Mechanism of natural killer T cells in experimental myocarditis
| Project/Area Number |
18K15834
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 53020:Cardiology-related
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| Research Institution | Health Sciences University of Hokkaido |
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Principal Investigator |
SAITO Akimichi 北海道医療大学, 予防医療科学センター, 講師 (40735502)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | ナチュラルキラーT細胞 / 心筋炎 / 薬剤性心筋障害 / 炎症性サイトカイン / α-ガラクトシルセラミド |
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| Outline of Final Research Achievements |
The purpose of this study was to elucidate the role of natural killer T (NKT) cells in myocarditis, which could cause dilated cardiomyopathy. An experimental autoimmune myocarditis model mouse was prepared and α-Galactosylceramide (α-GalCer), which specifically stimulates NKT cells, was administered to examine the degree of myocardial damage, but the model mouse was not stable and no significant difference was found. As a result, the effect of NKT cells on myocarditis could not be confirmed.
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| Academic Significance and Societal Importance of the Research Achievements |
今回の研究ではNKT細胞が心筋炎に果たす役割については検証できなかった。一方、同様に炎症を惹起する薬剤性心筋障害モデルにおけるNKT細胞の役割について検討を行い、α-GalCerによるNKT細胞の活性化は炎症を制御することで心筋障害を軽減させることを明らかにし、成果を学術誌および国際学会において報告した。
あらゆる心筋障害の発症・進展においてNKT細胞活性化により炎症を制御することで、心筋障害を軽減できる可能性を見出した。
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Report
(4 results)
Research Products
(18 results)
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[Presentation] Inhibition of Xanthine Oxidase in the Acute Phase Preserves Mitochondrial Function in Skeletal Muscle and Exercise Capacity in Heart Failure After Myocardial Infarction2018
Author(s)
Nambu H, Takada S, Maekawa S, Matsumoto J, Kakutani N, Shirakawa R, Katayama T, Yamanashi K, Obata Y, Furihata T, Saito A, Yokota T, Kinugawa S, Anzai T
Organizer
American Heart Association Scientific Sessions 2018
Related Report
Int'l Joint Research
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[Presentation] The Outer Mitochondrial Membrane Protein, mitoNEET, Sustains Structure of Mitochondrial Cristae2018
Author(s)
Furihata T, Kinugawa S, Takada S, Maekawa S, Katayama T, Shirakawa R, Nambu H, Obata Y, Yamanashi K, Kakutani N, Saito A, Fukushima A, Yokota T, Anzai T
Organizer
American Heart Association Scientific Sessions 2018
Related Report
Int'l Joint Research
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[Presentation] Excessive Mitochondrial Reactive Oxygen Species Emission From Circulating Blood Cells is Associated With Systemic Oxidative Stress, Severity of Heart Failure, and Exercise Intolerance2018
Author(s)
Shirakawa R, Yokota T, Nakajima T, Takada S, Yamane M, Saito A, Maekawa S, Kakutani N, Furihata T, Matsumoto J, Tsuda M, Katayama T, Nambu H, Yamanashi K, Obata Y, Nakano I, Fukushima A, Kinugawa S, Anzai T
Organizer
American Heart Association Scientific Sessions 2018
Related Report
Int'l Joint Research
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[Presentation] Empagliflozin improves exercise endurance via the activation of fatty acid oxidation in the skeletal muscle in murine model of post-infarct heart failure2018
Author(s)
Nambu H, Takada S, Fukushima A, Matsumoto J, Kakutani N, Maekawa S, Shirakawa R, Furihata T, Nakajima T, Katayama T, Tsuda M, Saito A, Yokota T, Kinugawa S, Anzai T
Organizer
European Society of Cardiology Congress 2018
Related Report
Int'l Joint Research
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[Presentation] Excessive mitochondrial reactive oxygen species emission from circulating blood cells is associated with severity of heart failure and exercise intolerance2018
Author(s)
Shirakawa R, Yokota T, Nakajima T, Takada S, Yamane M, Furihata T, Matsumoto J, Tsuda M, Katayama T, Maekawa S, Nambu H, Fukushima A, Saito A, Kinugawa S, Anzai T
Organizer
European Society of Cardiology Congress 2018
Related Report
Int'l Joint Research
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