Pathogenesis of persistent lymphatic vessel hyperplasia in chronic airway inflammation
J. Clin. Invest. Peter Baluk, et al. 115:247 doi:10.1172/JCI22037 [
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Figure 3Overexpression of VEGF family growth factors by adenoviral vectors. Tracheal lymphatic vessels (red) and blood vessels (green) 10 days after intranasal inoculation of nude mice with adenoviral vectors. (
A) Transduction of airway epithelial cells by adenovirus encoding LacZ (Adeno-LacZ), shown by X-gal staining (inset, blue), had no apparent effect on lymphatic vessels (arrows) or blood vessels (arrowheads). (
B) Adenoviral VEGF induced angiogenesis (arrowheads) but no detectable lymphangiogenesis (arrows). (
C) Adenoviral VEGF-C induced extensive lymphangiogenesis (arrows) but no angiogenesis (arrowheads). (
D) Adenoviral VEGF-D induced widespread lymphangiogenesis but no apparent change in blood vessels (arrowheads); lymphatic vessels appear to coalesce (arrows). Scale bar in
D (100 μm) applies to all figures. (
E) Northern blot showing human VEGF-C (hVEGF-C) and VEGF-D mRNA in extracts of lungs 10 days after inoculation with adenoviral LacZ, human VEGF-C, or human VEGF-D ΔNΔC. (
F) Results of ELISA showing VEGF-C and VEGF-D protein in lungs 10 days after inoculation with adenoviral LacZ, human VEGF165, VEGF-C, or VEGF-D ΔNΔC.
