Role of Interleukin-33 in Left Ventricular Remodeling After Myocardial Infarction

2014 Fiscal Year Final Research Report

• Project/Area Number: 25860620
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: Keio University
• Principal Investigator: ANZAI Atsushi 慶應義塾大学, 医学部, 助教 (50528164)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 炎症反応 / 心筋梗塞

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.

Free Research Field

循環器内科学