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Activation of invariant natural killer T cells by alpha-galactosylceramide ameliorates myocardial ischemia/reperfusion injury in mice

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Title: Activation of invariant natural killer T cells by alpha-galactosylceramide ameliorates myocardial ischemia/reperfusion injury in mice
Authors: Homma, Tsuneaki Browse this author
Kinugawa, Shintaro Browse this author →KAKEN DB
Takahashi, Masashige Browse this author
Sobirin, Mochamad Ali Browse this author
Saito, Akimichi Browse this author
Fukushima, Arata Browse this author →KAKEN DB
Suga, Tadashi Browse this author →KAKEN DB
Takada, Shingo Browse this author →KAKEN DB
Kadoguchi, Tomoyasu Browse this author
Masaki, Yoshihiro Browse this author
Furihata, Takaaki 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: Invariant natural killer T cells
Myocardial ischemia/reperfusion injury
Issue Date: Sep-2013
Publisher: Academic press ltd- elsevier science ltd
Journal Title: Journal of molecular and cellular cardiology
Volume: 62
Start Page: 179
End Page: 188
Publisher DOI: 10.1016/j.yjmcc.2013.06.004
PMID: 23774048
Abstract: Invariant natural killer T (iNKT) cells orchestrate tissue inflammation via regulating various cytokine productions. However the role of iNKT cells has not been determined in myocardial ischemia/reperfusion (I/R) injury. The purpose of this study was to examine whether the activation of iNKT cells by a-galactosylceramide (alpha-GC), which specifically activates iNKT cells, could affect myocardial I/R injury. I/R or sham operation was performed in male C57BL/6J mice. I/R mice received the injection of either alpha GC (I/R + aGC, n = 48) or vehicle (I/R + vehicle, n = 49) 30 min before reperfusion. After 24 h, infarct size/area at risk was smaller in I/R + alpha GC than in I/R + vehicle (37.8 +/- 2.7% vs. 47.1 +/- 2.5%, P < 0.05), with no significant changes in area at risk. The numbers of infiltrating myeloperoxidase- and CD3-positive cells were lower in I/R + alpha GC. Apoptosis evaluated by TUNEL staining and caspase-3 protein was also attenuated in I/R + alpha GC. Myocardial gene expression of tumor necrosis factor-a and interleukin (IL)-1 beta in I/R + alpha GC was lower to 46% and 80% of that in I/R + vehicle, respectively, whereas IL-10, IL-4, and interferon (IFN)-gamma were higher in I/R + alpha GC than I/R + vehicle by 2.0, 4.1, and 9.6 folds, respectively. The administration of anti-IL-10 receptor antibody into I/R + alpha GC abolished the protective effects of alpha GC on I/R injury (infarct size/area at risk: 53.1 +/- 5.2% vs. 37.4 +/- 3.5%, P < 0.05). In contrast, anti-IL-4 and anti-IFN-gamma antibodies did not exert such effects. In conclusion, activated iNKT cells by alpha GC play a protective role against myocardial I/R injury through the enhanced expression of IL-10. Therapies designed to activate iNKT cells might be beneficial to protect the heart from I/R injury. (C) 2013 Elsevier Ltd. All rights reserved.
Type: article (author version)
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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