Molecular biological approach of the arteriosclerosis onset mechanism by SAA derived from periodontal disease
| Project/Area Number |
25862065
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Periodontology
|
|---|
| Research Institution | Aichi Gakuin University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
|---|
| Keywords | 歯周病 / 動脈硬化症 / 血管内皮細胞 / 単球遊走因子 / 単球接着因子 / 毛管内皮細胞 |
|---|
| Outline of Final Research Achievements |
To reveal the molecular mechanism for periodontitis-induced atherosclerosis, I focused Serum amyloid A (SAA), an acute-phase protein. I investigated how do SAA affect human aortic endothelial cells (HAECs). As a result, SAA induced inflammatory molecules via TLR2, and then SAA also induced adhesion molecules. In addition, only the expression of MYD88 was lower in SAA- stimulated HAECs compared with unstimulated HAECs, it suggested that MyD88- independent pathway via TLR2 could be exist in this cascade. My result suggests that TLR2 may have a critical role to induce adhesion molecules following TLR2 signaling and the leukocyte cascade in SAA-stimulated HAECs. And SAA might be a predictive risk marker for atherosclerosis onset in patients with periodontitis.
|
Report
(5 results)
Research Products
(2 results)
