| Project/Area Number |
26293392
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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 |
Morphological basic dentistry
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| Research Institution | Ehime University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
李 智媛 愛媛大学, プロテオサイエンスセンター, 助教(特定教員) (70711274)
疋田 温彦 東京大学, 医学部附属病院, 特任准教授 (60443397)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥16,120,000 (Direct Cost: ¥12,400,000、Indirect Cost: ¥3,720,000)
Fiscal Year 2016: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2015: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Keywords | 骨代謝 / 骨粗鬆症 / 破骨細胞 / HIV / シグナル / 骨格 / 骨芽細胞 / ケモカイン / 骨 / 軟骨 / 形態形成 / 骨格形成 / 骨吸収性疾患 / イメージング / シミュレーション / 老化 / 恒常性 / 発生 |
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| Outline of Final Research Achievements |
The purpose of this research grant was to identify important genes during skeletal development, and further validate the role of candidate genes by analysis of knock-out mice. We identified some cc-chemokines expressing in developing skeletal tissues. One of prominent advance in this research was that a chemokine receptor CCR5, also a HIV co-receptor, was essential for osteoporosis. Clinical reports suggested that HIV treatment targeting CCR5 may cause less-susceptibility to bone-destructive diseases such as rheumatoid arthritis and osteoporosis. We uncovered that anti-CCR5 neutralization antibody as well as a CCR5 inhibitory drug, Maraviroc, blocked osteoclast differentiation and function through damaging their actin-ring formation. Moreover, CCR5-deficient mice were resistant to osteoporotic stimuli. These findings experimentally supports the clinical reports as mentioned above, and suggest that HIV therapy targeting CCR5 may provide skeletal merits.
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