2015 Fiscal Year Final Research Report
Role of age-associated BubR1 gene in atherogenesis and its molecular mechanism
Project/Area Number |
25462164
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Cardiovascular surgery
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Research Institution | Kyushu University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
MAEHARA Yoshihiko 九州大学, 医学研究院, 教授 (80165662)
FURUYAMA Tadashi 九州大学, 大学病院, 助教 (00419590)
FUKUNAGA Ryota 九州大学, 大学病院, 助教 (00529860)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | 細胞周期 / 動脈硬化 / マクロファージ / 増殖 |
Outline of Final Research Achievements |
BubR1 is an essential component of the spindle checkpoint. BubR1 insufficiency causes early aging-associated vascular phenotypes. We generated low-BubR1-expressing mutant (BubR1L/L) and apolipoprotein E-deficient (ApoE-/-) mice (BubR1L/L-ApoE-/- mice) to investigate the effects of BubR1 on atherosclerosis. 8W old male BubR1L/L-ApoE-/- mice and age-matched ApoE-/- mice were used. Atherosclerotic lesion development after being fed a high-cholesterol diet for 12 weeks was inhibited in BubR1L/L-ApoE-/- mice compared with ApoE-/- mice, and was accompanied by decreased accumulation of macrophages. To address the relative contribution of BubR1 on bone marrow-derived cells compared with non-bone marrow-derived cells, we performed bone marrow transplantation in ApoE-/- and BubR1L/L-ApoE-/- mice. Decreased BubR1 in bone marrow cells and non-bone marrow-derived cells decreased the atherosclerotic burden. BubR1 may represent a promising new target for regulating atherosclerosis.
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Free Research Field |
血管外科
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