| Project/Area Number |
16K08932
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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 |
Laboratory medicine
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| Research Institution | Gunma Paz University |
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Principal Investigator |
Makoto Osada 群馬パース大学, 保健科学部, 教授 (20569628)
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| Co-Investigator(Kenkyū-buntansha) |
井上 修 山梨大学, 大学院総合研究部, 特任准教授 (00432154)
井上 克枝 山梨大学, 大学院総合研究部, 教授 (10324211)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | S100A13 / CLEC-2 / 血管平滑筋 / 動脈硬化 / 血小板活性化 / ELISA / 血管平滑筋細胞 |
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| Outline of Final Research Achievements |
In the present study, we investigated whether S100A13 in serum could be an atherosclerotic marker and also tried to clarify the mechanism of S100A13 expression on the surface of smooth muscle cell at atherosclerotic lesion. The serum concentration of S100A13 obtained from atherosclerotic patients was significantly higher than that from healthy volunteers. This result indicates that serum S100A13 can be a marker for atherosclerosis. In addition, serum S100A13 is significantly increased in patients with renal impairment compared with that in normal subjects, suggesting that the measurement of serum S100A13 may be useful for the estimation of the renal function.
Although the mechanism of S100A13 expression in vascular smooth muscle cells has not been studied sufficiently, serum S100A13 may be a useful and novel marker in the patients with vascular diseases.
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| Academic Significance and Societal Importance of the Research Achievements |
動脈硬化によるプラークが破裂すると，血小板が活性化して血栓を形成し，心筋梗塞，脳梗塞等の動脈血栓症となる．癌に次ぐ日本人の死因である動脈血栓症の治療・予防は重要な課題である．血液検査により動脈硬化を客観的に測定する指標は存在しない．早期動脈硬化病変の血管平滑筋細胞にS100A13が発現しており，血小板のCLEC-2が結合することで血栓形成が促進される．この際血管平滑筋表面のS100A13が血中に遊離するため，血中S100A13が動脈硬化の指標となり得ると考えた．ヒト血中S100A13濃度は，動脈硬化症群で有意に高値となったため，動脈硬化の客観的な指標となると考えられた．
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