Fig. 5

Cortistatin-deficient brain endothelium shows deregulated gene pathways. Comparison of gene expression profiles from BECs isolated from Cort^+/+ vs Cort^−/− mice cultured as described in Fig. 2a. Each biological replicate (Rep) was pooled from 3 mice per genotype. a, d Volcano plots illustrate differentially expressed genes (DEGs) from Cort^−/− vs Cort^+/+ BECs incubated under NX/NG for 24 h (a) or under 4 h oxygen–glucose deprivation followed by 20 h reoxygenation (OGD-R) (d). Each dot represents one gene. Grey dots represent not significantly altered genes. The number of enriched (up, red) and decreased (down, blue) genes (with false discovery rate, FDR, p < 0.05) for cortistatin-deficient BECs is shown in the legend. Full description of DEGs is in Additional file 2: Tables S3 and S4. b, e Heatmaps and unsupervised hierarchical clustering of 613 DEGs (b) and 407 DEGs (e) in Cort^−/− vs Cort^+/+ BECs exposed to NX/NG and OGD-R, respectively. The expression values are represented in shades of red and blue, indicating expression above and below the median value across all samples. c, f Gene ontology (GO) terms for biological processes significantly overrepresented in Cort^−/− vs Cort^+/+ BECs incubated under NX/NG (c) or OGD-R (f). Data were grouped into similar gene sets and manually annotated into several networks, such as immune response, cellular matrix and remodelling, cell signalling and transcription, cell fate, brain endothelium dynamics, cell adhesion and migration, and cell metabolism. Red and blue bar-segments correspond to the numbers of upregulated and downregulated DEGs, respectively. All DEGs for each GO term are listed in Additional file 2: Tables S5 and S6. TGF-β, transforming growth factor beta; ECM, extracellular matrix; MAPK, mitogen-activated protein kinase; ERK, extracellular-signal-regulated kinase; VEGF, vascular endothelial growth factor; PDGFRβ, platelet-derived growth factor receptor beta; EMT, epithelial to mesenchymal transition