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. 2018 Apr 25;31:190–201. doi: 10.1016/j.ebiom.2018.04.021

Fig. 2.

Fig. 2

N-PRβ-KO adult mice show severe retinal blood vessel defects.

(a) N-PRβ-KO mice show retinal blood vessel defects in both males and females at the adult stage (8–12 weeks old). Immunofluorescence of CD31 (red) and collagen type IV (cyan) depict retinal vasculature and blood vessel specific ECM deposition of N-PRβ-KO mice compared with WT. (b and c) Ratio of the CD31-positive area compared to the whole area of the retina. N-PRβ-KO mice showed significantly higher ratios for both males (b) and females (c) compared with WT in the adult stage. n = 15 for males and females. (d and e) Ratio of the collagen type IV-positive area compared to the whole area of the retina. N-PRβ-KO mice showed significantly higher ratios for both males (d) and females (e) compared with WT in the adult stage. n = 15 for males and females. (f) Multi-colour representative immunofluorescence images of WT (upper row) and N-PRβ-KO mice (bottom row) at 10 weeks old. CD31-positive blood vessels (red), CD13-positive pericytes (green), collagen type IV deposition (cyan). Arrowheads indicate empty sleeves. (g and h) Percentage of pericyte coverage on the retinal vasculature of N-PRβ-KO mice. N-PRβ-KO mice showed significantly lower coverage rates for both males (g) and females (h) compared with WT in the adult stage. n = 20 randomly selected areas (20× objective lens) from 5 retinas of males and females. All values represent the mean ± SEM. ***, p < 0.001, compared to WT. Scale bar = 1 mm (a), 100 μm (f).