Pathophysiological role of uridine adenosine tetraphosphate in diabetic vasculopathy
Project/Area Number |
24790265
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
General pharmacology
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Research Institution | Hoshi University |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2014-03-31
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Project Status |
Completed (Fiscal Year 2013)
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Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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Keywords | 糖尿病 / 血管機能障害 / 血管平滑筋細胞 / 血管内皮細胞 / 糖尿病性血管機能障害 / 内皮由来因子 |
Research Abstract |
We have assessed responses to Up4A, a novel endothelium-derived contracting factor, shown by renal arteries (RAs) from type 2 diabetic Goto-Kakizaki (GK) rats. Up4A-induced contraction was greater in RA from the GK (vs. age-matched Wistar control). Inhibition of nitric oxide synthase increased the response to Up4A, whereas cyclooxygenase (COX) inhibition, antagonism of thromboxane (TX) receptor (TP) and P2 receptor decreased the response. In GK RA (vs. Wistar) ,COXs expression and TP agonist-induced contraction were greater, whereas the production of TXA2 by Up4A did not differ between groups. Our data indicate that the Up4A-induced contraction is closely associated with activation of COX/TP receptor axis. Clarifying the signal transduction and control of vascular tone by Up4A may be of significance to understanding the patho- physiology and advancing treatment of diabetes-associated vascular complications.
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Report
(3 results)
Research Products
(14 results)
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[Presentation] 2型糖尿病ラット摘出頸動脈におけるエンドセリン-1収縮に対するエピガロカテキンガレート慢性投与の影響2014
Author(s)
松本貴之, 渡邊駿, 川村隆輔, 金津智絵, 鳥羽美貴子, 新井隆三, 上原千晶, 佐川なつ実, 山田浩介, 田口久美子, 小林恒雄
Organizer
日本薬学会第134年会
Place of Presentation
熊本大学
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