Analysis of genetic risk factors in periodontal diseses ― Effect of cellular aging on damage of cells ―
| Project/Area Number |
12557178
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
矯正・小児・社会系歯学
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
HASEGAWA Tomokazu Hokkaido Univ., Grad. School of Dent., Inst., 大学院・歯学研究科, 助手 (50274668)
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| Co-Investigator(Kenkyū-buntansha) |
KIKUIRI Takashi Hokkaido Univ., Grad. School of Dent., Inst., 大学院・歯学研究科, 助手 (10322819)
SAITOH Akira Hokkaido Univ., Grad. School of Dent., Inst., 大学院・歯学研究科, 助手 (20301913)
SHIRAKAWA Tetsuo Hokkaido Univ., Dent. Hospital, Lec., 歯学部・附属病院, 講師 (00187527)
FUKUMOTO Satoshi Nagasaki Univ., School of Dent., Inst., 歯学部, 助手 (30264253)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥10,700,000 (Direct Cost: ¥10,700,000)
Fiscal Year 2001: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2000: ¥8,600,000 (Direct Cost: ¥8,600,000)
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| Keywords | genetic risk factor / periodontal disease / Down syndrome / telomere DNA length / cellular aging / Interferon receptor / STAT1 / Interleukin-6 / 先天性リスクファクター / STA1 / 特異的発現遺伝子 / DNA chip / Microarray |
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| Research Abstract |
1. Telomere DNA length of human fibroblasts derived from healthy and Down syndrome patients was analyzed by Southern blotting. After 5 times cell replication, it was shown that telomere DNA length was more short in fibroblasts from Down syndrome than from healty fibroblasts.
2. Fibroblasts derived from Down syndrome patients expressed interferon alpha/ beta (IMF-α/β) receptor subunit, IFNAR1, stronger than fibroblasts from healthy patients.
3. STAT1, one of transcriptional factors in the downstream of IMF receptor, was activated by the treatment of INF- γ. Western blotting demonstrated that activated STAT1 in Down fibroblasts was expressed stronger than in healthy fibroblasts after the treatment of INF-γ. However, in the presence of anti-INF-β antibody, activated STAT1 was reduced by the treatment of INF-γ.
4. Interleukin-6 (IL-6), one of inflammatory cytokines, was induced by the treatment of INF -γ. ELISA demonstrated that IL-6 production in Down fibroblasts increased more abundantly than in healthy fibroblasts by the treatment of INF- γ.
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Report
(3 results)
Research Products
(6 results)
