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Exosomes derived from regulatory T cells ameliorate acute myocardial infarction by promoting macrophage M2 polarization
IUBMB Life ( IF 4.6 ) Pub Date : 2020-08-25 , DOI: 10.1002/iub.2364
Hao Hu 1 , Jiawei Wu 1 , Cheng Cao 1 , Likun Ma 1
Affiliation  

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.

中文翻译:

来自调节性 T 细胞的外泌体通过促进巨噬细胞 M2 极化改善急性心肌梗死

急性心肌梗死(AMI)是一种严重的缺血性心脏病。调节性 T 细胞 (Tregs) 参与 AMI。本文旨在研究 Tregs 在 AMI 中的作用机制。我们构建了AMI小鼠模型。然后,用 Tregs 或 Treg 衍生的外泌体处理 AMI 小鼠和小鼠巨噬细胞(RAW264.7)。检测小鼠的心功能。进行三苯基四唑氯化物和 TdT 介导的 dUTP 缺口末端标记染色以检测心肌梗死面积或细胞凋亡。通过流式细胞术分析巨噬细胞的比例。进行酶联免疫吸附测定和定量实时 PCR 以估计细胞因子和基因的水平。我们发现 Tregs 改善了心脏功能,减少了心肌梗死面积并抑制了 AMI 小鼠的心肌细胞凋亡。而且,Treg衍生的外泌体减少了AMI小鼠的心肌梗死面积并抑制了心肌细胞的凋亡。此外,Treg 衍生的外泌体抑制 M1 巨噬细胞标志物的表达,并促进 AMI 小鼠和 RAW264.7 细胞心肌组织中 M2 巨噬细胞标志物的表达。总之,我们的工作表明,源自 Treg 的外泌体通过促进巨噬细胞 M2 极化来改善 AMI。因此,Tregs 可能是 AMI 治疗的必要细胞。我们的工作表明,源自 Treg 的外泌体通过促进巨噬细胞 M2 极化来改善 AMI。因此,Tregs 可能是 AMI 治疗的必要细胞。我们的工作表明,源自 Treg 的外泌体通过促进巨噬细胞 M2 极化来改善 AMI。因此,Tregs 可能是 AMI 治疗的必要细胞。
更新日期:2020-08-25
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