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Publication : Transmembrane protein ESDN promotes endothelial VEGF signaling and regulates angiogenesis.

First Author  Nie L Year  2013
Journal  J Clin Invest Volume  123
Issue  12 Pages  5082-97
PubMed ID  24177422 Mgi Jnum  J:207629
Mgi Id  MGI:5559263 Doi  10.1172/JCI67752
Citation  Nie L, et al. (2013) Transmembrane protein ESDN promotes endothelial VEGF signaling and regulates angiogenesis. J Clin Invest 123(12):5082-97
abstractText  Aberrant blood vessel formation contributes to a wide variety of pathologies, and factors that regulate angiogenesis are attractive therapeutic targets. Endothelial and smooth muscle cell-derived neuropilin-like protein (ESDN) is a neuropilin-related transmembrane protein expressed in ECs; however, its potential effect on VEGF responses remains undefined. Here, we generated global and EC-specific Esdn knockout mice and demonstrated that ESDN promotes VEGF-induced human and murine EC proliferation and migration. Deletion of Esdn in the mouse interfered with adult and developmental angiogenesis, and knockdown of the Esdn homolog (dcbld2) in zebrafish impaired normal vascular development. Loss of ESDN in ECs blunted VEGF responses in vivo and attenuated VEGF-induced VEGFR-2 signaling without altering VEGF receptor or neuropilin expression. Finally, we found that ESDN associates with VEGFR-2 and regulates its complex formation with negative regulators of VEGF signaling, protein tyrosine phosphatases PTP1B and TC-PTP, and VE-cadherin. These findings establish ESDN as a regulator of VEGF responses in ECs that acts through a mechanism distinct from neuropilins. As such, ESDN may serve as a therapeutic target for angiogenesis regulation.
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