XB-IMG-23636
Xenbase Image ID: 23636
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Fig. 3. Defective lymphatic vessel development in compound Foxc1+/−; Foxc2−/− mutants. (A–D) Immunohistochemical analysis to detect a lymphatic endothelial cell marker, Prox1, using transverse sections at the level of the heart at E10.5 (A, B) and E11.5 (C, D). (A, B) Although compound Foxc1+/−; Foxc2−/− mutant embryos (B) show the budding of lymphatic endothelial cells (arrows) from the cardinal vein, the number of Prox1-positive cells appears to be reduced compared to the wild type (A). (C, D) At E11.5, wild-type embryos (C) have well-formed lymph sacs (asterisks) and the sprouting of lymphatic endothelial cells (arrows). By contrast, abnormal formation of the lymph sacs and the reduced sprouting of lymphatic endothelial cells are observed in compound Foxc1+/−; Foxc2−/− mutants (D). (E) Quantitative analysis of Prox1-positive cells in wild-type and compound Foxc1+/−; Foxc2−/− mutant embryos at E10.5 and E11.5. The number of Prox1-positive cells is significantly reduced in compound Foxc1+/−; Foxc2−/− mutants at both E10.5 (P < 0.01) and E11.5 (P < 0.01). Data are collected from three embryos per genotype. (F–M) Section in situ hybridization at E10.5 (F–I) and E11.5 (J–M) at the level of the heart. In adjacent sections of wild-type embryo at E10.5 (F–H), expression domains of Foxc1 (F) and Foxc2 (G) in the developing lymphatic region are partially overlapped with those of VEGF-C (H) as indicated by arrows. VEGF-C expression is significantly reduced in compound Foxc1+/−; Foxc2−/− mutant embryos at E10.5 (I) and E11.5 (K), compared to wild-type embryos (H, J). By contrast, expression levels of VEGFR-3 in lymphatic endothelial cells (arrowheads) are normal in compound Foxc1+/−; Foxc2−/− mutant (M), compared to wild-type embryo (L). cv, cardinal vein; da, dorsal aorta. Scale bars, 50 μm (A–D) and 100 μm (I and M). Image published in: Seo S et al. (2006) Copyright © 2006. Image reproduced with permission of the Publisher, Elsevier B. V. Larger Image Printer Friendly View |