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IL-6-miR-210 Suppresses Regulatory T Cell Function and Promotes Atrial Fibrosis by Targeting Foxp3

  • Chen, YingWei (Department of Cardiology, The First Affiliated Hospital of Zheng Zhou University) ;
  • Chang, GuoDong (Department of Cardiology, The First People's Hospital of Shangqiu) ;
  • Chen, XiaoJie (Department of Cardiology, The First Affiliated Hospital of Zheng Zhou University) ;
  • Li, YunPeng (Department of Cardiology, The First Affiliated Hospital of Zheng Zhou University) ;
  • Li, HaiYu (Department of Cardiology, The First Affiliated Hospital of Zheng Zhou University) ;
  • Cheng, Dong (Department of Cardiology, The First Affiliated Hospital of Zheng Zhou University) ;
  • Tang, Yi (Department of Cardiology, The First Affiliated Hospital of Zheng Zhou University) ;
  • Sang, HaiQiang (Department of Cardiology, The First Affiliated Hospital of Zheng Zhou University)
  • Received : 2018.06.26
  • Accepted : 2018.10.01
  • Published : 2020.05.31

Abstract

The aim of this study was to explore the role of IL-6-miR-210 in the regulation of Tregs function and atrial fibrosis in atrial fibrillation (AF). The levels of interleukin (IL)-6 and IL-10 in AF patients were detected by using ELISA. Proportions of Treg cells were detected by fluorescence activated cell sorting analysis in AF patients. The expression of Foxp3, α-SMA, collagen I and collagen III were determined by western blot. The atrial mechanocytes were authenticated by vimentin immunostaining. The expression of miR-210 was performed by quantitative real-time polymerase chain reaction (qRT-PCR). TargetScan was used to predict potential targets of miR-210. The cardiomyocyte transverse sections in AF model group were observed by H&E staining. The myocardial filaments were observed by masson staining. The level of IL-6 was highly increased while the level of IL-10 (Tregs) was significantly decreased in AF patients as compared to normal control subjects, and IL-6 suppressed Tregs function and promoted the expression of α-SMA, collagen I and collagen III. Furthermore, miR-210 regulated Tregs function by targeting Foxp3, and IL-6 promoted expression of miR-210 via regulating hypoxia inducible factor-1α (HIF-1α). IL-6-miR-210 suppresses regulatory T cell function and promotes atrial fibrosis by targeting Foxp3.

Keywords

References

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