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. 2019 Sep 2;9:211. doi: 10.1038/s41398-019-0542-2

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© The Author(s) 2019

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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Fig. 2 — a Interrogation of lithium-responsive astroglial genes against BD databases DISGENET(5.0) and BDGene^34,35 identified 61 potential outcome markers that are present in both groups. b Unsupervised hierarchical clustering illustrates the overriding effect of lithium to downregulate BD-associated astroglial genes. c GO analysis identifies receptor signalling and ECM organisation as major astroglial biological processes regulated by lithium and associated with BD; Tgfb1 was found in all the GO terms apart from the five indicated with asterisks. d NEST analysis of lithium-responsive astroglial genes associated with BD predicted a major interaction between LOX and Elastin with TGFβ1 and MMP9 as the mechanism for astroglial ECM regulation and potential surrogate markers in BD (PPI enrichment p = 9.55e−15 p < 0.001; coloured nodes represent top biological pathways: green = ECM organisation (p < 0.001), blue = G-protein couple receptor signalling (GPCR) pathways (p < 0.001)