2015 Fiscal Year Final Research Report
Ca Load Induces Vascular Smooth Muscle Cell Mineralization Partly Mediated by TRPV
| Project/Area Number |
25461255
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | Showa University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
OGATA Hiroaki 昭和大学, 横浜市北部病院内科, 准教授 (30296959)
|
|---|
| Project Period (FY) |
2013-04-01 – 2016-03-31
|
| Keywords | 血管石灰化 / 血管平滑筋細胞 / カルシウム / TRPVチャネル |
|---|
| 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.
|
| Free Research Field |
血管石灰化
|
