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首页> 美国卫生研究院文献>BioMed Research International >LPS Increases MUC5AC by TACE/TGF-α/EGFR Pathway in Human Intrahepatic Biliary Epithelial Cell
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LPS Increases MUC5AC by TACE/TGF-α/EGFR Pathway in Human Intrahepatic Biliary Epithelial Cell

机译：LPS通过人肝内胆管上皮细胞中的TACE /TGF-α/ EGFR途径增加MUC5AC

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Background. Mucin 5AC (MUC5AC) overproduction plays important roles in stone formation and recurrence of hepatolithiasis. We aim to investigate the involved mechanism and the potential target to block this process. Methods. 42 bile duct samples from hepatolithiasis and 15 normal bile duct samples from hemangioma patients were collected for detecting MUC5AC expression by immunohistochemistry. MUC5AC and phosphoepidermal growth factor receptor (pEGFR) expressions in human intrahepatic biliary epithelial cells (HIBECs) cultured with or without lipopolysaccharide (LPS) were detected by real-time PCR and western blot analysis. Transforming growth factor-α (TGF-α) secretion in HIBECs was detected by ELISA. Results. MUC5AC was overexpressed in bile ducts of hepatolithiasis samples compared with bile ducts from hemangioma samples. LPS upregulated MUC5AC expression in HIBECs. LPS promoted EGFR activation, and inhibiting EGFR activation by AG1478 significantly decreased LPS-induced MUC5AC overexpression in HIBECs. Moreover, LPS increased TGF-α secretion, and inhibiting tumor necrosis factor-α converting enzyme (TACE), which has been implicated in ectodomain cleavage of TGF-α, significantly inhibited LPS-induced EGFR activation and subsequent MUC5AC overexpression in HIBECs. Conclusion. Our results suggested that LPS increases MUC5AC expression through the TACE/TGF-α/EGFR pathway in HIBECs. This new finding might give light to the prevention of stone formation and recurrence of hepatolithiasis.
机译：背景。 Mucin 5AC（MUC5AC）过量生产在结石形成和肝结石复发中起重要作用。我们旨在调查涉及的机制和阻止此过程的潜在目标。方法。收集42例肝结石患者的胆管样品和15例血管瘤患者的正常胆管样品，通过免疫组织化学检测MUC5AC的表达。通过实时PCR和Western印迹分析检测在有或没有脂多糖（LPS）的情况下培养的人肝内胆管上皮细胞（HIBECs）中MUC5AC和磷酸表皮生长因子受体（pEGFR）的表达。 ELISA检测HIBECs中转化生长因子-α（TGF-α）的分泌。结果。与来自血管瘤样品的胆管相比，MUC5AC在肝结石病样品的胆管中过表达。 LPS上调了HIBEC中MUC5AC的表达。 LPS促进EGFR激活，而AG1478抑制EGFR激活则显着降低HIBEC中LPS诱导的MUC5AC过表达。此外，LPS增加了TGF-α的分泌，并抑制了肿瘤坏死因子-α转化酶（TACE），该酶与TGF-α的胞外域裂解有关，可显着抑制LPS诱导的EGFR激活和随后在HIBECs中的MUC5AC过表达。结论。我们的结果表明，LPS通过HIBECs中的TACE /TGF-α/ EGFR途径增加MUC5AC表达。这一新发现可能为预防结石形成和肝结石复发提供参考。

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