Additional file 1 of Three-dimensional microenvironment regulates gene expression, function, and tight junction dynamics of iPSC-derived blood–brain barrier microvessels

Additional file 1: Figure S1. Characterization of iBMEC phenotype following differentiation in 1 mL or 2 mL of medium. Figure S2. TEER and permeability measurements of 2D iBMEC confluent monolayers. Figure S3. Media volume effect on phenotype of 2D iBMEC confluent monolayers. Figure S4. Details of bulk RNA sequencing and iPC characterization. Figure S5. Benchmarking iBMEC gene expression to brain microvessel, endothelial, and epithelial datasets. Figure S6. Abundance measurements of endothelial and epithelial transcripts across cell sources and model types. Figure S7. Images of angiogenic sprouts across models. Figure S8. Assessment of tight junction dynamics in confluent iBMEC monolayers. Figure S9. Time course of morphological metrics across cell types. Figure S10. Violin plots of metrics across cell types. Figure S11. Response of three-dimensional iBMEC microvessels to wound formation by laser ablation. Figure S12. Comparison of morphological metrics between homeostasis, ablation, and melittin exposure. Figure S13. Monolayer area dynamics during wound healing and melittin exposure. Table S1. Summary of bulk RNA transcriptomes used in this study. Table S2. Antibodies used in this study. Note S1. Validation of media volume effect on TEER. Note S2. Variability of iBMEC differentiation. Note S3. Mechanisms of media volume effect on iBMEC phenotype. Note S4. Calculation of permeability in 2D and 3D. iBMEC differentiation. Transwell barrier characterization. Oxygen and glucose recordings. Pericyte differentiation and characterization.