| Project/Area Number |
23592748
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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 |
Functional basic dentistry
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| Research Institution | Showa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KATAGIRI Takenobu 埼玉医科大学, ゲノム医学研究センター病態生理部門, 教授 (80245802)
MIYAMOTO Yoichi 昭和大学, 歯学部口腔生化学講座, 准教授 (20295132)
YAMADA Atsushi 昭和大学, 歯学部口腔生化学講座, 講師 (50407558)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | pH / 骨芽細胞 / 軟骨細胞 / 炭酸脱水酵素 / モノカルボン酸輸送体 / MCT / 細胞内pH / 細胞分化 / carbonic anhydrase / MCT-1 |
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| Research Abstract |
We found that carbonic anhydrase-9 (CA9) is expressed in mouse chondrocytes and monocarboxylate transporter-1 (MCT1) in osteoblasts, respectively. Hence we investigated the roles of CA9 and MCT1 in differentiation of chondrocytes and osteoblasts, respectively. CA9 was expressed in proliferating but not in hypertrophic chondrocytes in the growth plates of mice. Suppression of CA9 expression by its siRNA induced the hypertrophic differentiation in mouse primary chondrocytes, indicating that CA9 has a role to suppress hypertrophic differentiation of chondrocytes. Suppression of the expression of MCT1 in mouse osteoblasts induced lowered expression of alkaline phosphatase (ALP), while lactate, an MCT1 substrate, augmented the expression of ALP in osteoblasts. We also found that MCT1 positively regulates phosphorylation and nuclear translocation of Smad1/5/8 in osteoblasts after stimulation by bone morphogenetic protein-2.
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