| Project/Area Number |
23791216
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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 |
Pediatrics
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| Research Institution | Research Institute, Osaka Medical Center for Maternal and Child Health |
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Principal Investigator |
YAMAZAKI Miwa 地方独立行政法人大阪府立病院機構大阪府立母子保健総合医療センター(研究所), その他部局等, 研究員 (50455549)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | Pit-1 / リン / りん / くる病 |
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| Outline of Final Research Achievements |
Type III sodium phosphate cotransporter, Pit-1, is ubiquitously expressed in mammalian tissues and plays a role as intracellular phosphate transporter, although the function of Pit-1 remains unclear. We have reported that extracellular phosphate and FGF23, a phosphaturic hormone, trigger the signal transduction via Pit-1 and FGF receptor and the signaling shares the same downstream cascade and interacts. In the current study, we have isolated the cells of osteoblasts and osteocytes lineage from Hyp mice, a murine model for X-linked hypophosphatemia, and wild type mice, and obtained the Fgf23 and Pit-1 expression profiles. Increased Pit-1 expression in osteoblasts and osteocytes from adult Hyp mice may be a compensatory mechanism to adapt to the decrease in extracellular Pi levels after birth.
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