Apoptosis inhibitor of macrophage depletion decreased M1 macrophage accumulation and the incidence of cardiac rupture after myocardial infarction in mice.

Autor: Shohei Ishikawa, Takahisa Noma, Hai Ying Fu, Takashi Matsuzaki, Makoto Ishizawa, Kaori Ishikawa, Kazushi Murakami, Naoki Nishimoto, Akira Nishiyama, Tetsuo Minamino
Jazyk: angličtina
Rok vydání: 2017
Předmět:
Zdroj: PLoS ONE, Vol 12, Iss 11, p e0187894 (2017)
Druh dokumentu: article
ISSN: 1932-6203
DOI: 10.1371/journal.pone.0187894
Popis: Cardiac rupture is an important cause of death in the acute phase after myocardial infarction (MI). Macrophages play a pivotal role in cardiac remodeling after MI. Apoptosis inhibitor of macrophage (AIM) is secreted specifically by macrophages and contributes to macrophage accumulation in inflamed tissue by maintaining survival and recruiting macrophages. In this study, we evaluated the role of AIM in macrophage accumulation in the infarcted myocardium and cardiac rupture after MI.Wild-type (WT) and AIM‒/‒ mice underwent permanent left coronary artery ligation and were followed-up for 7 days. Macrophage accumulation and phenotypes (M1 pro-inflammatory macrophage or M2 anti-inflammatory macrophage) were evaluated by immunohistological analysis and RT-PCR. Matrix metalloproteinase (MMP) activity levels were measured by gelatin zymography. The survival rate was significantly higher (81.1% vs. 48.2%, P
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