Simultaneous Boron Ion-Channel/Growth Factor Receptor Activation for Enhanced Vascularization

Patricia Rico, Aleixandre Rodrigo-Navarro, Marcos de la Peña, Vladimira Moulisová, Mercedes Costell, Manuel Salmerón-Sánchez

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8 Citations (Scopus)


Boron ion is essential in metabolism and its concentration is regulated by ion-channel NaBC1. NaBC1 mutations cause corneal dystrophies such as Harboyan syndrome. Here a 3D molecular model for NaBC1 is proposed and it is shown that simultaneous stimulation of NaBC1 and vascular endothelial growth factor receptors (VEGFR) promotes angiogenesis in vitro and in vivo with ultralow concentrations of VEGF. Human umbilical vein endothelial cells' (HUVEC) organization into tubular structures is shown to be indicative of vascularization potential. Enhanced cell sprouting is found only in the presence of VEGF and boron, the effect abrogated after blocking NaBC1. It is demonstrated that stimulated NaBC1 promotes angiogenesis via PI3k-independent pathways and that α5β1vβ3 integrin binding is not essential to enhanced HUVEC organization. A novel vascularization mechanism that involves crosstalk and colocalization between NaBC1 and VEGFR receptors is described. This has important translational consequences; just by administering boron, taking advantage of endogenous VEGF, in vivo vascularization is shown in a chorioallantoic membrane assay.

Original languageEnglish
Article number1800220
JournalAdvanced Biosystems
Issue number1
Publication statusPublished - Jan 2019
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biomaterials
  • Biomedical Engineering
  • General Biochemistry,Genetics and Molecular Biology


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