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Durré, Tania; Morfoisse, Florent; Erpicum, Charlotte; Ebroin, Marie; Blacher, Silvia; García-Caballero, Melissa; Deroanne, Christophe; Louis, Thomas; Balsat, Cédric; Van de Velde, Maureen; Kaijalainen, Seppo; Kridelka, Frédéric; Engelholm, Lars; Struman, Ingrid; Alitalo, Kari; Behrendt, Niels; Paupert, Jenny; Noel, Agnès
Nature communications, 12/2018, Letnik: 9, Številka: 1Journal Article, Web Resource
The development of new lymphatic vessels occurs in many cancerous and inflammatory diseases through the binding of VEGF-C to its receptors, VEGFR-2 and VEGFR-3. The regulation of VEGFR-2/VEGFR-3 heterodimerisation and its downstream signaling in lymphatic endothelial cells (LECs) remain poorly understood. Here, we identify the endocytic receptor, uPARAP, as a partner of VEGFR-2 and VEGFR-3 that regulates their heterodimerisation. Genetic ablation of uPARAP leads to hyperbranched lymphatic vasculatures in pathological conditions without affecting concomitant angiogenesis. In vitro, uPARAP controls LEC migration in response to VEGF-C but not VEGF-A or VEGF-CCys156Ser. uPARAP restricts VEGFR-2/VEGFR-3 heterodimerisation and subsequent VEGFR-2-mediated phosphorylation and inactivation of Crk-II adaptor. uPARAP promotes VEGFR-3 signaling through the Crk-II/JNK/paxillin/Rac1 pathway. Pharmacological Rac1 inhibition in uPARAP knockout mice restores the wild-type phenotype. In summary, our study identifies a molecular regulator of lymphangiogenesis, and uncovers novel molecular features of VEGFR-2/VEGFR-3 crosstalk and downstream signaling during VEGF-C-driven LEC sprouting in pathological conditions.
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