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KAKEN_25860620seika.pdf
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Download
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:734.3 KB
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| Last updated |
:Apr 11, 2016 |
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: 691 |
Total downloads since Apr 11, 2016 : 691
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| Title |
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心筋梗塞後左室リモデリングにおけるInterleukin-33の役割解明
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| Kana |
シンキン コウソクゴ サシツ リモデリング ニ オケル Interleukin-33 ノ ヤクワリ カイメイ
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Shinkin kosokugo sashitsu rimoderingu ni okeru Interleukin-33 no yakuwari kaimei
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Role of Interleukin-33 in Left Ventricular Remodeling After Myocardial Infarction
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安西, 淳
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アンザイ, アツシ
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Anzai, Atsushi
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慶應義塾大学・医学部・助教
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Research team head
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科研費研究者番号 : 50528164
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2015
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科学研究費補助金研究成果報告書
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2014
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マウス心筋梗塞モデルを用いて, interleukin-33の発現が梗塞後に上昇し, その発現細胞が線維芽細胞であることを見出した。Interleukin-33ノックアウトマウスでは心筋梗塞後の心機能が改善傾向にあり, 炎症性サイトカインやマトリックスメタロプロテイナーゼの発現が抑制されていた。ノックアウトマウスの梗塞部に浸潤するマクロファージの極性が抗炎症性有意であり, interleukin-33の受容体であるST2の発現がCD11b陽性細胞で上昇していたことから, 梗塞部で発現したinterleukin-33が主にマクロファージに作用して, 梗塞後左室リモデリングを増悪させることが予想された。
The expression of interleukin-33 was increased after permanent coronary ligation in mice. We identified that the main source of interleukin-33 was cardiac fibroblasts in the murine infarcts. Interleukin-33 knockout mice exhibited improved cardiac function and better survival rate 28 days after myocardial infarction. The expression of inflammatory cytokines and matrix metalloprotainase was reduced in the knockout mice and anti-inflammatory M2 macrophages are dominant infiltrating-cells in the infarcts 7 days after myocardial infarction. As Interleukin-33 receptor, ST2, strongly expressed on the CD11b+ cells, interleukin-33 might have detrimental role in the tissue healing after myocardial infarction, partly through controlling inflammatory and anti-inflammatory macrophage function.
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研究種目 : 若手研究(B)
研究期間 : 2013～2014
課題番号 : 25860620
研究分野 : 循環器内科学
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