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. Author manuscript; available in PMC: 2015 Feb 28.
Published in final edited form as: Circ Res. 2014 Jan 15;114(5):806–822. doi: 10.1161/CIRCRESAHA.114.303119

Figure 6. VEGFR-2 and VEGFR-3 in trachea of CCSP-VEGF-C mice.

Figure 6

A-D, Strong VEGFR-2 immunoreactivity (red) in tracheal blood vessels (arrowheads) and weak VEGFR-2 staining in lymphatics (arrows) compared to strong VEGFR-3 staining in lymphatics of CCSP-VEGF-C mice on water or doxycycline from P0 to P7 or P70 to P77. E, Expression of VEGFR-2 and VEGFR-3 mRNA in trachea of same groups as in A-D (N = 8 per group). *P < 0.05 vs. baseline at corresponding age. F, Western blots for VEGFR-2 and VEGFR-3 in trachea of same groups as in E (N = 10 per group). Loading control is beta-actin. In neonates, VEGFR-2 protein was increased 2-fold and VEGFR-3 was increased 7-fold after doxycycline. In adults, VEGFR-2 protein was increased 2-fold and VEGFR-3 was increased 4-fold after doxycycline. G, J, Lymphatics stained for LYVE-1 (red) in tracheal whole mounts of neonatal (G) or adult (J) mice after doxycycline plus PBS, anti-VEGFR-2 antibody DC101, anti-VEGFR-3 antibody mF4-31C1, or both antibodies for 7 days. Scale bar: 80 μm (A-D); 200 μm (G, J). H, I, K, Extent of inhibition of lymphangiogenesis in CCSP-VEGF-C mice treated with doxycycline and inhibitory antibodies used in G and J. LYVE-1-positive lymphatics were assessed over entire trachea of neonatal mice at P7 (H) or by measuring sprouts over cartilage rings at P7 (I) or P77 (K). * P < 0.05 vs. PBS. † P < 0.05 vs. mF4-31C1.