Fig. 3

Characterisation of GLAST-HIF-1α^fl/fl mouse line. A PCR genotyping demonstrates excision of floxed HIF-1α exon 2 in genomic DNA from brain cortices of tamoxifen (LoF) or oil (Ctrl) treated GLAST-CreER^T2; HIF-1α^fl/fl mice. Tamoxifen treatment led to generation of a short 300 bp truncated product of HIF-1α (HIF-1α^Δ) compared to the 1.1kbp full-length product (HIF-1α^F). B Co-immunostaining of GLAST-CreER^T2; HIF-1α^fl/fl brain sections for GFAP (green) and Cre recombinase (red) in the brain cortex. Scale bar = 50 µm. C Immunoblot of brain cytoplasmic and nuclear fractions confirm tamoxifen-induced nuclear translocation of Cre recombinase in GLAST-CreER^T2; HIF-1α^fl/fl mice. β-actin was used as loading control. D Glut1 and VEGF mRNA expression in primary astrocytes isolated from GLAST-CreER^T2; HIF-1α^fl/fl mice after tamoxifen (2 µM) or vehicle treatment and 48 h hypoxic exposure (1% O₂). Two-way ANOVA, mean ± SD, n = 3–5, **p < 0.01, ***p < 0.001 compared to Hx Ctrl