| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Outline of Final Research Achievements |
The expression of interleukin-33 was increased after permanent coronary ligation in mice. We identified that the main source of interleukin-33 was cardiac fibroblasts in the murine infarcts. Interleukin-33 knockout mice exhibited improved cardiac function and better survival rate 28 days after myocardial infarction. The expression of inflammatory cytokines and matrix metalloprotainase was reduced in the knockout mice and anti-inflammatory M2 macrophages are dominant infiltrating-cells in the infarcts 7 days after myocardial infarction. As Interleukin-33 receptor, ST2, strongly expressed on the CD11b+ cells, interleukin-33 might have detrimental role in the tissue healing after myocardial infarction, partly through controlling inflammatory and anti-inflammatory macrophage function.
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