Analysis of the disorder on cell function induced by advanced glycation end-product (AGE) in dental pulp, gingival and alveolar bone tissues
| Project/Area Number |
15K15701
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Conservative dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
中島 由紀子 徳島大学, 病院, 助教 (70709526)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 歯周病 / 糖尿病 / 老化 / 歯髄 / 歯肉 / 骨 / 最終糖化産物 |
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| Outline of Final Research Achievements |
This study investigated the effects of advanced glycation end-product (AGE) on 3-type cultured cells; dental pulp cells, bone cells and gingival cells. In some cell cultures, additive effects of AGE with P-gingivalis-derived lipopolysaccharide (P-LPS) were studied. In dental pulp cells, AGE induced pulp calcification by the increase of S100A and A9 expression via RAGE-MAPK pathway. In osteoblastic cells, AGE and P-LPS independently reduced alkaline phosphatase activity and bone nodule formation. The addition of both AGE and LPS further decreased these markers. AGE markedly decreased the protein levels of type 1 collagen and osteocalcin, and increased IL1β and S100A8. In gingival fibroblasts, AGE increased expression of IL-6 and ICAM1, and the ICAM1 expression decreased by NF-κB inhibitors. These results demonstrate that AGE may be a potent indicator in dental pulp and periodontal diseases of diabetic and aging patients.
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Report
(3 results)
Research Products
(11 results)
