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. 2017 Nov 1;7:14841. doi: 10.1038/s41598-017-14929-1

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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SMOX, Akt pathway and acrolein are required for bile canalicular lumen formation. Cells (5 × 10⁵ cells for each treatments) were transfected with siSMOX or treated with 10 µM Akt inhibitor 1L6-hydroxymethyl-chiro-inositol-2-(R)-2-O-methyl-3-O-octadecyl-sn-glycerocarbonate, 5 nM PI3K inhibitor 17β-hydroxywortmannin, 1 mM N-acetylcysteine (NAC), 1 mM N-benzylhydroxylamine (N-BHA), 4 mM pyruvate or 10⁴ units/mL catalase for 3 days. The number of bile canalicular lumen were counted and expressed as numbers of lumen/100 cells. Values are expressed as mean + SD of three independent experiments. ***p < 0.001 against DMSO (dimethylsulfoxide).