2017 Fiscal Year Final Research Report
The analysis of Nsd1 cause phenotypic change of vascular smooth muscle cells
| Project/Area Number |
15K09161
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Cardiovascular medicine
|
|---|
| Research Institution | University of the Ryukyus |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
松下 正之 琉球大学, 医学(系)研究科(研究院), 教授 (30273965)
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
MANABE Ichiro 千葉大学, 大学院医学研究科, 教授 (70359628)
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Keywords | 平滑筋細胞 / 動脈硬化 |
|---|
| 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.
|
| Free Research Field |
血管生物学
|
