| Project/Area Number |
15K10493
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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 |
Orthopaedic surgery
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| Research Institution | Keio University |
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Principal Investigator |
SATO KAZUKI 慶應義塾大学, 医学部(信濃町), 准教授 (60235322)
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| Co-Investigator(Kenkyū-buntansha) |
宮本 健史 慶應義塾大学, 医学部(信濃町), 特任准教授 (70383768)
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| Research Collaborator |
MITO Kazuaki
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | ニコチン / α7nAchR / 骨代謝 / 喫煙 / 副交感神経 |
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| Outline of Final Research Achievements |
The nicotinic receptor α7nAchR reportedly regulates vagal nerve targets in brain and cardiac tissues, and the parasympathetic nervous system; however, ite roles in bone metabolism were remained to be elucidated. Moreover, smoking is known as a risk of osteoporosis development, however, the mechanisms underlying have not been clarified. Our study revealed that α7nAchR suppressed TNFαexpression in macrophages, decreased osteoprotegerin/RANKL ratio via the parasympathetic nervous system and upregulated osteoclastogenesis, resulting in loss of bone mass. Nicotine, the ligand of α7nAchR, activated the system. We now clarified a novel mechanism underlying controlling bone metabolism by the parasympathetic nervous system, and how nicotine, a main bioactive substance taken by smoking, affected bone.
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