Fig. 1: Effects of selective VEGFR2 and/or VEGFR3 activation on postnatal lymphangiogenesis.
From: VEGFR2 is required for VEGF-C–VEGFR3–PI3Kα-mediated sprouting lymphangiogenesis
a VEGF-VEGFR interactions and experimental scheme for AAV-mediated overexpression of VEGF ligands in the ear. Whole mount immunofluorescence of mouse ear dermis two weeks after injection of AAVs encoding different VEGFs showing their different effects on lymphatic capillaries (b) and collecting vessels (c). Dashed boxed areas are magnified on the right (b). d Diameter of collecting vessels in AAV-treated mice, represented as mean ± s.d. (WT: n = 4 (Control), 3 (VEGF-C C156S), 4 (VEGF-A164) mice; Vegfr2flox/flox;Vegfr1-CreERT2: n = 4 (Control), 4 (VEGF-A164) mice). ****p < 0.0001; One-way ANOVA followed by Tukey’s multiple comparison test. e Overexpression of VEGF in the ear of a mouse lacking Vegfr2 in BECs and treated with the VEGF-C trap, showing only small vascular lesions (arrowheads) due to expansion of residual unrecombined cells, and no lymphatic vessel alterations, quantified in (d). Similar results were observed in 4/4 mice with confirmed VEGF overexpression. Scale bar: 200 µm (b,e, overviews), 50 µm (b, e, high magnification, c). Illustrations in (a, e) created using BioRender (https://www.biorender.com).
