| Project/Area Number |
25461255
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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 | Showa University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
OGATA Hiroaki 昭和大学, 横浜市北部病院内科, 准教授 (30296959)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2014: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2013: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | 血管石灰化 / 血管平滑筋細胞 / カルシウム / TRPVチャネル / Ca / TRPV / アポトーシス |
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| Outline of Final Research Achievements |
Although hypercalcemia is a risk factor for vascular calcification, little is known about the involvement of calcium (Ca) in the process of vascular calcification. Human aortic VSMCs were incubated in a low Ca media (LCa), normal Ca media (NCa), and a high Ca media (HCa). VSMC mineralization, and gene expression of markers for osteogenic process and a Ca channel (TRPV-2) was determined. RNA interference for TRPV-2 was performed to study the effect of TRPV2 on the mineralization. VSMC mineralization was induced in a dose dependent manner with the induction of an osteogenic process which was confirmed by the increase in Runx2 mRNA and ALP mRNA expression. We confirmed the up-regulation of TRPV-2 in the HCa. When TRPV-2 mRNA was knocked-down, the mineralization was significantly suppressed in HCa.
These results suggest that Ca load induced VSMC mineralization which is partly mediated by TRPV2. Thus Ca load is a considerable factor for the process of VSMC mineralization.
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