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Activation of Natural Killer T Cells Ameliorates Postinfarct Cardiac Remodeling and Failure in Mice

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Title: Activation of Natural Killer T Cells Ameliorates Postinfarct Cardiac Remodeling and Failure in Mice
Authors: Sobirin, Mochamad Ali Browse this author
Kinugawa, Shintaro Browse this author →KAKEN DB
Takahashi, Masashige Browse this author
Fukushima, Arata Browse this author →KAKEN DB
Homma, Tsuneaki Browse this author
Ono, Taisuke Browse this author
Hirabayashi, Kagami Browse this author
Suga, Tadashi Browse this author →KAKEN DB
Azalia, Putri Browse this author
Takada, Shingo Browse this author →KAKEN DB
Taniguchi, Masaru Browse this author →KAKEN DB
Nakayama, Toshinori Browse this author →KAKEN DB
Ishimori, Naoki Browse this author →KAKEN DB
Iwabuchi, Kazuya Browse this author →KAKEN DB
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Keywords: natural killer T cells
myocardial infarction
inflammation
heart failure
cytokines
Issue Date: 28-Sep-2012
Publisher: American Heart Association
Journal Title: Circulation Research
Volume: 111
Issue: 8
Start Page: 1037
End Page: 1047
Publisher DOI: 10.1161/CIRCRESAHA.112.270132
PMID: 22887770
Abstract: Rationale: Chronic inflammation in the myocardium is involved in the development of left ventricular (LV) remodeling and failure after myocardial infarction (MI). Invariant natural killer T (iNKT) cells have been shown to produce inflammatory cytokines and orchestrate tissue inflammation. However, no previous studies have determined the pathophysiological role of iNKT cells in post-MI LV remodeling. Objective: The purpose of this study was to examine whether the activation of iNKT cells might affect the development of LV remodeling and failure. Methods and Results: After creation of MI, mice received the injection of either α-galactosylceramide (αGC; n=27), the activator of iNKT cells, or phosphate-buffered saline (PBS; n=31) 1 and 4 days after surgery, and were followed during 28 days. Survival rate was significantly higher in MI+αGC than MI+PBS (59% vs 32%, P<0.05). LV cavity dilatation and dysfunction were significantly attenuated in MI+αGC, despite comparable infarct size, accompanied by a decrease in myocyte hypertrophy, interstitial fibrosis, and apoptosis. The infiltration of iNKT cells were increased during early phase in non-infarcted LV from MI and αGC further enhanced them. It also enhanced LV interleukin (IL)-10 gene expression at 7 days, which persisted until 28 days. Anti IL-10 receptor antibody abrogated these protective effects of αGC on MI remodeling. The administration of αGC into iNKT cell-deficient Jα18^[-/-] mice had no such effects, suggesting that αGC was a specific activator of iNKT cells. Conclusions: iNKT cells play a protective role against post-MI LV remodeling and failure through the enhanced expression of cardioprotective cytokines such as IL-10.
Type: article (author version)
URI: http://hdl.handle.net/2115/52273
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 絹川 真太郎

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