LPS stimulates MUC5AC expression in human biliary epithelial cells: whether there exists a possible pathway of PKC/NADPH/ROS?

LPS stimulates MUC5AC expression in human biliary epithelial cells: whether there exists a possible pathway of PKC/NADPH/ROS?
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LPS刺激人胆道上皮细胞MUC5AC表达:是否存在PKC/NADPH/ROS可能的通路?

DOI:
10.1007/s11010-013-1817-1
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发表时间:
2013
影响因子:
4.3
通讯作者:
Yongnan Li
Yongnan Li
中科院分区:
生物学3区
文献类型:
--
作者:
Min Li;Yu Tian;Shuodong Wu;Hong Yu;Yongnan Li

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先前的研究表明,脂多糖(LPS)可以上调气道上皮细胞的MUC5AC。然而,细菌感染与胆道粘液分泌改变之间的关系和机制尚不清楚。用LPS诱导人胆道上皮细胞,用特异性试剂盒检测细胞上清中h2o2的产生,用实时荧光定量PCR、Western blot和免疫组织化学检测MUC5AC的表达。h2o2产量呈剂量依赖性增加,LPS上调MUC5AC mRNA和蛋白水平的表达,而特异性抑制剂可降低MUC5AC的高表达。活性氧通过上调MUC5AC的分泌参与LPS的过程。此外,PKC和NADPH氧化酶调节lps挑战的人胆道上皮细胞MUC5AC的产生。
Previous studies have shown that lipopolysaccharide (LPS) can upregulate MUC5AC in airway epithelial cells. However, the relationship and mechanism between bacterial infection and altered mucus secretion in the biliary tract remains unclear. Human biliary epithelial cells were induced by LPS, H2O2production in the cell supernatants were detected by specific kit and expression of MUC5AC were detected by real-time PCR, Western blot, and immunohistochemistry. H2O2production increased in a dose-dependent manner, LPS upregulate MUC5AC expression in both mRNA and protein level while specific inhibitors can reduce this high expression. Reactive oxygen species participates in the process of LPS by upregulating MUC5AC secretion. Moreover, PKC and NADPH oxidase regulate MUC5AC production in LPS-challenged human biliary epithelial cells.
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影响因子: 6.4
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