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Eosinophils improve cardiac function after myocardial infarction.
Liu, Jing; Yang, Chongzhe; Liu, Tianxiao; Deng, Zhiyong; Fang, Wenqian; Zhang, Xian; Li, Jie; Huang, Qin; Liu, Conglin; Wang, Yunzhe; Yang, Dafeng; Sukhova, Galina K; Lindholt, Jes S; Diederichsen, Axel; Rasmussen, Lars M; Li, Dazhu; Newton, Gail; Luscinskas, Francis W; Liu, Lijun; Libby, Peter; Wang, Jing; Guo, Junli; Shi, Guo-Ping.
Afiliação
  • Liu J; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Yang C; Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
  • Liu T; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Deng Z; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Fang W; Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
  • Zhang X; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Li J; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Huang Q; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Liu C; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Wang Y; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Yang D; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Sukhova GK; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Lindholt JS; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Diederichsen A; Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
  • Rasmussen LM; Department of Cardiothoracic and Vascular Surgery, Odense University Hospital, Odense, Denmark.
  • Li D; Elitary Research Centre of personalised medicine in arterial disease (CIMA), Odense University Hospital, Odense, Denmark.
  • Newton G; Cardiovascular Research Unit, Viborg Hospital, Viborg, Denmark.
  • Luscinskas FW; Elitary Research Centre of personalised medicine in arterial disease (CIMA), Odense University Hospital, Odense, Denmark.
  • Liu L; Department of Cardiology, Odense University Hospital, Odense, Denmark.
  • Libby P; Elitary Research Centre of personalised medicine in arterial disease (CIMA), Odense University Hospital, Odense, Denmark.
  • Wang J; Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, Odense, Denmark.
  • Guo J; Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
  • Shi GP; Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
Nat Commun ; 11(1): 6396, 2020 12 16.
Article em En | MEDLINE | ID: mdl-33328477
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-ß-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.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Miócitos Cardíacos / Eosinófilos / Infarto do Miocárdio Tipo de estudo: Risk_factors_studies Limite: Aged / Animals / Female / Humans / Male Idioma: En Ano de publicação: 2020 Tipo de documento: Article
Texto completo
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Miócitos Cardíacos / Eosinófilos / Infarto do Miocárdio Tipo de estudo: Risk_factors_studies Limite: Aged / Animals / Female / Humans / Male Idioma: En Ano de publicação: 2020 Tipo de documento: Article