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首页> 美国卫生研究院文献>Journal of Cellular and Molecular Medicine >Neutrophil extracellular traps activate lung fibroblast to induce polymyositis‐related interstitial lung diseases via TLR9‐miR‐7‐Smad2 pathway
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Neutrophil extracellular traps activate lung fibroblast to induce polymyositis‐related interstitial lung diseases via TLR9‐miR‐7‐Smad2 pathway

机译：中性粒细胞胞外陷阱通过TLR9-miR-7-Smad2途径激活肺成纤维细胞诱导多发性肌炎相关的间质性肺疾病

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Excessive neutrophil extracellular trap (NET) formation may contribute to polymyositis (PM)‐associated interstitial lung diseases (ILD), but the underlying mechanism is not fully revealed. In this study, we found that NET accelerated the progression of ILD and promoted pulmonary fibrosis (PF) in vivo. miR‐7 expression was down‐regulated in lung tissue of PM group than control group, and NETs further decreased miR‐7 expression. TLR9 and Smad2 were up‐regulated in lung tissue of PM group than control group, and NETs further increased TLR9 and Smad2 expressions. In vitro experiments showed that PMA‐treated NETs accelerated the proliferation of LF and their differentiation into myofibroblast (MF), whereas DNase I decreased the promotion effect of NETs. Neutrophil extracellular trap components myeloperoxidase (MPO) and histone 3 also promoted the proliferation and differentiation of LF. In addition, we demonstrated that TLR9 involved in the regulation of NETs on LF proliferation and differentiation, and confirmed the interaction between miR‐7 and Smad2 in LF. Finally, miR‐7‐Smad2 pathway was confirmed to be involved in the regulation of TLR9 on LF proliferation and differentiation. Therefore, NETs promote PM‐related ILD, and TLR9‐miR‐7‐Smad2 signalling pathway is involved in the proliferation of LFs and their differentiation into MFs.
机译：过度的中性粒细胞胞外陷阱（NET）形成可能与多发性肌炎（PM）相关的间质性肺病（ILD）有关，但其潜在机制尚未完全揭示。在这项研究中，我们发现NET在体内加速了ILD的进程并促进了肺纤维化（PF）。与对照组相比，PM组肺组织中的miR-7表达下调，而NETs进一步降低了miR-7的表达。 PM组肺组织中TLR9和Smad2的表达高于对照组，而NETs进一步增加了TLR9和Smad2的表达。体外实验表明，经PMA处理的NETs促进了LF的增殖及其向肌纤维母细胞（MF）的分化，而DNase I降低了NETs的促进作用。中性粒细胞胞外陷阱成分髓过氧化物酶（MPO）和组蛋白3也促进了LF的增殖和分化。此外，我们证明了TLR9参与了NET对LF增殖和分化的调控，并证实了miR-7和Smad2在LF中的相互作用。最后，证实了miR-7-Smad2通路参与了TLR9对LF增殖和分化的调控。因此，NETs促进了PM相关的ILD，而TLR9-miR-7-Smad2信号通路参与了LF的增殖及其向MF的分化。

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