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首页> 外文期刊>Experimental Lung Research >The human Cathelicidin LL-37 induces MUC5AC mucin production by airway epithelial cells via TACE-TGF-α-EGFR pathway
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The human Cathelicidin LL-37 induces MUC5AC mucin production by airway epithelial cells via TACE-TGF-α-EGFR pathway

机译：人类Cathelicidin LL-37通过TACE-TGF-α-EGFR途径诱导气道上皮细胞产生MUC5AC粘蛋白

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Aim: To investigate the mechanism for LL-37 inducing MUC5AC mucin production in airway epithelial cells. Materials and Methods: The airway epithelial NCI-H292 cells were stimulated with various concentrations of LL-37 synthetic peptide and scrambled LL-37 (sLL-37) synthetic peptide ranged from 2.5 to 10 μg/mL. The effects of LL-37 and sLL-37 on TNF-α-converting enzyme (TACE) and EGFR activation and MUC5AC mucin production were evaluated by fluorescence resonance energy transfer (FRET) assay, Western blotting and ELISA respectively. Furthermore, we measured changes of transforming growth factor-alpha (TGF-α) in culture supernatants. A serious of inhibitors including TACE inhibitor TAPI-1, EGFR inhibitor AG1478, EGFR-neutralizing antibody, TGF-α-neutralizing antibody, amphiregulin (AR)-neutralizing antibody, and heparin binding-epidermal growth factor (HB-EGF)-neutralizing antibody were used to block the signaling pathway. Human serum and FBS were also used to investigate the effects of serum on LL-37-induced MUC5AC mucin production. Results: LL-37 induced TACE and EGFR activation, as well as TGF-α and MUC5AC mucin production by NCI-H292 cells in a dose-dependent manner. EGFR-neutralizing antibody and AG1478 inhibited LL-37-induced EGFR activation and subsequent MUC5AC mucin production, whereas TGF-α- neutralizing antibody increased LL-37-induced TGF-α production. TAPI-1 inhibited LL-37-induced TGF-α production, EGFR activation and subsequent MUC5AC mucin production, whereas TGF-α-neutralizing antibody, but not AR-or HB-EGF-neutralizing antibody, inhibited LL-37-induced EGFR activation and subsequent MUC5AC mucin production in NCI-H292 cells. The sLL-37 had no effect on TACE and EGFR activation and MUC5AC mucin production. Additionally, Human serum, rather than FBS, inhibited LL-37-induced MUC5AC mucin production. Conclusions: LL-37 induces MUC5AC mucin production by airway epithelial cells via TACE-TGF-α-EGFR pathway.
机译：目的：探讨LL-37诱导气道上皮细胞产生MUC5AC粘蛋白的机制。材料与方法：用各种浓度的LL-37合成肽和2.5至10μg/ mL的加扰的LL-37（sLL-37）合成肽刺激气道上皮NCI-H292细胞。分别通过荧光共振能量转移（FRET）法，Western印迹法和ELISA法评估了LL-37和sLL-37对TNF-α转化酶（TACE），EGFR激活和MUC5AC粘蛋白产生的影响。此外，我们测量了培养上清液中转化生长因子-α（TGF-α）的变化。大量抑制剂包括TACE抑制剂TAPI-1，EGFR抑制剂AG1478，EGFR中和抗体，TGF-α中和抗体，双调蛋白（AR）中和抗体以及肝素结合表皮生长因子（HB-EGF）中和抗体被用来阻断信号通路。还使用人血清和FBS来研究血清对LL-37诱导的MUC5AC粘蛋白产生的影响。结果：NCI-H292细胞以剂量依赖的方式诱导LL-37诱导TACE和EGFR活化，以及TGF-α和MUC5AC粘蛋白的产生。 EGFR中和抗体和AG1478抑制LL-37诱导的EGFR激活和随后的MUC5AC粘蛋白产生，而TGF-α中和抗体则增加LL-37诱导的TGF-α产生。 TAPI-1抑制LL-37诱导的TGF-α产生，EGFR激活和随后的MUC5AC粘蛋白产生，而TGF-α中和抗体抑制LL-37诱导的EGFR激活，而不是AR-或HB-EGF中和抗体。以及随后在NCI-H292细胞中产生MUC5AC粘蛋白。 sLL-37对TACE和EGFR活化以及MUC5AC粘蛋白产生没有影响。另外，人血清而不是FBS抑制LL-37诱导的MUC5AC粘蛋白产生。结论：LL-37通过TACE-TGF-α-EGFR途径诱导气道上皮细胞产生MUC5AC粘蛋白。

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