Elucidate of deteriorating mechanism of diabetic and periodontitis via receptor of advanced glycation endproducts
| Project/Area Number |
22792088
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Periodontal dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
UCHIDA Yushi 広島大学, 大学院・医歯薬学総合研究科, 助教 (40363080)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | S100タンパク質 / 歯肉上皮細胞 / 歯肉線維芽細胞 / IL-8 / 細胞間コミュニケーション / connexin43 / 骨髄由来間葉系幹細胞 / 石灰化能 / 糖尿病 / 歯周病 / 糖最終産物 / S100 / 歯肉繊維芽細胞 |
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| Research Abstract |
S100 protein increased the IL-8 levels in HGEC. Amounts of IL-8 in HGEC stimulated by S100 protein were 1. 5 times higher than non-stimulated cells for 48 hours. Production of connexin43 in HGEC was induced by 1. g/ ml S100 protein for 6 hours. However, production of connexin43 declined in HGEC stimulated by 10. g/ ml S100 protein for 24 hours. Gap junctional intercellular communication was induced by 1. g/ ml S100 protein for 12 hours, but inhibited by 10. g/ ml S100 protein for 24 hours. Porphynomonas gingivalis might induce IL-8 in HGEC via Receptor of advanced glycation endproducts.
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Report
(3 results)
Research Products
(2 results)
