| Project/Area Number |
17592184
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Social dentistry
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
YAMAGUCHI Noboru Kyushu University, Faculty of Dental Science, Preventive Dentistry, Research Associate, 歯学研究院, 助手 (00230368)
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| Co-Investigator(Kenkyū-buntansha) |
舛廣 善和 九州大学, 大学院・歯学研究院, 助手 (00336083)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2006: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | diabetes / periodontal disease / periodontopathic bacteria / osteoclast / adiponectin / RANKL / NF-KB / nitric oxide / NF-kappaB / 免疫学 / 細胞 / Toll-like receptor |
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| Research Abstract |
Our previous epidemiologic studies suggested that periodontal disease is closely related to obesity and glucose tolerance. Since the level of adiponectin, an adipocyte-derived cytokine, in plasma had been reported to decrease in obese and type 2 diabetes patients, we explored the role of adiponectin in the etiology of periodontitis by using the D clone of RAW 264, which clone exhibits highly efficient osteoclast formation, to determine whether adiponectin acts as a regulatory molecule in osteoclast formation stimulated by lipopolysaccharide (LPS) of periodontopathic bacteria.
We observed that adiponectin acted as a potent inhibitor of osteoclast formation stimulated by Toll-like receptor 4 (TLR4) ligand and receptor activator of NF-κB ligand (RANKL). Since NF-κB is an important transcriptional factor in osteoclast formation, we examined the effect of the adiponectin on its transcriptional activity. Our luciferase assay showed that adiponectin was able to inhibit the TLR4-mediated NF-κB activity in RAW 264 cells. In addition, we observed that the cytokine was actually able to inhibit TLR4-mediated expression of the gene for inducible nitric oxide synthase and production of nitric oxide in the cells. These observations strongly suggest that adiponectin may function as a negative regulator of LPS/RANKL-mediated osteoclast formation in periodontal disease.
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