| Project/Area Number |
25870258
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
Applied pharmacology
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| Research Institution | Hoshi University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| 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 |
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| Outline of Final Research Achievements |
Many various complications (cardiovascular disease and atherosclerosis etc.) are caused by affection of long-term diabetes. The vascular disorder is the characteristic in common. This leads to impaired endothelial function, which has become a serious public-health threat, and so we designed the present study to elucidate mechanism to control the vascular function, and to suggest that GRK2 (G protein coupled receptor kinase 2) uncovers new molecular targets for the treatment of diabetic complications. As a result, we found that in the endothelium under high glucose condition, GRK2 was up-regulated by the stimulation of insulin or angiotensin II, and let to a stronger inhibition of insulin-induced Akt/eNOS/NO production pathway. Furthermore, we confirmed that the endothelium-dependent vasorelaxation that attenuated in diabetes was improved by giving GRK2 siRNA to spontaneous type 2 diabetes mice, suggesting that GRK2 is a precipitating factor on the development of diabetic complications.
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