| Project/Area Number |
16K19044
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
General medical chemistry
|
|---|
| Research Institution | National Cardiovascular Center Research Institute |
|---|
Principal Investigator |
|
|---|
| Research Collaborator |
NAKAGAWA OSAMU
WATANABE YUSUKE
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | Tmem100 / 血管形成 / 血管内皮 / 胎生期 / 胎生期心血管 / 遺伝子発現制御 / 発生・分化 / 発現制御 |
|---|
| Outline of Final Research Achievements |
We previously demonstrated that the expression of transmembrane protein No.100 (TMEM100) was markedly induced by the activation of ALK1 signaling in cultured human endothelial cells. Tmem100 was expressed in arterial endothelial cells during mouse embryo development, and Tmem100 null mice showed embryonic lethality due to impairment of endothelial differentiation and vascular morphogenesis. However, the regulatory mechanisms of TMEM100 expression in embryonic vasculature are largely unknown. We identified a well-conserved endothelial enhancer of mouse Tmem100/human TMEM100 through BAC-based reporter analysis in mouse embryos. The reporter expression pattern was restricted to intermediate to large arteries and distinct from broader expression of the Alk1 knock-in LacZ reporter in the smaller caliber-vessels. These results suggest that the TMEM100 expression in embryonic endothelial cells is likely to be controlled by a unique combination of BMP-ALK1 and other signaling pathways.
|
