Investigation of the modulator of inflammatory response after myocardial infarction

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19365
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: University of Tsukuba
• Principal Investigator: KIMURA Taizo 筑波大学, 附属病院, 病院講師 (00636508)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 心筋梗塞 / テネイシンC / マクロファージ / 心室リモデリング / toll like receptor 4

Outline of Final Research Achievements

Left ventricular remodeling after myocardial infarction (MI), which is major cause of heart failure,is one of the important clinical issues.
In this study, we showed that Tenascin-C (TNC), an extracellular matrix glycoprotein,increased the infiltration of pro-inflammatory macrophages and decreased the infiltration of anti-inflammatory macrophages in infarcted myocardium of mice and aggravated left ventricular remodeling after MI.In vitro analysis, induction of anti-inflammatory macrophages from mouse bone marrow derived cells was significantly suppressed by adding TNC and this effect was inhibited by toll like receptor 4 inhibitor. These findings suggest, TN-C aggravates the left ventricular remodeling after MI partly through the promotion of inflammatory response via the regulation of macrophage subsets.
TNC might be a new biotarget to prevent adverse ventricular remodeling after MI.

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