| Project/Area Number |
25860257
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Human genetics
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| Research Institution | National Institute of Genetics |
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Principal Investigator |
HIROFUMI Nakaoka 国立遺伝学研究所, 総合遺伝研究系, 特任研究員 (70611193)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
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| Keywords | 脳動脈瘤 / くも膜下出血 / 網羅的遺伝子発現解析 / 炎症 / マクロファージ / トランスクリプトーム / 炎症反応 / 転写因子 / 転写調節 / トランスクリプトーム解析 / 破裂 / マクロファージ浸潤 |
|---|
| Outline of Final Research Achievements |
We compared gene expression profiles in aneurysmal domes between unruptured and ruptured intracranial aneurysms (UIAs and RIAs, respectively) to elucidate biological mechanisms predisposing to the rupture. By classifying the samples into subgroups showing similar gene expression patterns, we demonstrated RIAs segregated into 2 distinct subgroups (early and late RIAs). Comparing gene expression levels between early RIAs and UIAs, we identified 430 upregulated and 617 downregulated genes in early RIAs. The results suggest that macrophage-mediated inflammation is a key biological pathway for IA rupture. The identified genes can be good candidates for molecular markers of rupture-prone IAs and therapeutic targets.
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