2012 Fiscal Year Final Research Report
A basic study of de novo function of PTH in mineral metabolism disorders
| Project/Area Number |
23792105
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
MINAMIZAKI Tomoko 広島大学, 大学院・医歯薬保健学研究院, 助教 (30452593)
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| Research Collaborator |
YOSHIKO Yuji 広島大学, 大学院・医歯薬保健学研究院, 教授 (20263709)
YOSHIOKA Hirotaka 広島大学, 大学院・医歯薬保健学研究院, 助教 (50523411)
KOZAI Katsuyuki 広島大学, 大学院・医歯薬保健学研究院, 教授 (10178212)
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| Project Period (FY) |
2011 – 2012
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| Keywords | 細胞・組織 / 骨代謝 / リン代謝 / PTH / FGF23 |
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| Research Abstract |
PTH increased the promoter activity of Fgf23 in rat calvaria-derived osteoblast cell cultures, however, there was no significant change in the levels of Fgf23mRNA expression and production. In combination with dihydroxyvitamin D3(1,25D), on the other hand, PTH decreased 1,25D-induced Fgf23mRNA expression and production. One of the reasons for this effect is that the expression of vitamin D receptor and type III sodium-dependent phosphate transporter (Pit1) was suppressed by PTH. Further, PTH promoted MKP1 phosphorylation via PKA pathway, and thereby attenuated the signal FGF23 signaling.
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