| Project/Area Number |
17209057
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Nagasaki University |
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Principal Investigator |
NAKAYAMA Koji Nagasaki University, Graduate School of Biomedical Sciences, Professor (80150473)
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Toru Nagasaki University, Graduate School of Biomedical Sciences, Professor (00211029)
YOSHMURA Atsutoshi Nagasaki University, Graduate School of Biomedical Sciences, Associate Professor (70253680)
SAKAI Eiko Nagasaki University, Graduate School of Biomedical Sciences, Assistant Professor (10176612)
NAITO Mariko Nagasaki University, Graduate School of Biomedical Sciences, Assistant Professor (20244072)
AMANO Atsuo Osaka University, Graduate School of Dental Science, Professor (50193024)
大原 直也 長崎大学, 大学院・医歯薬学総合研究科, 助教授 (70223930)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥49,530,000 (Direct Cost: ¥38,100,000、Indirect Cost: ¥11,430,000)
Fiscal Year 2007: ¥14,430,000 (Direct Cost: ¥11,100,000、Indirect Cost: ¥3,330,000)
Fiscal Year 2006: ¥14,430,000 (Direct Cost: ¥11,100,000、Indirect Cost: ¥3,330,000)
Fiscal Year 2005: ¥20,670,000 (Direct Cost: ¥15,900,000、Indirect Cost: ¥4,770,000)
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| Keywords | Infectious Disease / Bacteria / Dental Science / Circulation ・ High Blood Pressure / Immunoloey / 骨代謝 |
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| Research Abstract |
The periodontopathic bacterium Porphyromonas gingivalis has the ability to agglutinate human erythrocytes. We found that the Hgp44 domain protein, which is encoded by gingipain-related genes of P. gingivalis, can agglutinate erythrocytes by using a recombinant Hgp44 protein. The target molecule on the cell surface of erythrocytes against Hgp44 was found to be glycophorin. Also, we found that a peptide encoded by a DNA region backward of the region encoding Hgp44 has the inhibitory effect on the Hgp44-mecliated hemagglutination.
P. gingivalis cell-induced platelet aggregation is particularly important for interaction between periodontal disease and cardiovascular disease. It has been believed that P. gingivalis-mediated platelet aggregation is caused by activation of PAR receptor on platelets by Arg-gingipain. However, we found that P. gingivalis cell-mediated platelet aggregation does not depend on Arg-gingipain but Hgp44 protein on the bacterial cell surface, anti-P. gingivalis antibody in serum, and FcγRIIa and GPIlb/IIIa on platelets.
Alveolar bone resorption is one of the characteristic symptoms in periodontal disease, which results in tooth loss. Tooth loss causes loss of the gingival crevice that is an anatomical niche for periodontal pathogens such as P. gingivalis. We found that culture supernatants of P. gingivalis have the ability to inhibit in vitro osteoclastogenesis from bone marrow macrophages and determined that a hemoglobin receptor protein (HbR), which is a major protein in the culture supernatants, is the inhibitor to osteoclast formation. The HbR protein inhibited RANKL-induced Akt phosphorylation and expression of NFATc1 and c-Fos.
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