Fig. 9: Smad2 genetic deficiency rescues the vascular malformation in TfamECKO mice. | Nature Communications

Fig. 9: Smad2 genetic deficiency rescues the vascular malformation in TfamECKO mice.

From: Mitochondrial dysfunction induces ALK5-SMAD2-mediated hypovascularization and arteriovenous malformations in mouse retinas

Fig. 9

Retinal tissues from WT, TfamECKO, Smad2ECKO and double knockout (DKO) mice were harvested at P15. ac Attenuation of arterialization and microaneurysm formation in the DKO retinas. Whole mount co-staining with α-SMA, endomucin (EMCN) and CD31. Arrowheads indicate normal or normalized vessels and arrows indicate microaneurysm in the mutant retinas. Asterisks indicate arterialized microvessels. α-SMA coverage (α-SMA/CD31 ratio) and vascular density were quantified. n = 6 mice per group. A: artery/arterial; V: vein. df Whole mount staining for CD31. Vasculatures in three retinal layers (surface, intermediate and deep) were imaged by confocal microscopy analyses, and pseudo-colored by red, blue and green, respectively. TfamECKO retinas had only the surface vessels with malformation and microaneurysms (arrows). Normal (WT and Smad2ECKO) or normalized capillaries in DKO are indicated by arrowheads. Vessel density and branch points were quantified. n = 6 mice per group. Data are means ± SEM. P values are indicated, using one-way ANOVA followed by Tukey’s multiple comparisons test. Scale bar: 50 μm (a); 25 μm (d). Source data are provided as a Source Data file.

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