Figure 6. Reduced Notch signaling augments the loss of Eogt in retinal angiogenesis.
(A) Images of vessel density in P5 retinas from Eogt−/− compared to compound mutant mice. (B) Scatter plots represent branch point numbers in P5 retinas from Eogt−/− compared with compound mutant mice, normalized to Eogt+/+ mice. The average number of branch points for the Eogt+/+ used to compare mice with an N1− or Rbpj− allele was 237 ± 5, and for the Eogt+/+ compared to mice with an N12f or N1lbd allele was 380 ± 36 (500 X 500 μm field (n = 3–8 fields per retina), N = 2–6 mice). (C) Scatter plots showing the number of filopodia in P5 compound mutant mice as compared to Eogt−/− mice, normalized to Eogt+/+ mice. Each symbol represents the average number of filopodia per mouse (250 × 250 µm field (n = 4–12 fields per mouse), N = 2–4 mice. The average for Eogt+/+ compared to mice with a N1- or Rbpj- allele was 30 ± 1 per mm and for mice with a N112f or N1lbd allele was 36 ± 4 per mm, taken as 1.0 for normalization. (D) Images of branch points in P15 retinas comparing Eogt−/− to compound mutant mice as indicated. (E) Scatter plots shows branch points in compound mutants compared to Eogt−/− P15 retinas, normalized to Eogt+/+ mice. The average of the Eogt+/+ used to compare mice with a with a N1− or Rbpj− allele was 73 ± 3, and for mice with a N112f or N1lbd allele it was 69 ± 12 (500 x 500 µm field (n = 3–8 fields per retina), N = 3–6 mice. Data represent mean ± standard error except for P5 Eogt+/+Notch1+/− filopodia and P5 Eogt+/+Notch1+/lbd branch points and filopodia that are represented as mean ± range; p values were calculated by unpaired two-tailed Student’s t-test. *p≤0.05; **p≤0.01; ***p≤0.001.