Figure 5. Endothelial Sema3G contributes to the coordination of vascular remodeling.

(A) Representative images showing increased empty collagen IV–positive (green) but IB4-negative (magenta) matrix sleeves (yellow arrowheads) at the angiogenic front and in remodeling plexus of P6 Cdh5-Cre Sema3G^fl/fl mice. (B) Quantification of the ratio of IB4-positive vessels to collagen IV–positive vessels at the P6 angiogenic front (left, Sema3G^fl/fl, n = 7 mice; Cdh5-Cre Sema3G^fl/fl, n = 6 mice) and in remodeling plexus (right, n = 6 mice for each group). (C) Confocal images of anti–VE-cadherin–stained (green) and IB4-stained (red) (upper panel) or anti-desmin–stained (green) and IB4-stained (red) (lower panel) vascular plexus in P6 retinas. Arrowheads indicate EC-EC contacts with absent VE-cadherin signals. (D) Quantitation of vessel segments without a continuous junctional VE-cadherin signal (left, normalized to total IB4-labeled segments, n = 5 mice) and desmin-positive pericyte coverage in remodeling plexus (right, n = 4 mice). (E) Schematic illustration of the postnatal retinal angiogenesis model in Sema3G^fl/fl and Cdh5-Cre Sema3G^fl/fl mice. The postnatal retinal angiogenesis model could proceed as an overshooting reaction followed by the pruning of excessive vessels. Endothelial Sema3G deletion causes a hyperpruned vascular network in growing retinal vessels. Error bars represent mean ± SEM. *P < 0.05; **P < 0.01; 2-tailed Student’s t tests. Scale bars: 100 μm (A and C); magnified images: 50 μm (A and C).