Abstract
Lymphangiogenesis, the formation of lymphatic vessels, plays key roles in embryonic development and wound healing. We and other groups have reported that impaired blood vessel formation suppresses compensatory lung growth after pneumonectomy (PNX). However, the role of lymphatics in regenerative lung growth remains unknown. Here we find that lymphangiogenesis is stimulated in the mouse lung after PNX and expression of PROX1, which plays key roles in lymphatic development, and a major lymphatic growth factor, VEGFR3 is higher in the post-PNX mouse lungs compared to that in sham-operated control mice. Diphtheria toxin-induced depletion of lymphatic vessels or treatment with VEGFR3 inhibitor inhibits post-PNX lung growth. VEGFC stimulates lymphatic vessel formation in the gel implanted on the mouse lungs, while VEGFR3 inhibitor inhibits the effects. These results suggest that lymphangiogenesis is stimulated during lung growth after PNX through VEGFC-VEGFR3 signaling. Modulation of lymphangiogenesis may provide a novel strategy for lung regeneration.
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