Role of oxygen-derived free radicals and BubR1 expression
Project/Area Number |
22591408
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
General surgery
|
Research Institution | Kyushu University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
MAEHARA Yoshihiko 九州大学, 医学研究院, 教授 (80165662)
|
Project Period (FY) |
2010 – 2012
|
Project Status |
Completed (Fiscal Year 2012)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | 血管外科学 / 動脈硬化 / 老化 / 活性酸素 / 細胞周期 / 平滑筋細胞 / 内皮細胞 / 血管 |
Research Abstract |
BubR1 expression and hAoSMC proliferative ability were significantly decreased in the aged hAoSMC. Angiotensin II and H2O2 upregulated BubR1 expression in young hAoSMC, and the upregulation was abrogated by a p38 MAPK inhibitor or an inhibitor of the NADH/NADPH oxidase. siRNA against BubR1 reduced proliferative activity and increased ROS production in hAoSMC. These findings demonstrate BubR1 mRNA expression decreases along with proliferation in aged hAoSMC. Aging-related loss of BubR1 and subsequent impairment of reactivity to ROS may explain reduced proliferative capacity of aged smooth muscle cells.These findings demonstrate BubR1 mRNA expression decreases along with proliferation in aged hAoSMC. Aging-related loss of BubR1 and subsequent impairment of reactivity to ROS may explain reduced proliferative capacity of aged smooth muscle cells.
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Report
(4 results)
Research Products
(4 results)