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. 2020 Jan 31;10:1597. doi: 10.1038/s41598-020-58482-w

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© The Author(s) 2020

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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Effects of HIF PHD inhibitors on hypoxia gene expression. Expression of hypoxia genes, HIF1α, Bnip3, Phd2, Vegf, Pfkfb1, Pfkfb3, Ldha, after treatment with 100 µM PHD inhibitors in normoxia for 24 hours were normalised to β-actin levels. Significant upregulation of Bnip3 and Vegf was seen with FG4592 and Bay85-3934. Phd2 was significant upregulated by FG4592. Pfkfb3 was significantly upregulated by DMOG, FG2216, FG492, GSK1278863, and Bay85-3934. Ldha was significantly upregulated by FG2216, GSK1278863 and Bay85-3934. HIF1α was not changed by any of the HIF PHD inhibitors. Each data point represented the mean and standard deviation of the relative fold change with respect to 1% DMSO-treated sample normalised to reference gene β-actin level. The dotted line represented basal gene expression. Statistical significance was indicated as *P < 0.05 (Two-way ANOVA, Tukey’s post-hoc analysis).