| Project/Area Number |
16591876
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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 |
Functional basic dentistry
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| Research Institution | Aichi Gakuin University |
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Principal Investigator |
ARAI Michitsugu Aichi Gakuin University, SCH. DENT., ASSISTANT PROF. (20097538)
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| Co-Investigator(Kenkyū-buntansha) |
TOGARI Akifumi AICHI-GAKUIN UNIVERSTTY, SCH. DENT., PROFESSOR (80126325)
HIRUKAWA Koji AICHI-GAKUIN UNIVERSTTY, SCH. DENT., RESEARCH ASSOCIATE (60340147)
茂木 眞希雄 愛知学院大学, 歯学部, 講師 (00174334)
森田 あや美 愛知学院大学, 歯学部, 助手 (70301629)
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| Project Period (FY) |
2004 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,390,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥90,000)
Fiscal Year 2007: ¥390,000 (Direct Cost: ¥300,000、Indirect Cost: ¥90,000)
Fiscal Year 2006: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2005: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2004: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | neuropeptide Y / isoprenaline / osteoclastogenesis / bone marrow cell / sympathetic nerve / bone metabolism / cAMP / Y1 receptor / ニューロペプチドY骨髄細胞 / 骨芽細胞 / 破骨細胞 / アドレナリン |
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| Research Abstract |
In this project, we demonstrated a physiological role of neuropeptide Y (NPY), a co-transmitter with noradrenaline in peripheral sympathetic nerve fibers, in the nerve regulation of bone metabolism. The effect of NPY on the osteoclastogenesis in mouse bone marrow cell cultures treated with isoprenaline, a β-adrenergic receptor (β-AR) agonist, was examined. The mouse bone marrow cells constitutively expressed mRNAs for the NPY-Y1 receptor and β2-AR. NPY inhibited the formation of osteoclast-like cells induced by isoprenaline but not that by 1α, 25-dihydroxyvitamin D_3 (1a, 25(OH)_2D_3) or soluble receptor activator of nuclear factor-B_K ligand (RANKL); and it suppressed the production of RANKL and cyclic AMP (cAMP) increased by isoprenaline but not those increased by 1α, 25(OH)_2D_3. NPY also inhibited osteoclastogenesis induced by forskolin, an activator of adenylate cyclase; however, it did not inhibit that induced by exogenously supplied dibutyryl cAMP, a cell-permeable cAMP analog that activates cAMP-dependent protein kinase. These results demonstrate that NPY inhibited the isoprenaline-induced osteoclastogenesis by blocking the agonist-elicited increases in the production of cAMP and RANKL in mouse bone marrow cells, suggesting an interaction between NPY and β-AR agonist in bone resorption.
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