| Project/Area Number |
17K10842
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurosurgery
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| Research Institution | Kurume University (2019)
Kumamoto University (2017-2018) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
宮田 敬士 熊本大学, 大学院生命科学研究部(医), 特任准教授 (50398228)
大森 雄樹 熊本大学, 病院, 助教 (60599116)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 慢性炎症 / 動脈硬化 / Angptl2 / アンジオポエチン様タンパク質２ |
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| Outline of Final Research Achievements |
Immunostaining of CD68, a marker for Angptl2 and macrophages, was performed in samples of human carotid plaques, and it was revealed that macrophages infiltrated the plaques. Moreover, it was confirmed that Angptl2 was highly expressed in the infiltrated macrophages. Therefore, it was suggested that macrophages are the main secretory source of Angptl2 in plaques.
The present study suggests that human carotid plaque contains a large amount of chronic inflammation Angptl2, and that its expression induces vascular inflammation and is involved in the pathogenesis of carotid plaque.
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| Academic Significance and Societal Importance of the Research Achievements |
血管における局所的なAngptl2の発現が血管炎症を惹起し、病態形成および進展に関与していると考えられる。そのため頸動脈プラークの発生、増大、破綻の病態に慢性炎症、特にAngptl2が関与していることが強く推測される。その関与が明らかにされれば、Angptl2が頸動脈プラークに対する薬物治療や、さらには急性冠症候群や閉塞性動脈硬化症などを含めた全身の動脈硬化の治療標的になる可能性があると考えられる。
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