Elucidation of the arteriosclerosis pathogenesis through periodontal disease derived from serum amyloid A (SAA).
| Project/Area Number |
25862062
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Periodontology
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| Research Institution | Aichi Gakuin University (2015)
Matsumoto Dental University (2013-2014) |
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Principal Investigator |
MUTO AKINORI 愛知学院大学, 歯学部, 助教 (50549433)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 歯周病 / 動脈硬化 / 動脈硬化症 / 血清アミロイドA |
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| Outline of Final Research Achievements |
We noticed that elevated serum amyloid A (SAA) is an acute inflammation markers in mice was induced periodontal disease were analyzed the effect on arteriosclerosis of SAA.
Expression of arteriosclerosis induced factor VCAM-1, ICAM-1, MCP-1 was significantly increased by SAA in human vascular endothelial cells. And their expression was significantly reduced by the TLR2 neutralizing antibody which is one of SAA receptors. So the TLR2 neutralizing antibody, was injected to easy formation mouse (ApoE deficient mice). The results that TLR2 injected group was decrease of lipid deposition site more than control group. In this experiment, SAA would bind to TLR2 on the endothelial cells and increase the adhesion molecules expressions. We suggest that this is one of the pathways that SAA could accelerate the atherosclerosis.
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Report
(4 results)
Research Products
(6 results)
