| Project/Area Number |
15K09161
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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 |
Cardiovascular medicine
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| Research Institution | University of the Ryukyus |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
松下 正之 琉球大学, 医学(系)研究科(研究院), 教授 (30273965)
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| Co-Investigator(Renkei-kenkyūsha) |
MANABE Ichiro 千葉大学, 大学院医学研究科, 教授 (70359628)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 平滑筋細胞 / 動脈硬化 / 血管平滑筋 / 内膜肥厚 / 血管平滑筋細胞 / 血管生物学 / 細胞分化 / ヒストン修飾 |
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| Outline of Final Research Achievements |
The mechanism of smooth muscle cells (SMCs) phenotypic change is one of the most important question in vascular diseases, yet, little is known regarding what plays the role of SMCs switch. SRF acts as the key transcription factor controlling SMCs specific genes, and many factors regulate SRF positively or negatively. Here we show that histone methyltransferase, Nsd1 is upregulated in synthetic SMCs compare with contractile SMCs, and knocking down Nsd1 using small interfering RNA occur SMC phenotypic change from synthetic state to contractile state in cultured high passage rat SMCs. Homozygous Nsd1 mutant mice exhibited little neointimaformation after vascular injury. Our present study suggested that Nsd1 act as SMC phenotyping switch, then inhibition of Nsd1 expression or activity could be available in vascular injury.
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