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Fig. 7 | Journal of Neuroinflammation

Fig. 7

From: Cortistatin deficiency reveals a dysfunctional brain endothelium with impaired gene pathways, exacerbated immune activation, and disrupted barrier integrity

Fig. 7

Transcriptional alterations in cortistatin-deficient brain endothelium. Gene sets for Cort+/+ and Cort−/− BECs displayed in Figs. 5 and 6 were manually annotated into gene modules relevant for key BBB features and functions: a extracellular matrix components; b cell–cell contact mediators; c BBB dynamics; d cell fate agents; e endothelial transporters; f immune response; g response to oxygen; h others, (genes with the highest fold change from different categories); and i signalling pathways. Differential expression patterns of selected DEGs modulated by the lack of cortistatin are represented in each module based on criteria defined in the legend box. Genes that do not have significant expression changes are displayed by a white box. Relative fold change expression (log2FC) in each experimental group is shown by shades of red (upregulated) and blue (downregulated). MMPs matrix metalloproteinases, TFs transcription factors, Aa amino acids, LDL low density lipoprotein, MAPKs mitogen-activated protein kinases

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