Abstract:
:Although VEGFR-3 deficiency disrupts blood vascular development during early embryogenesis, the underlying mechanism was not clear. To characterize its function in angiogenesis and lymphangiogenesis, we employed two genetically modified mouse models in this study, targeting the coding region for the ligand-binding domain (Vegfr3(ΔLBD)) or the tyrosine kinase domain with an inactivation point mutation (Vegfr3(TKmut)). We show that lymphatic growth was disrupted in Vegfr3(ΔLBD/ΔLBD) and Vegfr3(TKmut/TKmut) mice, but blood vessels developed normally in both embryo and yolk sac. Interestingly, in Vegfr3(ΔLBD/ΔLBD) but not Vegfr3(TKmut/TKmut) mice, lymph sac was present but there was lack of lymphangiogenic sprouting. We further demonstrate that both the wild-type and mutant forms of VEGFR-3 could form heterodimers with VEGFR-2, and decreased the level of phospho-VEGFR-2 and the downstream phospho-Erk1/2 in endothelial cells when they were treated with VEGF-A. These findings indicate that signaling mediated via VEGFR-3 activation by its cognate ligands (VEGF-C/-D) is not required for angiogenesis, and that VEGFR-3 may play a role in this process by modulating VEGFR-2-mediated signals.
journal_name
Cell Resjournal_title
Cell researchauthors
Zhang L,Zhou F,Han W,Shen B,Luo J,Shibuya M,He Ydoi
10.1038/cr.2010.116subject
Has Abstractpub_date
2010-12-01 00:00:00pages
1319-31issue
12eissn
1001-0602issn
1748-7838pii
cr2010116journal_volume
20pub_type
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