost: ¥6,300,000)
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| Keywords | Rheumatoid Arthritis / CDKI / Gene Therapy / p16 / Adenovirus / p21 / アデノウィルス |
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| Research Abstract |
The synovia affected by rheumatoid arthritis (RA) is characterized by synovial proliferation which leads to irreversible cartilage and bone destruction. Current and experimental treatments have been aimed largely at correction of the underlying immune abnormalities, but these treatments often prove ineffective in preventing the invasive destruction. We studied the expression of cyclin dependent kinase inhibitors in rheumatoid synovial cells as a means of suppressing synovial cell proliferation. The results showed that the synoviial cells derived from hypertrophic synovia readily express pl6TNK4A when they were growth-inhibited. This was not. observed in other types of fibroblasts. In vivo adenoviral gene therapy with the plGINK4A gene efficiently inhibited the pathology in an animal model of RA.These observations indicated that the induction of pl6TNK4A may provide a novel approach to the effective treatment of RA.
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Report
(4 results)
Research Products
(8 results)
