2010 Fiscal Year Final Research Report
Regulatory mechanisms of Ca^<2+> oscillations and transcription factor NFAT in osteoclastogenesis.
| Project/Area Number |
20390475
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Fukuoka Dental College |
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Principal Investigator |
OKABE Koji Fukuoka Dental College, 歯学部, 教授 (80224046)
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| Co-Investigator(Kenkyū-buntansha) |
OKAMOTO Fujio 福岡歯科大学, 歯学部, 講師 (60153938)
KAJIYA Hiroshi 福岡歯科大学, 歯学部, 講師 (80177378)
INOUE Ryuji 福岡大学, 医学部, 教授 (30232573)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 破骨細胞 / Ca^<2+>オシレーション / TRPチャネル / NFAT / 破骨細胞分化 |
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| Research Abstract |
The receptor activator of NFκB ligand (RANKL) induces Ca^<2+> oscillations and activates the Nuclear Factor of Activated T cells 1 (NFATc1) during osteoclast differentiation (osteoclastogenesis). Ca^<2+> oscillations are an important trigger signal for osteoclastogenesis, however the molecular basis of Ca^<2+> permeable influx pathways serving Ca^<2+> oscillations has not yet been identified. Using a DNA microarray, we found that Transient Receptor Potential Vanilloid channels 2 (TRPV2) are expressed significantly in RANKL-treated RAW264.7 cells (preosteoclasts) compared to untreated cells. Therefore, we further investigated the expression and functional role of TRPV2 on Ca^<2+> oscillations and osteoclastogenesis. In conclusion, Ca^<2+> oscillations in preosteoclasts are triggered by RANKL-dependent TRPV2 and SOCE activation and intracellular Ca^<2+> release. Subsequent activation of NFATc1 promotes osteoclastogenesis.
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