Fig. 4
From: aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability
aPKCλ regulates c-Myc abundance and signaling via miR-34c. a Expression of miR-34c in control or PRKCI KD siRNA treated HUVEC. Data represent mean ± S.E.M. two-tailed unpaired t-test *p < 0.05 (n = 5). b Expression of miR-34c in PrkciiΔEC and control P6 retina. Data represent mean ± S.E.M. two-tailed unpaired t-test *p < 0.05 (n ≥ 8). c Expression of miR34c after overnight serum starvation with and without aPKC kinase inhibitor treatment in HUVEC; Data represents mean + /- S.E.M., Mann Whitney test; **p < 0.01 (n ≥ 8). d ChIP of FoxO1-CA and FoxO1-CA/D from the FoxO1 binding site of the miR-34c promoter region in HUVEC. Data represent mean ± S.E.M. one-way ANOVA with Bonferroni post-hoc analyses; ns p > 0.05; *p < 0.05 (n = 4). e Staining of c-Myc (green) and IB4 (red) with c-Myc channel alone in right panels in P6 PrkciiΔEC and control mouse retina after treatment with anti-miR-34c or scrambled control. Representative staining of > 3 animals of each genotype and treatment; Scale bar represents 100 μm. f Percentage of c-Myc positive EC cells per field (upper) and endothelial cell coverage region in P6 retina of PrkciiΔEC after treatment with anti-miR-34c or scrambled control. Data represent mean ± S.E.M. two-way ANOVA with Bonferroni post-hoc analyses; **p < 0.01; *p < 0.05; ns p > 0.05 (n = 3–5). g IB4 (red) and ERG1/2/3 (green) staining in the P6 retina of PrkciiΔEC after treatment with anti-miR-34c or scrambled control. Representative staining of > 3 animals of each genotype and treatment; Scale bar represents 200 μm. h Relative expression of FoxO1-regulated genes involved in c-Myc signaling measured by RT-PCR in HUVEC. Data represent mean ± S.E.M. two-tailed unpaired t-test ns p > 0.05; *p < 0.05; **p < 0.01 (n ≥ 3)
