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. 2017 Oct 10;7:12879. doi: 10.1038/s41598-017-12861-y

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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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DUSP5 regulates ERK1/2-dependent inflammatory gene expression in adipocytes. (A) Adipocytes were pretreated (30 min) with the MEK1/2 inhibitor U0126 prior to stimulation with vehicle (H₂0) or TNFα (100 pM). RNA was isolated 30 min post-TNFα stimulation and qPCR used to assess inflammatory gene expression of CCL2, COX-2, and IL-16. (B) Adipocytes (n = 3/group) were transiently transfected with small, non-targeting control (100 nM) siRNAs or siRNAs (100 nM) targeting independent regions of the DUSP5 gene for 48 hrs prior to stimulation with TNFα. RNA was isolated 30 min post-TNFα stimulation and assessed for CCL2, COX-2 and IL-16 mRNA expression. Statistical analysis was completed by ANOVA followed by Tukey’s post-hoc using GraphPad Prism software to determine significance p < 0.05.