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. 2015 Nov 3;125(12):4572–4586. doi: 10.1172/JCI82045

Figure 8. DLL4 expression is dependent on active VEGFR3 and VEGFR2 signaling.

Figure 8

(A) Whole-mount immunostaining of DLL4 (white, arrow) on lacteals (LYVE1, red) of mice treated with control IgG, αVEGFR2, or αVEGFR3 blocking antibodies. Perinuclear DLL4 intensity/lacteal volume (mean ± SD); n = 3. (B) Serum-starved LECs transfected with control, VEGFR2, VEGFR3, and VEGFR2/VEGFR3 (R2+R3) siRNA were treated for 24 hours with either BSA or VEGFC and analyzed by Western blotting. Data are representative of 2 independent experiments. (C) Serum-starved LECs were treated with BSA, VEGFC, and VEGFC C156S for 24 hours and analyzed by Western blotting. Data are representative of 2 independent experiments. (D) Quantification of lacteal filopodia after αVEGFR2 or αVEGFR3 treatment. LEC filopodia/villus (mean ± SD); n = 3. (E) Representative whole-mount images of intestinal villus blood capillaries (PECAM1, green) and lacteals (LYVE1, red) after αVEGFR2 or αVEGFR3 treatment. Lacteal length (mean ± SD) binned for given lengths after 2 weeks of antibody administration; n = 3. Scale bars: 10 μm, A; 50 μm, E. *P < 0.05, **P < 0.01, ***P < 0.001, 2-tailed unpaired Student’s t test (E) or 1-way ANOVA with Bonferroni correction (A and D).