Figure 7.

Loss of Cav-1 reduces NG2 on enlarged branch retinal veins without affecting mural cell coverage and increases concomitant venous αSMA immunoreactivity. A–H: Retinas from WT and Cav-1 KO mice were immunostained with antibodies against mural cell markers, NG2 (green) (A and F), PDGFRβ (blue) (C and G), and αSMA (red) (D and H). Cav-1 deficiency in branch retinal veins significantly reduced NG2 expression and increased αSMA expression (F and H), compared with WT (B and D), but loss of Cav-1 did not noticeably decrease PDGFRβ in either genotype (C and G). I–L: Higher magnification images correspond to boxed regions in panels A and E. Cav-1 KO veins are not devoid of NG2⁺ cells (K and L), with weakly NG2⁺ cells visible on branch retinal veins (arrowheads), but the intensity is significantly weaker than in WT (I and J). M–P: Retinas from WT (M and N) and Cav-1 KO (O and P) mice were stained against CD31 (red) and NG2 (green). CD31 immunoreactivity was similar in both genotypes. Q: Fluorescence intensity was quantified from CD31, NG2, PDGFRβ, and αSMA staining in WT and Cav-1 KO retinal vasculature. Results suggest an intrinsic mural cell phenotype alteration due to the loss of Cav-1, rather than to altered mural cell coverage. Data are expressed as means ± SEM. n = 5–8 per group. ^∗P < 0.05, ^∗∗∗∗P < 0.0001 versus WT. Scale bars: 50 μm (A–H); 10 μm (I–L); and 20 μm (M–P).