The role of IL-22 in myocardial injury after ischemia-reperfusion
Project/Area Number |
16K20406
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Emergency medicine
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Research Institution | Kurume University |
Principal Investigator |
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Project Period (FY) |
2016-04-01 – 2018-03-31
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Project Status |
Completed (Fiscal Year 2017)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | 急性心筋梗塞 |
Outline of Final Research Achievements |
The aim of this study was to determine whether IL-22 administration could activate myocardial STAT3 signaling pathway and prevent the myocardial ischemia-reperfusion injury (IRI) in mice.Immunostaining revealed that phospho-STAT3 positive cardiomyocytes were markedly higher in IL-22-treated mice compared to PBS-treated mice. Real-time PCR revealed that IL-22 receptor subunit alpha 1 (IL-22RA1) was expressed in the heart. Next, we examined the effect of IL-22 on the myocardial infarction after IRI.Evans blue and TTC staining after a 24 h reperfusion showed a significant reduction in myocardial infarct size in IL-22-treated mice compared to PBS-treated mice. TUNEL staining revealed that apoptotic cells were significantly decreased in IL-22-treated mice compared to PBS-treated mice.Thus, IL-22 treatment directly activates myocardial STAT3 signaling pathway and prevents the myocardial infarction and apoptosis after IRI.
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Report
(3 results)
Research Products
(2 results)
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[Presentation] IL-10 Family Cytokine IL-22 Directly Activates Myocardial STAT3 Signaling Pathway and Prevents Myocardial Ischemia-Reperfusion Injury2018
Author(s)
Jinya Takahashi, Mai Yamamoto, Hideo Yasukawa, Takanobu Nagata, Koutatsu Shimozono, Shoichiro Nohara, Toshiyuki Yanai, Daisuke Fukui, Tomoko Sasaki, Tatsuhiro Shibata, Kazutoshi Mawatari, Yoshihiro Fukumoto
Organizer
The 82nd Annual Scientific Meeting of the Japanese Circulation Society, Osaka
Related Report
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