Role of a Zing Finger Protein in Atherosclerosis via Regulation of Macrophage Differentiation and Function
Project/Area Number |
15K09160
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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 medicine
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Research Institution | Kyushu University |
Principal Investigator |
Kitamoto Shiro 九州大学, 医学研究院, 共同研究員 (00380436)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
Keywords | 動脈硬化 / マクロファージ / シグナル伝達 / 生体分子 / 遺伝子調節 |
Outline of Final Research Achievements |
Zing Finger Protein 329 (ZFP329) was suggested to play a role as a atherosclerosis-promoting factor by inducing proinflammatory M1 macrophage population, enhancing macrophage foam cell formation via suppression of cholesterol transporter protein expression, and inhibiting intracellular signal transduction of TGF-β (Transforming growth factor-β), which ameliorates and stabilizes atherosclerosis, from in vitro experiments. We are now continuing to generate ZFP329 deficient mice and are planning to perform further analysis of ZFP329 function utilizing these mice in future.
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Report
(4 results)
Research Products
(2 results)
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[Journal Article] Suppression of abdominal aortic aneurysm formation by AR-R17779, an agonist for the α7 nicotinic acetylcholine receptor.2016
Author(s)
Watanabe A, Ichiki T, Kojima H, Takahara Y, Hurt-Camejo E, Michaelsson E, Sankoda C, Ikeda J, Inoue E, Tokunou T, Kitamoto S, Sunagawa K.
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Journal Title
Atherosclerosis.
Volume: 244
Pages: 113-20
DOI
Related Report
Peer Reviewed
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