Exosomes derived from regulatory T cells ameliorate acute myocardial infarction by promoting macrophage M2
Hao Hu1, Jiawei Wu1, Cheng Cao1
1Department of Cardiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, China.
Acute myocardial infarction (AMI) is a serious ischemic heart disease. Regulatory T cells (Tregs) participate in AMI. This article aims to investigate the mechanism of action of Tregs in AMI. We constructed AMI mouse model. Then, AMI mouse and mouse macrophages (RAW264.7) were treated with Tregs or Treg-derived exosomes. The cardiac function of mice was detected. Triphenyl-tetrazolium chloride and TdT-mediated dUTP nick-end labeling staining were performed to detect the myocardial infarct size or apoptosis. The proportions of macrophages were analyzed by flow cytometry. Enzyme linked immunosorbent assay and quantitative real-time PCR was performed to estimate the levels of cytokines and genes. We found that Tregs ameliorated cardiac function, reduced myocardial infarct size and inhibited apoptosis of myocardial cells in AMI mice. Moreover, Treg-derived exosomes reduced myocardial infarct size and repressed apoptosis of myocardial cells in AMI mice. Furthermore, Treg-derived exosomes suppressed the expression of M1 macrophage markers, and promoted the expression of M2 macrophage markers in myocardial tissues of AMI mice and RAW264.7 cells. In conclusion, our work demonstrates that exosomes derived from Tregs ameliorate AMI by promoting macrophage M2 polarization. Thus, Tregs may be an essential cell for AMI treatment.
Acute myocardial infarction (AMI) is a serious ischemic heart disease. Regulatory T cells (Tregs) participate in AMI. This article aims to investigate the mechanism of action of Tregs in AMI. We constructed AMI mouse model. Then, AMI mouse and mouse macrophages (RAW264.7) were treated with Tregs or Treg-derived exosomes. The cardiac function of mice was detected. Triphenyl-tetrazolium chloride and TdT-mediated dUTP nick-end labeling staining were performed to detect the myocardial infarct size or apoptosis. The proportions of macrophages were analyzed by flow cytometry. Enzyme linked immunosorbent assay and quantitative real-time PCR was performed to estimate the levels of cytokines and genes. We found that Tregs ameliorated cardiac function, reduced myocardial infarct size and inhibited apoptosis of myocardial cells in AMI mice. Moreover, Treg-derived exosomes reduced myocardial infarct size and repressed apoptosis of myocardial cells in AMI mice. Furthermore, Treg-derived exosomes suppressed the expression of M1 macrophage markers, and promoted the expression of M2 macrophage markers in myocardial tissues of AMI mice and RAW264.7 cells. In conclusion, our work demonstrates that exosomes derived from Tregs ameliorate AMI by promoting macrophage M2 polarization. Thus, Tregs may be an essential cell for AMI treatment.
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