| Project/Area Number |
17K11994
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Periodontology
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| Research Institution | Nihon University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
中山 洋平 日本大学, 松戸歯学部, 准教授 (30434088)
高井 英樹 日本大学, 松戸歯学部, 講師 (30453898)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 接合上皮 / アメロチン / ODAM / FDC-SP / 歯周病 / 予防 / 炎症 / TNF-α / 歯肉上皮細胞 / 歯周炎 |
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| Outline of Final Research Achievements |
Amelotin (AMTN) and Follicular dendritic cell secreted protein (FDC-SP) are secreted proteins expressed in junctional epithelium (JE). To elucidate the transcriptional regulation of AMTN and FDC-SP genes in inflamed gingiva, we have analyzed the effect of TNF-α on the expression of both genes in Ca9-22 human gingival epithelial cells. TNF-α increased AMTN and FDC-SP mRNA and protein levels after 12 h. TNF-α induced luciferase (LUC) activities of human AMTN and FDC-SP gene promoter constructs in Ca9-22 cells. TNF-α induced LUC activities were partially inhibited in the mutation -353AMTN constructs that included mutations in C/EBP1, C/EBP2 and YY1 elements. Transcriptional stimulations by TNF-α were partially inhibited in the -345FDCSP constructs that included mutations in the YY1, GATA, C/EBP2 and C/EBP3. Transcriptional activities induced by TNF-α were inhibited by tyrosine kinase, MEK1/2 and phosphoinositide 3-kinase inhibitors.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究の成果により、接合上皮で発現するアメロチン(AMTN)、ODAMおよびFDC-SPの転写調節機構および相互作用と機能の一部が解明され、接合上皮内での発現制御による歯周病予防に関する基盤データーが得られる可能性がある。その結果、将来的に歯周病の予防だけでなく、「接合上皮発現タンパク質の制御による新たな治療法」につながる可能性があり、意義は大きく、社会的貢献度が高いテーマであると思われる。
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