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. 2018 Sep 11;8:13638. doi: 10.1038/s41598-018-31835-2

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© The Author(s) 2018

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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A STAT3-microRNA signaling is involved in lipid accumulation. (a) dHepaRG cells were treated with sodium oleate 250 μM for 4 days or vehicle treated (Ctrl) and co-treated for the subsequent 48 hours with sodium oleate 250 μM plus S3I-201 100 μM or S3I-201 alone. Total RNA were extracted and miRNAs levels were analyzed by qPCR (TaqMan MicroRNA Assay, Applied Biosystems), samples were normalized to the RNU38B endogenous control. Histograms show mean value expressed as fold induction of treated versus control cells. (b) C5BL6 mice were fed a high-fat diet (HFD) or normal diet (ND) for 16 weeks. Upper panel: total RNA were extracted from mice liver and q-PCR quantification of miR-21 expression was normalized to the snoRNA234 endogenous control. Lower panel: densitometric analysis (ImageJ software) of pSTAT3 protein levels from liver mice total protein extracts analyzed by immunoblotting. Histograms show mean value expressed as fold induction of HFD samples versus ND samples. (Bars indicate S.D.; asterisks indicate p-value). Immunoblot is available in Supplementary Fig. 6e.