| ○種別 (必須): | □ | 学術論文 (審査論文)
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| ○言語 (必須): | □ | 英語
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| ○審査 (推奨): |
| ○カテゴリ (推奨): |
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| ○学究種別 (推奨): |
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| ○著者 (必須): | 1. | 島田 健司 ([徳島大学.病院.先端医科医療開発研究プロジェクト]/[徳島大学.病院.診療科.脳·神経·精神科.脳神経外科])
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| 2. | (英) Furukawa Hjime (日) (読)
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| 3. | (英) Wada Kousuke (日) (読)
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| 4. | (英) Kohrai Masaaki (日) (読)
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| 5. | (英) Wei Yuan (日) (読)
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| 6. | 多田 恵曜 ([徳島大学.大学院医歯薬学研究部.医学域.先端医学教育研究プロジェクト]/[徳島大学.大学院医歯薬学研究部.医学域.医科学部門.外科系.脳神経外科学])
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| 7. | (英) Kuwahara Atsushi (日) (読)
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| 8. | (英) Shikata Fumiaki (日) (読)
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| 9. | (英) Kitazato T. Keiko (日) (読)
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| 10. | 永廣 信治
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| 11. | (英) Lawton T. Michael (日) (読)
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| 12. | (英) Hashimoto Tomoki (日) (読)
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| ○題名 (必須): | □ | (英) Protective role of peroxisome proliferator-activated receptor- in the development of intracranial aneurysm rupture (日)
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| ○要約 (任意): | □ | (英) Inflammation is emerging as a key component of the pathophysiology of intracranial aneurysms. Peroxisome proliferator-activated receptor-γ (PPARγ) is a nuclear hormone receptor of which activation modulates various aspects of inflammation. Using a mouse model of intracranial aneurysm, we examined the potential roles of PPARγ in the development of rupture of intracranial aneurysm. A PPARγ agonist, pioglitazone, significantly reduced the incidence of ruptured aneurysms and the rupture rate without affecting the total incidence aneurysm (unruptured aneurysms and ruptured aneurysms). PPARγ antagonist (GW9662) abolished the protective effect of pioglitazone. The protective effect of pioglitazone was absent in mice lacking macrophage PPARγ. Pioglitazone treatment reduced the mRNA levels of inflammatory cytokines (monocyte chemoattractant factor-1, interleukin-1, and interleukin-6) that are primarily produced by macrophages in the cerebral arteries. Pioglitazone treatment reduced the infiltration of M1 macrophage into the cerebral arteries and the macrophage M1/M2 ratio. Depletion of macrophages significantly reduced the rupture rate. Our data showed that the activation of macrophage PPARγ protects against the development of aneurysmal rupture. PPARγ in inflammatory cells may be a potential therapeutic target for the prevention of aneurysmal rupture. (日)
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| ○キーワード (推奨): | 1. | (英) Aneurysm, Ruptured (日) (読)
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| 2. | (英) Anilides (日) (読)
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| 3. | (英) Animals (日) (読)
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| 4. | (英) Cerebral Arteries (日) (読)
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| 5. | 細胞質分裂 (cytokinesis)
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| 6. | (英) Hypoglycemic Agents (日) (読)
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| 7. | (英) Intracranial Aneurysm (日) (読)
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| 8. | (英) Macrophages (日) (読)
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| 9. | (英) Mice (日) (読)
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| 10. | ノックアウトマウス (knockout mice)
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| 11. | (英) PPAR gamma (日) (読)
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| 12. | (英) Thiazolidinediones (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Stroke ([American Heart Association])
(pISSN: 0039-2499, eISSN: 1524-4628)
| ○ISSN (任意): | □ | 1524-4628
ISSN: 0039-2499
(pISSN: 0039-2499, eISSN: 1524-4628) Title: StrokeTitle(ISO): StrokePublisher: American Heart Association (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 46
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| ○号 (必須): | □ | 6
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| ○頁 (必須): | □ | 1664 1672
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2015年 6月 初日 (平成 27年 6月 初日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1161/STROKEAHA.114.007722 (→Scopusで検索)
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| ○PMID (任意): | □ | 25931465 (→Scopusで検索)
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| ○CRID (任意): |
| ○WOS (任意): | □ | 000354941800052
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| ○Scopus (任意): | □ | 2-s2.0-84942924464
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| ○指導教員 (推奨): |
| ○備考 (任意): | 1. | (英) Article.ELocationID: 10.1161/STROKEAHA.114.007722 (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, N.I.H., Extramural (日)
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| 4. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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| 5. | (英) OtherID: NIHMS678779 [Available on 06/01/16] (日)
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| 6. | (英) OtherID: PMC4447500 [Available on 06/01/16] (日)
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| 7. | (英) KeywordList.Keyword: inflammation (日)
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| 8. | (英) KeywordList.Keyword: intracranial aneurysm (日)
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| 9. | (英) KeywordList.Keyword: subarachnoid hemorrhage (日)
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