| Project/Area Number |
17K10435
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | Kanazawa University |
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Principal Investigator |
Taki Junichi 金沢大学, 医学系, 准教授 (10251927)
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| Co-Investigator(Kenkyū-buntansha) |
小川 数馬 金沢大学, 新学術創成研究機構, 教授 (30347471)
柴 和弘 金沢大学, 学際科学実験センター, 教授 (40143929)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | ventricular remodeling / myocardial infarction / C-14-methionine / I-125-RGD / macrophage / postconditioning / angiogenesis / apoptosis / LV remodeling / RGD / annexin V |
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| Outline of Final Research Achievements |
Serial C-14-methionine imaging, that mainly reflects macrophage infiltration, after 30min myocardial ischemia and reperfusion and subsequent left ventricular remodeling at 2 months was investigated under condition with post-conditioning and colchicine treatment. In rats with post-conditioning, peaked methionine uptake at day 3 was not suppressed compared with control rats, however, subsequent resolution of methionine uptake at 1 to 2 weeks was accelerated and ventricular remodeling at 2 months was attenuated. In rats treated with colchicine during 1 to 6 day after infarction, peaked methionine uptake at day 3 and subsequent 1 to 2 weeks was all suppressed and ventricular remodeling at 2 months was attenuated. As an inflammatory imaging, C-14-methionine imaging could be used to monitor the effect of treatments on post-infarction inflammation and to predict left ventricular remodeling at chronic phase.
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| Academic Significance and Societal Importance of the Research Achievements |
心筋梗塞における救急での再灌流療法により急性期の死亡率は著明に改善された。しかしその後の心拡大や機能低下、いわゆる左室リモデリングにより心不全となり予後不良となることが問題視されている。この左室リモデリングの要因として梗塞後の持続する炎症性変化の関与が示唆されている。我々は以前の研究で梗塞後の炎症は主にマクロファージが関与しており、メチオニンが集積することを報告してきた。今回この梗塞後の炎症性変化に対する治療的介入として臨床で実施可能なpost-conditioningとコルヒチン治療により左室リモデリングが抑制され、炎症性変化のモニターがメチオニンイメージングで可能であることを示した。
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