| Project/Area Number |
24390192
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Hokkaido University |
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Principal Investigator |
TSUTSUI Hiroyuki 北海道大学, 医学(系)研究科(研究院), 教授 (70264017)
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| Co-Investigator(Kenkyū-buntansha) |
KINUGAWA Shintaro 北海道大学, 大学院医学研究科, 講師 (60399871)
ISHIMORI Naoki 北海道大学, 北海道大学病院, 准教授 (70399848)
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| Co-Investigator(Renkei-kenkyūsha) |
TOKUHARA Satoshi 北見赤十字病院, 循環器内科, 副部長
SAITO Akimichi 北海道大学, 大学院医学研究科, 医員 (40735502)
NISHIKAWA Mikito 帯広協会病院, 循環器内科, 医員
TAKAHASHI Masashige 市立釧路総合病院, 心臓血管内科, 医師
FUKUSHIMA Arata University of Alberta Cardiovascular Research Centre, doctoral fellow
SUGA Tadashi 立命館大学, スポーツ健康科学部, 研究員 (30708673)
TAKADA Shingo 北海道大学, 北海道大学病院, COI研究員 (60722329)
KADOGUCHI Tomoyasu 順天堂大学, 大学院医学研究科, 博士研究員
MASAKI Yoshihiro 砂川市立病院, 循環器内科, 医長
FURIHATA Takaaki 北海道大学, 大学院医学研究科
ONO Taisuke 北見赤十字病院, 循環器内科, 医員
HIRABAYASHI Kagami 苫小牧市立病院, 循環器内科, 医長
HOMMA Tsuneaki 国立病院機構北海道医療センター, 循環器内科, 医師
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥17,940,000 (Direct Cost: ¥13,800,000、Indirect Cost: ¥4,140,000)
Fiscal Year 2014: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2012: ¥7,020,000 (Direct Cost: ¥5,400,000、Indirect Cost: ¥1,620,000)
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| Keywords | 分子心臓学 / 心不全 / 心筋リモデリング / 慢性炎症 / ナチュラルキラーT細胞 / Th1/Th2バランス |
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| Outline of Final Research Achievements |
The purpose of this study was to elucidate the role of natural killer T (NKT) cells in myocardial remodeling and failure. The infiltration of NKT cells was increased in the heart from the mice after myocardial infarction (MI). The administration of α-Galactosylceramide (α-GalCer), which specifically activates NKT cells, to the MI mice further enhanced the NKT cell infiltration and LV interleukin-10 gene expression, and inhibited LV remodeling. α-GalCer also inhibited LV remodeling after ischemia/reperfusion injury.
α-GalCer-pulsed human dendritic cells (α-GalCer/DC), which differentiated from autologous peripheral blood mononuclear cells, can efficiently activate NKT cells. α-GalCer/DC were administered to nude mice under the GLP standard and any toxicity was observed throughout the follow-up period, suggesting that α-GalCer/DC may be a novel therapeutic strategy against heart failure. Now we are preparing for the phase I study of α-GalCer/DC in patients with heart failure.
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