Fig. 2: Dysfunctional BMECs in hypoxia block OPC differentiation.

a The mRNA level of classic hypoxia-related genes of control, CoCl₂- and OGD-treated BMECs (n = 4 independent primary cell cultures/group). b, c Representative images and quantifications of endothelial proliferation (EdU⁺) and apoptosis (TUNEL⁺) (n = 5 independent primary cell cultures/group). Scale bar, 20 μm. d Immunofluorescent staining of ZO-1 or Claudin-5 in BMECs (n = 5 independent primary cell cultures/group). Scale bar, 20 μm. e, f Immunoblotting showing ZO-1, Claudin-5, Occludin expression of BMECs with or without ischemia. Results represent the mean for the relative band intensity of five replicates. g, h Proliferating OPCs (Ki67⁺PDGFRα⁺Olig2⁺) grown in control CM and CoCl₂−, OGD-treated CM and its quantification (n = 5 independent primary cell cultures/group). Scale bar, 20 μm. i–k Representative immunofluorescent images and quantifications showing the percentage of OPC differentiation (n = 5 independent primary cell cultures/group). Scale bar, 20 μm. l, m Immunoblotting analyses of PDGFRα, MBP, CNPase expression in OPCs of 3 groups. Results represent the mean for the relative band intensity of five replicates. For immunoblotting experiments, protein samples derived from the same experiment and gels/blots were processed in parallel. All data are presented as the mean ± SD. The data were compared by one-way ANOVA with Tukey post hoc test. Source data are provided as a Source Data file.