FIGURE 3.

Combined inactivation of Phd2 and Phd3 but not inactivation of Phd2 alone promotes cerebral vascular expansion. A, Representative immunofluorescent images of frozen brain sections from Cre⁻ control, NG2‐Phd2^−/−, NG2‐Phd2^−/−Phd3^−/− (NG2‐Phd2,3^−/−) and NG2‐Phd1^−/−Phd2^−/−Phd3^−/− (NG2‐Phd1‐3^−/−) mice stained for PDGFRB, CD31 and collagen IV; scale bar, 100 µm. B, Quantification of cortical PDGFRB‐, CD31‐ and collagen IV‐positive areas expressed as percentage of Cre⁻ control (n = 3‐6). C, Relative cortical mRNA transcript levels in homogenates from cortex of Cre⁻ control, NG2‐Phd2^−/−, NG2‐Phd2^−/−Phd3^−/− and NG2‐Phd1^−/−Phd2^−/−Phd3^−/− mice expressed as fold‐change compared to Cre⁻ control (n = 4‐11). D, Phd3 transcript levels in striatum (ST), hypothalamus (HYT); cortex (CTX) and hippocampus (HP) from Cre⁻ control and NG2‐Phd2^−/− mice. Data are represented as mean ± SEM; one‐way ANOVA followed by Tukey's post hoc analysis; *P < .05, ^† P < .01 and ^‡ P < .001 compared with Cre⁻ control; ^f P < 0.05, ^ff P < 0.01, and ^fffP < 0.001 compared with NG2‐Phd2^−/−Phd3^−/− mice. Angpt1, angiopoietin 1; Angpt2, angiopoietin 2; Cxcl12, C‐X‐C motif chemokine 12; Fgf2, fibroblast growth factor 2; Tgfb1, transforming growth factor beta 1; Vegfa, vascular endothelial growth factor A