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Eosinophils improve cardiac function after myocardial infarction.
- Source :
-
Nature communications [Nat Commun] 2020 Dec 16; Vol. 11 (1), pp. 6396. Date of Electronic Publication: 2020 Dec 16. - Publication Year :
- 2020
-
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 H <subscript>2</subscript> O <subscript>2</subscript> - 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.
- Subjects :
- Aged
Animals
Cell Death
Diphtheria Toxin toxicity
Electrocardiography
Eosinophils drug effects
Eosinophils pathology
Female
Fibroblasts pathology
Fibroblasts physiology
Humans
Interleukin-4 genetics
Interleukin-4 metabolism
Male
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Transgenic
Myocardium pathology
Ribonucleases genetics
Ribonucleases metabolism
Eosinophils physiology
Myocardial Infarction physiopathology
Myocytes, Cardiac pathology
Subjects
Details
- Language :
- English
- ISSN :
- 2041-1723
- Volume :
- 11
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Nature communications
- Publication Type :
- Academic Journal
- Accession number :
- 33328477
- Full Text :
- https://doi.org/10.1038/s41467-020-19297-5