Additional file 1 of Cortistatin deficiency reveals a dysfunctional brain endothelium with impaired gene pathways, exacerbated immune activation, and disrupted barrier integrity

Additional file 1: Extended methods for animals, b.End5 and BECs cells, human BBB model, endothelial permeability assay, immunocytochemistry, determination of inflammatory factors, transendothelial migration assay, in vivo BBB permeability assay, RNA extraction and determination of gene expression, next-generation transcriptome sequencing. Table S1. Sequence of primers used for qPCR dynamic array. Table S2. Sequence of primers used for real-time PCR quantifications. Figure S1. Principal coordinates analysis (PCoA) and unsupervised hierarchical clustering of normalized RNA-Seq data. Figure S2. Expression profile of the components of the cortistatin pathway in b.End5 cells. Figure S3. Cortistatin modulates the immune function of activated b.End5 cells. Figure S4. Expression profile of the components of the cortistatin pathway in murine brain endothelial cells. Figure S5. Characterization of cortistatin in human brain endothelium Figure S6. Lack of barrier integrity and altered expression profile in cortistatin-deficient cells. Figure S7. Analysis of specific markers in BECs and validation of gene expression. Figure S8. Characterization of gene pathways in wild type vs cortistatin-deficient brain endothelium. Figure S9. Characterization of gene pathways in the dynamics of brain endothelium. Figure S10. Cortistatin restores the integrity of injured brain endothelial cells.