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首页> 外文期刊>Stem Cell Research & Therapy >Vagal-α7nAChR signaling promotes lung stem cells regeneration via fibroblast growth factor 10 during lung injury repair
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Vagal-α7nAChR signaling promotes lung stem cells regeneration via fibroblast growth factor 10 during lung injury repair

机译：vagal-α7nAchr信号传导通过成纤维细胞生长因子10在肺损伤修复期间促进肺干细胞再生

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BACKGROUND:Proliferation and transdifferentiation of lung stem cells (LSCs) could promote lung injury repair. The distal airways of the lung are innervated by the vagus nerve. Vagal-alpha7 nicotinic acetylcholine receptor (α7nAChR) signaling plays a key role in regulating lung infection and inflammation; however, whether this pathway could regulate LSCs remains unknown.METHODS:LSCs (Sca1sup+/supCD45sup-/supCD31sup-/sup cells) were isolated and characterized according to a previously published protocol. α7nAChR knockout mice and wild-type littermates were intratracheally challenged with lipopolysaccharide (LPS) to induce lung injury. A cervical vagotomy was performed to study the regulatory effect of the vagus nerve on LSCs-mediated lung repair. α7nAChR agonist or fibroblast growth factor 10 (FGF10) was intratracheally delivered to mice. A single-cell suspension of lung cells was analyzed by flow cytometry. Lung tissues were collected for histology, quantitative real-time polymerase chain reaction (RT-PCR), and immunohistochemistry.RESULTS:We found that LSCs maintained multilineage differentiation ability and transdifferentiated into alveolar epithelial type II cells (AEC2) following FGF10 stimulation in vitro. Vagotomy or α7nAChR deficiency reduced lung Ki67sup+/sup LSCs expansion and hampered the resolution of LPS-induced lung injury. Vagotomy or α7nAChR deficiency decreased lung FGF10 expression and the number of AEC2. The α7nAChR agonist-GTS-21 reversed the reduction of FGF10 expression in the lungs, as well as the number of Ki67sup+/sup cells, LSCs, Ki67sup+/sup LSCs, and AEC2 in LPS-challenged vagotomized mice. Supplementation with FGF10 counteracted the loss of Ki67sup+/sup LSCs and AEC2 in LPS-challenged α7nAChR knockout mice.CONCLUSIONS:The vagus nerve deploys α7nAChR to enhance LSCs proliferation and transdifferentiation and promote lung repair in an FGF10-dependent manner during LPS-induced lung injury.
机译：背景：肺干细胞（LSCs）的增殖和转介质可以促进肺损伤修复。肺的远端气道被迷走神经受到了声号。 vagal-alpha7烟碱乙酰胆碱受体（α7nAChr）信号传导在调节肺部感染和炎症方面发挥着关键作用;但是，该途径是否可以调节LSCs仍然未知。方法：LSCs（SCA1 + CD45 - cd31 - 细胞）根据先前发布的协议。 α7NACHR敲除小鼠和野生型凋落物用脂多糖（LPS）脑内攻击，以诱导肺损伤。进行宫颈迷离术，以研究迷走神经对LSC介导的肺修复的调节作用。 α7NACHR激动剂或成纤维细胞生长因子10（FGF10）被脑内递送至小鼠。通过流式细胞术分析肺细胞的单细胞悬浮液。收集肺组织的组织学，定量实时聚合酶链反应（RT-PCR）和免疫组化。结果：我们发现LSCs保持多线分化能力并在体外FGF10刺激后转化为肺泡上皮II细胞（AEC2）。迷走术或α7NACHR缺乏减少肺部Ki67 + LSCs膨胀，阻碍了LPS诱导的肺损伤的分辨率。阴道术或α7NACHR缺乏减少肺FGF10表达和AEC2的数量。 α7NAChR激动剂-GTS-21反转肺中FGF10表达的减少，以及Ki67 + 细胞，LSC，Ki67 + Lscs和AEC2的数量LPS挑战迷重术小鼠。用FGF10补充抵消了LPS挑战α7NACHR敲除小鼠的KI67 + LSC和AEC2的丧失。结论：迷走神经部署α7NACHR以增强LSCs增殖和转染，以FGF10依赖的方式促进肺部修复在LPS诱导的肺损伤期间。

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