| Project/Area Number |
22390159
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | The University of Tokushima |
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Principal Investigator |
SATA Masataka 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (80345214)
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| Co-Investigator(Kenkyū-buntansha) |
SOEKI Takeshi 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (60393211)
HIRATA Yasunobu 東京大学, 医学部附属病院, 特任准教授 (70167609)
黒部 裕嗣 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (30380083)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥18,720,000 (Direct Cost: ¥14,400,000、Indirect Cost: ¥4,320,000)
Fiscal Year 2012: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2011: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2010: ¥8,060,000 (Direct Cost: ¥6,200,000、Indirect Cost: ¥1,860,000)
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| Keywords | 動脈硬化 / 血管新生 / 慢性炎症 / HMGB-1 / 急性冠症候群プラーク破裂 / 循環器・高血圧 / 急性冠症候群 / プラーク破裂 / プラーク / 自然免疫 / マクロファージ / サイトカイン / 生活習慣病 |
|---|
| Research Abstract |
We tried to elucidate molecular mechanism of plaque destabilization by analyzing clinical samples and utilizing animal models. The concentration of HMGB1, a non-histone nuclear protein, increased at coronary sinus in patients with coronary artery disease. Particularly, acute coronary syndrome, such as acute myocardial infarction or unstable angina pectoris, was associated with ten times elevated HMGB1 level. Animal experiments revealed that HMGB1-DNA complex signal contributed destabilization of vessel wall by activating Toll-like receptor 9 in the bone marrow-derived cells.
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