Investigation of molecular mechanism of S100A8 in diabetes-associated periodontitis
| Project/Area Number |
15H06451
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Periodontology
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| Research Institution | The University of Tokushima |
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Principal Investigator |
HIROSHIMA Yuka 徳島大学, 先端酵素学研究所(プロテオ), 特任助教 (60545143)
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 終末糖化産物 / 歯周病 / カルプロテクチン / 糖尿病 / S100A8 / 歯肉上皮細胞 |
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| Outline of Final Research Achievements |
Advanced glycation end-products (AGEs) in gingival tissues of diabetes patients aggravate periodontal disease, but the mechanisms are unknown. The aim of this study is to investigate effects of AGE and Porphyromonas gingivalis lipopolysaccharide (PgLPS) on calprotectin (S100A8/S100A9) expression in human gingival epithelial cells. Results demonstrate that AGE acts in synergy with PgLPS to increase S100A8 and S100A9 expression through the p38, JNK MAPK, and NF-κB and modulate localization of S100A8 and S100A9 in gingival epithelial cells. Calprotectin may be involved in the pathogenesis of diabetes-associated periodontitis.
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Report
(3 results)
Research Products
(2 results)
