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. 2017 Oct 3;7:12628. doi: 10.1038/s41598-017-13051-6

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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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LpPLA₂ is released by Hofbauer cells and increased in GDM. (a–c): Immunofluorescence staining of placental tissue. Images are representative of 3 independent experiments (N = 3). (a) van Willebrandt factor (vWF, green) was localized to the placental vessel lumen. LpPLA₂ (red) was localized to villous stroma and sub-endothelial connective tissue layers. EC = endothelial cells, SEL = sub-endothelial layer. (b) Trophoblast marker Cytokeratin 7 (CK7, green) was present in the fused syncytial layer of the villous; LpPLA₂ (red) was localized to villous stroma. SC = Syncytium. (c) Co-localization of LpPLA₂ (red) with CD163 (green), a marker of Hofbauer cells, was observed within villous stroma. HBC = Hofbauer cells. (d) LpPLA₂ activity secreted by HBCs isolated from healthy and GDM placenta (mean ± SD; N = 5 HBC isolations/group; two-way ANOVA). (e) LpPLA₂ activity is abolished by addition of 150 nM Darapladib, a specific LpPLA₂-inhibitor (mean ± SD, N = 4).