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. 2017 Sep 8;7:11006. doi: 10.1038/s41598-017-11212-1

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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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Blocking MGAT5-mediated N-glycosylation suppresses Gal-1-induced hepatic stellate cell (HSC) migration. (A) Schematic representation of N-glycan biosynthesis. (B) An N-glycan inhibitor (swainsonine, SW) inhibits L-PHA binding to LX-2 cells. (C) SW inhibits Gal-1 binding to LX-2 cells. (D) SW suppresses Gal-1-induced LX-2 cell migration. (E) Knockdown of MGAT5 inhibits L-PHA binding to LX-2 cells. (F) MGAT5 siRNAs suppress MGAT5 expression. (G) MGAT5 siRNAs inhibit Gal-1-induced LX-2 cell migration. LX-2 cells were treated with SW or transfected with MGAT5 siRNA for 48 h followed by incubation with L-PHA and Gal-1-488 to detect their binding to LX-2 cells using flow cytometry. The black line represents the binding of LX-2 cells with DyLight® 488 strepavidin alone and the brown line represents LX-2 cells without staining. To measure the migratory ability, cells were treated with 500 nM Gal-1 for 16 h. Migrated cells were counted, and results are presented as the mean ± SEM of three independent experiments. *p < 0.05.