| Project/Area Number |
24659841
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathobiological dentistry/Dental radiology
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| Research Institution | Kyushu Dental College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ARIYOSHI Wataru 九州歯科大学, 歯学部, 准教授 (40405551)
沖永 敏則 九州歯科大学, 歯学部, 助教 (60582773)
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| Co-Investigator(Renkei-kenkyūsha) |
OKINAGA Toshinori 九州歯科大学, 歯学部, 助教 (60582773)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | マクロファージ / β1-3グルカン / dectin-1 / インフラマソーム |
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| Research Abstract |
Several immune system cell-surface receptors are reported to be associated with osteoclastogenesis. Dectin-1, a lectin receptor for beta-glucan, is found predominantly on cells of the myeloid lineage. In the present study, we examined the effect of dectin-1 agonist, curdlan, on osteoclastogenesis. In dectin-1 over-expressing RAW 264.7 cells (d-RAW), curdlan suppressed receptor activator of nuclear factor-kappaB (NF-kappaB) ligand (RANKL)-induced osteoclast differentiation, bone resorption and actin-ring formation. Furthermore, curdlan inhibited RANKL-induced nuclear factor of activated T-cell cytoplasmic 1 (NFATc1) expression.
In conclusion, our results demonstrate that curdlan potentially inhibits osteoclast differentiation, especially NFATc1 expression. This suggests activation of curdlan-dectin-1 interaction critically regulates the genes required for osteoclastogenesis.
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