| Project/Area Number |
16K09652
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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 |
Kidney internal medicine
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
大矢 昌樹 和歌山県立医科大学, 医学部, 講師 (90550301)
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| Project Period (FY) |
2016-10-21 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | FGF23 / 骨細胞 / 骨芽細胞 / ビタミンD / リン / FGF 23 / 活性型ビタミンD / 活性型ビタミンD受容体 / 線維芽細胞増殖因子23 / 高リン血症 / 骨組織 / 腎機能障害 / 骨細胞 Osteocyte / Klotho / 慢性腎臓病 (CKD) / 活性型Vitamin D / リン代謝 / 腎障害 |
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| Outline of Final Research Achievements |
We estimated the FGF23 production in vitro among isolated osteoblasts, osteocytes and osteoclast in bone constitution cells without osteocyte harvest. The osteoblastic Cell Line MC3T3-E1 cells have ability to be calcified spontaneously. We changed these cells into osteocytes by ascorbic acid and phosphate overload in vitro. We estimate the FGF23 mRNA expression at each stage from osteoblast to osteocyte. The both of matured osteoblast and immature osteocyte had the most effective production ability. We discovered that the most powerful stimulator on FGF23 is active vitamin D and analogues (vitamin D receptor activator), but not phosphate loading.
In addition, we were able to observe the even plasmatoid dendritic cell in spleen and calcified vessel as an ectopic calcification have also FGF23 production ability. These phenomena might explain the effect of FGF23 on cardiovascular events and immune system. This area is needed further investigation.
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| Academic Significance and Societal Importance of the Research Achievements |
FGF23は腎機能障害者においては、生命予後と密接に関係することが明らかとなりつつある。またFGF23受容体となるKlotho蛋白をコードするKlotho遺伝子は長寿遺伝子すなわち抗老化作用を有することが明らかとなった。
本研究成果は、この老化の本質的なメカニズムの一端を明らかにするものであり、今後の抗老化作用を有する創薬にもつながる成果である。さらには心血管病の進展や免疫系への作用など広い分野の研究領域を啓く可能性がある。
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