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首页> 外文期刊>Cell biology international. >M2 macrophages induce EMT through the TGF-/Smad2 signaling pathway
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M2 macrophages induce EMT through the TGF-/Smad2 signaling pathway

机译：M2巨噬细胞通过TGF-/ Smad2信号通路诱导EMT

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摘要

IPF is characterized by fibroblast accumulation, collagen deposition, and ECM remodeling, with myofibroblasts believed to be the effector cell type. Myofibroblasts develop due to EMT of lung alveolar epithelial cells, which can be induced by TGF-. M2 macrophages, a macrophage subpopulation, secrete large amounts of TGF-. To clarify the relationship between IPF, EMT, TGF-, and M2 macrophages, a bleomycin-induced pulmonary fibrosis mouse model was used. Seventeen days after mice were treated with bleomycin, the successful establishment of a pulmonary fibrosis model was confirmed by HE stain and Masson's trichrome stain. We found evidence in support of EMT, such as elevated protein levels of -SMA in lung tissue and decreased levels of E-cadherin and CK-18. Additionally, increased TGF- levels and TGF-/Smad2 signaling activation was observed. Macrophages were recruited to pulmonary alveoli. Alveolar macrophages were phenotyped and identified as M2 macrophages, with up-regulated CD206 on the cell surfaces. For in vitro studies, we treated RAW 264.7 cells with IL-4 for 24h, and the cells were then utilized as M2 macrophages. TGF- levels increased significantly in the culture supernatant. Forty-eight hours after lung epithelial cells (MLE-12) were co-cultured with the M2 macrophages, the expression of -SMA increased, and E-cadherin and CK-18 decreased. When a TGF- receptor inhibitor, LY2109761 was used, the EMT induced by M2 macrophages was blocked. In conclusion, we demonstrated that M2 macrophages induce EMT through the TGF-/Smad2 signaling pathway.
机译：IPF的特征在于成纤维细胞积累，胶原沉积和ECM重塑，肌纤维细胞被认为是效应细胞类型。由于肺肺泡上皮细胞的EMT，肌成纤维细胞产生，其可以通过TGF-诱导。 M2巨噬细胞，巨噬细胞亚群，分泌大量TGF-。为了阐明IPF，EMT，TGF-和M2巨噬细胞之间的关系，使用了一种博来霉素诱导的肺纤维化小鼠模型。用博来霉素治疗小鼠17天，通过他的染色和马隆的三色染色来确认肺纤维化模型的成功建立。我们发现支持EMT的证据，例如肺组织中的-SMA升高的蛋白质水平，并降低e-cadherin和CK-18。另外，观察到增加的TGF级和TGF-/ Smad2信号传导激活。巨噬细胞被募集到肺部肺泡。肺泡巨噬细胞被表型化并鉴定为M2巨噬细胞，细胞表面上具有上调的CD206。对于体外研究，我们用IL-4处理了264.7细胞24小时，然后用作M2巨噬细胞。培养上清液中的TGF级别显着增加。肺上皮细胞（MLE-12）与M2巨噬细胞共同培养，-SMA增加，E-Cadherin和CK-18的表达减少了40℃。当使用TGF受体抑制剂LY2109761时，由M2巨噬细胞诱导的EMT被抑制。总之，我们证明了M2巨噬细胞通过TGF / Smad2信号通路诱导EMT。

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  • 来源
    《Cell biology international.》 |2017年第9期|共9页
  • 作者

    Zhu Liangying; Fu Xiao; Chen Xiang; Han Xiaodong; Dong Ping;

  • 作者单位

    Nanjing Univ Sch Med Immunol &

    Reprod Biol Lab Hankou Rd 22 Nanjing 210093 Jiangsu Peoples R;

    Nanjing Univ Sch Med Immunol &

    Reprod Biol Lab Hankou Rd 22 Nanjing 210093 Jiangsu Peoples R;

    Nanjing Univ Sch Med Immunol &

    Reprod Biol Lab Hankou Rd 22 Nanjing 210093 Jiangsu Peoples R;

    Nanjing Univ Sch Med Immunol &

    Reprod Biol Lab Hankou Rd 22 Nanjing 210093 Jiangsu Peoples R;

    Nanjing Univ Sch Med Immunol &

    Reprod Biol Lab Hankou Rd 22 Nanjing 210093 Jiangsu Peoples R;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    bleomycin; collagen; EMT; M2 macrophages; myofibroblast; pulmonary fibrosis;

    机译：Bleomycin;胶原蛋白;EMT;M2巨噬细胞;肌纤维细胞;肺纤维化;

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