| Project/Area Number |
15K15089
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Pathological medical chemistry
|
|---|
| Research Institution | Keio University |
|---|
Principal Investigator |
Kubota Yoshiaki 慶應義塾大学, 医学部(信濃町), 教授 (50348687)
|
|---|
| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
|---|
| Keywords | 血管 / 血管新生 / VEGF / VEGFR2 / 網膜 / 発現制御 / 発生・分化 / 循環器・高血圧 |
|---|
| Outline of Final Research Achievements |
Blood vessels are distributed throughout the body during development. This developmental process depends on the signaling of vascular endothelial growth factor (VEGF) and its main receptor, VEGFR2. However, the precise role of VEGF on vascular endothelial cells, in particular the role in the maintenance of their stability is not clear. In this study, we generated tamoxifen-inducible endothelial VEGFR2 knockout mice (Cdh5-BAC-CreERT2+;Vegfr2flox./flox) and morphologically analyzed the retina of the mutant mice at a single cell level. We found not only abrogation of the formation of new vessels but also the striking regression of established ones. This phenotype was mostly recapitulated by neuron-specific VEGF knockout mice (Chx10-Cre+Vegfaflox/flox). Overall our study suggests that the VEGF/VEGFR2 signaling positively regulates the stability of established blood vessels.
|
