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Eosinophils improve cardiac function after myocardial infarction.

Nature communications (2020-12-18)
Jing Liu, Chongzhe Yang, Tianxiao Liu, Zhiyong Deng, Wenqian Fang, Xian Zhang, Jie Li, Qin Huang, Conglin Liu, Yunzhe Wang, Dafeng Yang, Galina K Sukhova, Jes S Lindholt, Axel Diederichsen, Lars M Rasmussen, Dazhu Li, Gail Newton, Francis W Luscinskas, Lijun Liu, Peter Libby, Jing Wang, Junli Guo, Guo-Ping Shi
ABSTRACT

Clinical studies reveal changes in blood eosinophil counts and eosinophil cationic proteins that may serve as risk factors for human coronary heart diseases. Here we report an increase of blood or heart eosinophil counts in humans and mice after myocardial infarction (MI), mostly in the infarct region. Genetic or inducible depletion of eosinophils exacerbates cardiac dysfunction, cell death, and fibrosis post-MI, with concurrent acute increase of heart and chronic increase of splenic neutrophils and monocytes. Mechanistic studies reveal roles of eosinophil IL4 and cationic protein mEar1 in blocking H2O2- and hypoxia-induced mouse and human cardiomyocyte death, TGF-β-induced cardiac fibroblast Smad2/3 activation, and TNF-α-induced neutrophil adhesion on the heart endothelial cell monolayer. In vitro-cultured eosinophils from WT mice or recombinant mEar1 protein, but not eosinophils from IL4-deficient mice, effectively correct exacerbated cardiac dysfunctions in eosinophil-deficient ∆dblGATA mice. This study establishes a cardioprotective role of eosinophils in post-MI hearts.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Eosin Y Solution, Alcoholic
Roche
In Situ Cell Death Detection Kit, Fluorescein, sufficient for ≤50 tests, suitable for detection
Sigma-Aldrich
Anti-Actin, α-Smooth Muscle - FITC antibody, Mouse monoclonal, clone 1A4, purified from hybridoma cell culture