| Project/Area Number |
15K21419
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Biological pharmacy
Pharmacology in pharmacy
|
|---|
| Research Institution | Hoshi University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | 血管内皮障害 / 糖尿病 / GRK2 / 血管内皮機能不全 / GRK２ / 分子薬理学 |
|---|
| Outline of Final Research Achievements |
We focused on vascular endothelial dysfunction to study the molecular preventative mechanism under GRK2 control in diabetes. We investigated vascular endothelial dysfunction in ob/ob mice and HUVECs treated high glucose and angiotensin II (Ang II). The present results clarified the relationship among hepatic GRK2, glucose homeostasis, and vascular endothelial function. Liver-targeting GRK2 siRNA delivery represents a novel therapeutic tool to restore glucose homeostasis and reduce endothelial dysfunction. Furthermore, the HUVECs data strongly indicate that high glucose and Ang II directly affect endothelial cells and the production of EEVs; the resultant EEVs aggravate endothelial dysfunction in mice aortas.
|
