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Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction

Author

Listed:
  • Juan Tang

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
    School of Basic Medical Sciences, Tianjin Medical University)

  • Yujun Shen

    (School of Basic Medical Sciences, Tianjin Medical University)

  • Guilin Chen

    (School of Basic Medical Sciences, Tianjin Medical University)

  • Qiangyou Wan

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences)

  • Kai Wang

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences)

  • Jian Zhang

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
    School of Basic Medical Sciences, Tianjin Medical University)

  • Jing Qin

    (Center for Genomic Sciences, LKS Faculty of Medicine, The University of Hong Kong
    School of Life Science, Chinese University of Hong Kong)

  • Guizhu Liu

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences)

  • Shengkai Zuo

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences)

  • Bo Tao

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences)

  • Yu Yu

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences)

  • Junwen Wang

    (Center for Genomic Sciences, LKS Faculty of Medicine, The University of Hong Kong
    Center for Individualized Medicine, Mayo Clinic
    Arizona State University, Scottsdale)

  • Michael Lazarus

    (International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba)

  • Ying Yu

    (Key Laboratory of Food Safety Research, CAS Center for Excellence in Molecular Cell Science, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences
    School of Basic Medical Sciences, Tianjin Medical University)

Abstract

Two distinct monocyte (Mo)/macrophage (Mp) subsets (Ly6Clow and Ly6Chigh) orchestrate cardiac recovery process following myocardial infarction (MI). Prostaglandin (PG) E2 is involved in the Mo/Mp-mediated inflammatory response, however, the role of its receptors in Mos/Mps in cardiac healing remains to be determined. Here we show that pharmacological inhibition or gene ablation of the Ep3 receptor in mice suppresses accumulation of Ly6Clow Mos/Mps in infarcted hearts. Ep3 deletion in Mos/Mps markedly attenuates healing after MI by reducing neovascularization in peri-infarct zones. Ep3 deficiency diminishes CX3C chemokine receptor 1 (CX3CR1) expression and vascular endothelial growth factor (VEGF) secretion in Mos/Mps by suppressing TGFβ1 signalling and subsequently inhibits Ly6Clow Mos/Mps migration and angiogenesis. Targeted overexpression of Ep3 receptors in Mos/Mps improves wound healing by enhancing angiogenesis. Thus, the PGE2/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6Clow Mos/Mps, indicating that Ep3 receptor activation may be a promising therapeutic target for acute MI.

Suggested Citation

  • Juan Tang & Yujun Shen & Guilin Chen & Qiangyou Wan & Kai Wang & Jian Zhang & Jing Qin & Guizhu Liu & Shengkai Zuo & Bo Tao & Yu Yu & Junwen Wang & Michael Lazarus & Ying Yu, 2017. "Activation of E-prostanoid 3 receptor in macrophages facilitates cardiac healing after myocardial infarction," Nature Communications, Nature, vol. 8(1), pages 1-14, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14656
    DOI: 10.1038/ncomms14656
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