Impact of macrophage transcription factor MafB on cardiac remodeling after myocardial infarction.

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860541
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: Yamagata University
• Principal Investigator: Hasegawa Hiromasa 山形大学, 医学部, 非常勤講師 (20715396)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: マクロファージ / 心筋梗塞 / リモデリング / 転写因子MafB

Outline of Final Research Achievements

Transcription factor MafB is expressed only in monocytes and macrophages among hematopoietic cells, which plays a role in the terminal differentiation of macrophages. MafB knockout mice die immediately after birth due to developmental anomalies of neurons in the respiratory center. We generated transgenic mice that express dominant negative (DN) MafB capable of suppressing endogenous MafB transcription activity only in macrophages. MafB inhibition promotes macrophage apoptosis. Macrophage apoptosis plays a role in cardiac remodeling after myocardial infarction. We investigated macrophage apoptosis, efferocytosis, cytokine production and macrophage polarization using peritoneal macrophages of DN-MafB mice and MafB knockdown RAW264.7 cells. MafB inhibition promotes macrophage polarization to M1 and secretion of various inflammatory cytokines which cause inflammation and tissue disruptive reaction. There was no difference in effecrocytosis between DN-MafB and wild type macrophages.

Free Research Field

循環器内科学