Identification of phosphate sensor channel in bone and endothelial cells suppressed the ectopic calcification
| Project/Area Number |
18590891
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ITO Mikiko The University of Tokushima, Institute of health biosciences, Graduate school, Assistant Professor (50314852)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | phosphate / transporter / channel / sensor / mineralization |
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| Research Abstract |
The hemodialysis patient with chronic renal failure keeps remarkably increasing by a diabetic every year. The hyperphosphatemia is observed at high ratio in these patients, and the phosphate (Pi) management is important because this leads of one's death by the cardiovascular disease by the ectopic calcification. Especially, Pi sensor (type IIc Na/Pi cotransporter) and Pi channel are key protein to clear the ectopic calcification in bone. In this research, we tried to clarify the calcification mechanism by characterization of the Pi sensor in the bone and/or the vascular endothelial.
We investigated the efflux of Pi from osteoclast-like cells derived by the treatment of RAW264.7 cells with RANKL. These studies suggest that osteoclast-like cells have a unique Pi uptake/efflux system and can prevent Pi accumulation within osteoclast. In addition, we studied the Pi sensor protein complex by the Yeast two-hybrid method. Several PDZ proteins may be involved in Pi sensor complex and bone mineral metabolism. To understand the role of Na/Pi-IIa and Na/Pi-IIc transporters in the overall maintenance of Pi homeostasis and bone mineralization, we have disrupted the mouse NaPi-IIa/NaPi-IIc gene and analyzed phenotypes of each mutant. The present study, Pi sensor may be important role of the ectopic calcification.
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Report
(3 results)
Research Products
(146 results)
