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

Homma, Tsuneaki; Kinugawa, Shintaro; Takahashi, Masashige et al.

Journal of molecular and cellular cardiology, 2013, 62, 179-188

Permalink : https://hdl.handle.net/2115/53280

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アクセス権
open access
URI
https://hdl.handle.net/2115/53280
タイトル
Activation of invariant natural killer T cells by alpha-galactosylceramide ameliorates myocardial ischemia/reperfusion injury in mice
著者
Homma, Tsuneaki ; Kinugawa, Shintaro ; Takahashi, Masashige ; Sobirin, Mochamad Ali ; Saito, Akimichi ; Fukushima, Arata ; Suga, Tadashi ; Takada, Shingo ; Kadoguchi, Tomoyasu ; Masaki, Yoshihiro ; Furihata, Takaaki ; Taniguchi, Masaru ; Nakayama, Toshinori ; Ishimori, Naoki ; Iwabuchi, Kazuya ; Tsutsui, Hiroyuki
著者名
Homma, Tsuneaki
e-Rad_Researcher
60399871
著者名
Kinugawa, Shintaro
著者名
Takahashi, Masashige
著者名
Sobirin, Mochamad Ali
著者名
Saito, Akimichi
e-Rad_Researcher
40706553
著者名
Fukushima, Arata
e-Rad_Researcher
30708673
著者名
Suga, Tadashi
e-Rad_Researcher
60722329
著者名
Takada, Shingo
著者名
Kadoguchi, Tomoyasu
著者名
Masaki, Yoshihiro
e-Rad_Researcher
60782505
著者名
Furihata, Takaaki
e-Rad_Researcher
80110310
著者名
Taniguchi, Masaru
e-Rad_Researcher
50237468
著者名
Nakayama, Toshinori
e-Rad_Researcher
70399848
著者名
Ishimori, Naoki
e-Rad_Researcher
20184898
著者名
Iwabuchi, Kazuya
e-Rad_Researcher
70264017
著者名
Tsutsui, Hiroyuki
言語
英語
キーワード
Invariant natural killer T cells
Myocardial ischemia/reperfusion injury
Inflammation
Cytokines
発行日
2013-09
出版者
Academic press ltd- elsevier science ltd
収録物名
Journal of molecular and cellular cardiology
巻(号)
62
ページ
179-188
抄録
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.
資源タイプ
学術雑誌論文
出版タイプ
Accepted Manuscript
PISSN
0022-2828
NCID
AA00702819
関連情報
PMID
23774048
関連情報 (isVersionOf)
出版社版DOI
https://doi.org/10.1016/j.yjmcc.2013.06.004