| Project/Area Number |
26293401
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Okayama University |
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Principal Investigator |
OHARA Naoya 岡山大学, 医歯(薬)学総合研究科, 教授 (70223930)
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| Co-Investigator(Kenkyū-buntansha) |
中山 真彰 岡山大学, 医歯(薬)学総合研究科, 助教 (10579105)
大原 直子 岡山大学, 医歯(薬)学総合研究科, 助教 (80301365)
井上 哲圭 岡山大学, 医歯(薬)学総合研究科, 助教 (20223258)
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| Research Collaborator |
TAGUCHI Yuko
KANO Konami
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥16,510,000 (Direct Cost: ¥12,700,000、Indirect Cost: ¥3,810,000)
Fiscal Year 2016: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2015: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2014: ¥10,270,000 (Direct Cost: ¥7,900,000、Indirect Cost: ¥2,370,000)
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| Keywords | 歯周病原細菌 / 歯周病 / ジンジパイン / PI3K/Akt / 歯周病細菌 / PI3K/Akt経路 / 細菌 / 病原因子 / シグナル伝達 |
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| Outline of Final Research Achievements |
Periodontal diseases are chronic oral bacterial infectious diseases. In our study, Porphyromonas gingivalis, which is one of major oral pathogens, produces cysteine proteases called as gingipains. Gingipains attenuate PI3K/Akt signaling pathway, and which is associated with their protease activity from extracellular interaction without invasion of this organisms. Moreover, several downstream proteins of Akt, which are GSK3, mTOR, Bad, PRAS40, and MDM2, are also changed the their phosphorylation level by gingipains in gingival epithelial cells. On the basis of the results, their physiological activity might be dysregulated by gingipains in parallel with inactivation of PI3K/Akt in the cells.
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