HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
Peer-reviewed Journal Articles, etc >

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

Files in This Item:
CR111-8_1037-1047.pdf799.67 kBPDFView/Open
Data_Supplement.pdfData Supplement311.96 kBPDFView/Open
Please use this identifier to cite or link to this item:

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
Homma, Tsuneaki Browse this author
Ono, Taisuke Browse this author
Hirabayashi, Kagami Browse this author
Suga, Tadashi Browse this author
Azalia, Putri Browse this author
Takada, Shingo Browse this author
Taniguchi, Masaru Browse this author
Nakayama, Toshinori Browse this author
Ishimori, Naoki Browse this author →KAKEN DB
Iwabuchi, Kazuya Browse this author
Tsutsui, Hiroyuki Browse this author →KAKEN DB
Keywords: natural killer T cells
myocardial infarction
heart failure
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)
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

Export metadata:

OAI-PMH ( junii2 , jpcoar )


Feedback - Hokkaido University