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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
Suga, Tadashi Browse this author
Takada, Shingo Browse this author →KAKEN DB
Kadoguchi, Tomoyasu Browse this author
Masaki, Yoshihiro Browse this author
Furihata, Takaaki Browse this author
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
Inflammation
Cytokines
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)
URI: http://hdl.handle.net/2115/53280
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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