| ○種別 (必須): |
| ○言語 (必須): | □ | 英語
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| ○招待 (推奨): |
| ○審査 (推奨): |
| ○カテゴリ (推奨): |
| ○共著種別 (推奨): |
| ○学究種別 (推奨): |
| ○組織 (推奨): |
| ○著者 (必須): | 1. | (英) Tsujita Kenichi (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
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| 2. | (英) Kaikita Koichi (日) (読)
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| ○貢献度 (任意): |
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| 3. | (英) Hayasaki Takanori (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
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| 4. | (英) Honda Tsuyoshi (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 5. | (英) Kobayashi Hironori (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 6. | 坂下 直実
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 7. | (英) Suzuki Hiroshi (日) (読)
| ○役割 (任意): |
| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 8. | (英) Kodama Tatsuhiko (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 9. | (英) Ogawa Hisao (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| 10. | (英) Takeya Motohiro (日) (読)
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| ○貢献度 (任意): |
| ○学籍番号 (推奨): |
| [継承] |
| ○題名 (必須): | □ | (英) Targeted deletion of class A macrophage scavenger receptor increases the risk of cardiac rupture after experimental myocardial infarction. (日)
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| ○副題 (任意): |
| ○要約 (任意): | □ | (英) Class A macrophage scavenger receptor (SR-A) is a macrophage-restricted multifunctional molecule that optimizes the inflammatory response by modulation of the activity of inflammatory cytokines. This study was conducted with SR-A-deficient (SR-A(-/-)) mice to evaluate the relationship between SR-A and cardiac remodeling after myocardial infarction. Experimental myocardial infarction (MI) was produced by ligation of the left coronary artery in SR-A(-/-) and wild-type (WT) male mice. The number of mice that died within 4 weeks after MI was significantly greater in SR-A(-/-) mice than in WT mice (P=0.03). Importantly, death caused by cardiac rupture within 1 week after MI was 31% (17 of 54 mice) in SR-A(-/-) mice and 12% (6 of 51 mice) in WT mice (P=0.01). In situ zymography demonstrated augmented gelatinolytic activity in the infarcted myocardium in SR-A(-/-) mice compared with WT mice. Real-time reverse transcription-polymerase chain reaction at day 3 after MI showed that the expression of matrix metalloproteinase-9 mRNA increased significantly in the infarcted myocardium in SR-A(-/-) mice compared with WT mice. Furthermore, SR-A(-/-) mice showed augmented expression of tumor necrosis factor-alpha and reduction of interleukin-10 in the infarcted myocardium at day 3 after MI. In vitro experiments also demonstrated increased tumor necrosis factor-alpha and decreased interleukin-10 expression in activated SR-A(-/-) macrophages. The present findings suggest that SR-A deficiency might cause impairment of infarct remodeling that results in cardiac rupture via insufficient production of interleukin-10 and enhanced expression of tumor necrosis factor-alpha and of matrix metalloproteinase-9. SR-A might contribute to the prevention of cardiac rupture after MI. (日)
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| ○キーワード (推奨): | 1. | (英) Animals (日) (読)
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| 2. | (英) Cells, Cultured (日) (読)
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| 3. | (英) Crosses, Genetic (日) (読)
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| 4. | 細胞質分裂 (cytokinesis)
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| 5. | (英) Enzyme Induction (日) (読)
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| 6. | (英) Gene Deletion (日) (読)
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| 7. | (英) Heart Rupture (日) (読)
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| 8. | (英) Interleukin-10 (日) (読)
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| 9. | (英) Lipoproteins, LDL (日) (読)
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| 10. | (英) Macrophages, Peritoneal (日) (読)
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| 11. | 男性 (male)
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| 12. | (英) Matrix Metalloproteinase 2 (日) (読)
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| 13. | (英) Matrix Metalloproteinase 9 (日) (読)
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| 14. | (英) Mice (日) (読)
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| 15. | (英) Mice, Inbred C57BL (日) (読)
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| 16. | ノックアウトマウス (knockout mice)
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| 17. | (英) Myocardial Infarction (日) (読)
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| 18. | 心筋 (myocardium)
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| 19. | (英) Reverse Transcriptase Polymerase Chain Reaction (日) (読)
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| 20. | (英) Scavenger Receptors, Class A (日) (読)
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| 21. | (英) Tissue Inhibitor of Metalloproteinase-1 (日) (読)
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| 22. | (英) Tissue Inhibitor of Metalloproteinases (日) (読)
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| 23. | (英) Tumor Necrosis Factor-alpha (日) (読)
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| 24. | (英) Ventricular Remodeling (日) (読)
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| ○発行所 (推奨): |
| ○誌名 (必須): | □ | Circulation ([American Heart Association])
(pISSN: 0009-7322, eISSN: 1524-4539)
| ○ISSN (任意): | □ | 1524-4539
ISSN: 0009-7322
(pISSN: 0009-7322, eISSN: 1524-4539) Title: CirculationTitle(ISO): CirculationPublisher: American Heart Association (NLM Catalog)
(Scopus)
(CrossRef)
(Scopus information is found. [need login]) | [継承] |
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| ○巻 (必須): | □ | 115
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| ○号 (必須): | □ | 14
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| ○頁 (必須): | □ | 1904 1911
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| ○都市 (任意): |
| ○年月日 (必須): | □ | 西暦 2007年 3月 26日 (平成 19年 3月 26日)
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| ○URL (任意): |
| ○DOI (任意): | □ | 10.1161/CIRCULATIONAHA.106.671198 (→Scopusで検索)
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| ○PMID (任意): | □ | 17389263 (→Scopusで検索)
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| ○CRID (任意): |
| ○WOS (任意): |
| ○Scopus (任意): | □ | 2-s2.0-34247171613
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| ○評価値 (任意): |
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| ○指導教員 (推奨): |
| ○備考 (任意): | 1. | (英) Article.Affiliation: Department of Cell Pathology, Graduate School of Medical Sciences, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-8556, Japan. (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 3. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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