Molecular biological approach of the arteriosclerosis onset mechanism by SAA derived from periodontal disease

2016 Fiscal Year Final Research Report

• 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: Nishida Eisaku 愛知学院大学, 歯学部, 助教 (10512519)
• Project Period (FY): 2013-04-01 – 2017-03-31
• 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

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.

Free Research Field

歯周病学